MSc Biomedical Basis of Disease. Pain Theory for...

46
Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015 1 Pain Theory for Therapists Introducing the Biopsychosocial Model by Alan P Smith BSc(Hons) MSc DO 2 Alan Smith Osteopath since obtaining DO in 1994. MSc Biomedical Basis of Disease. Sheffield Hallam University, 1999. BSc(Hons) in Physical Science. Leicester University Contact Details [email protected] www.ebmseminars.co.uk 38 Barroon, Castle Donington, Derby DE74 2PE. Tel: 01332 853777 Objectives To Better Understand Pain Mechanisms To “Introduce” the Biopsyhcosocial Model To Learn New Clinical Skills in Treating Patients’ Pain Relevance of Understanding Pain Most patients will have pain Pain generates the anxiety that motivates the patient seek help The better we understand pain the more efficiently we can identify & treat the cause What Is Pain? IASP Definition Pain is "an unpleasant sensory and emotional experience associated with actual or potential tissue damage , or described in terms of such damage.“ Pain motivates us to withdraw from potentially damaging situations, protect a damaged body part while it heals, and avoid those situations in the future. International Association for the Study of Pain 1979 Pain is a Multidimensional Experience Sensory-Discriminitive Intensity, Location, Quality Affective-Motivational Unpleasantness, Suffering, Urge to Escape Cognitive-Evaluative Appraisal, Threat past experiences, conditioning

Transcript of MSc Biomedical Basis of Disease. Pain Theory for...

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

1

Pain Theory for Therapists Introducing the Biopsychosocial Model

by Alan P Smith BSc(Hons) MSc DO

2

Alan Smith bull Osteopath since obtaining DO in 1994

bull MSc Biomedical Basis of Disease

Sheffield Hallam University 1999

bull BSc(Hons) in Physical Science

Leicester University

Contact Details

alan_smith_ostyahoocouk

wwwebmseminarscouk

38 Barroon Castle Donington Derby DE74 2PE Tel 01332 853777

Objectives

bull To Better Understand Pain Mechanisms

bull To ldquoIntroducerdquo the Biopsyhcosocial Model

bull To Learn New Clinical Skills in Treating Patientsrsquo Pain

bull To Earn More Money

Relevance of Understanding Pain

bull Most patients will have pain

bull Pain generates the anxiety that

motivates the patient seek help

bull The better we understand pain the more efficiently we can identify amp treat the cause

What Is Pain IASP Definition

Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue

damage or described in terms of such damageldquo

Pain motivates us to withdraw from potentially damaging situations protect a damaged body part while it heals and

avoid those situations in the future

International Association for the Study of Pain 1979

Pain is a Multidimensional Experience

Sensory-Discriminitive Intensity Location Quality

Affective-Motivational Unpleasantness Suffering Urge to Escape

Cognitive-Evaluative Appraisal Threat ndash past experiences conditioning

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

2

Pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply

determined by the magnitude of the painful stimulus but higher cognitive activities can influence perceived intensity and

unpleasantness

Pain can be treated not only by trying to cut down the sensory input but also by influencing the motivational-affective and

cognitive factors as well

Pain is a Multidimensional Experience

Cognitive activities may affect both sensory and affective experience or they may modify primarily the affective-motivational

dimension

Pain in the Absence of Physical Injury is sometimes referred to as

ldquoPhysiological Painrdquo

It Stops as soon as you Withdraw or ldquoEscaperdquo from the Stimulus

Pain in the Presence of Physical Injury (Pathology) is sometimes referred to as

ldquoPathophysiological Painrdquo

Here the stimulus will have a component from the products of Inflammation and Pain Impulses will Bombard the CNS for some

Considerable Time

Physiological amp Pathophysiological Pain

How Do We Treat PatientsrsquoPain

Find the Tissue Lesion

Treat the Lesioned Tissue - to assist healing

Resolution

This is the Traditional Physical Therapy Approach

Understanding amp Treating Pain

Tissue Injury

Nociceptor Firing

CNS

PAIN

Tissue Injury

Nociceptor Firing

CNS

PAIN

Gate

Anxiety Worry

Uncertainty lsquoThreatrsquo

THERAPY Belief Trust

Reassurance (Distraction)

Rubbing Shaking TENS

PathoanatomicalBiomedical Model (Bottom-up) Biopsychosocial Model (Bottom-up and Top-Down)

Professor Eyal Lederman DO PhD is the director of the Centre for Professional Development in Osteopathy and Manual Therapy London

2010

ldquoThe effectiveness of most medical interventions is derived partially from contextual or nonspecific factors commonly referred to as placebo effects These

effects have demonstrated remarkable potency for the alleviation of pain and under certain circumstances placebos have produced effect sizes

indistinguishable from established medications surgeries and other analgesic treatmentsrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

3

ldquoAlthough the effects of manual therapy are classically explained within a biomechanical paradigm research now points to the important role of

neurophysiological processes at both spinal and supraspinal levels in the modulation of nociceptive informationrdquo hellip ldquoin clinical practice manual therapy

articular mobilizations andor manipulations are seldom being used as an isolated interventionrdquohellip ldquocombining various strategies imparts a synergistic

effect on the brain-orchestrated analgesic systemrdquo

2015 Understanding amp Treating Pain

Tissue Injury

Nociceptor Firing

CNS

PAIN

Gate

Anxiety Worry

Uncertainty lsquoThreatrsquo

THERAPY Belief Trust

Reassurance (Distraction)

Rubbing Shaking TENS

Biopsychosocial Model (Bottom-up and Top-Down)

Targets for Treating Pain

1) Tissues Traditional Modalities 2) Gate Non-specific (lsquoplaceborsquo) 3) Consciousness Distraction

ldquoCognitive distraction could be mediated mainly by direct frontal-corticol somatosensory interactions without the engagement of brainstem pain-

control systemsrdquo ldquoPlacebo analgesia does not depend on active redirection of attention and that expectancy and distraction can be combined to maximize

pain reliefrdquo

2012

C Stimulus

Pain is Generated in the Brain

Reneacute Descartes

(1596-1650)

Descartes wrote ldquoThe flame particle jumps from the fire

touches the toe moves up the spinal cord until a little bell goes off in the brain and says lsquoouch It

hurtrsquordquo

Treatise of Man 1662

It is a disturbance which passes along nerve fibres to the brain

Reneacute Descartes ndash Pain is a disturbance that passes along nerve fibres to the brain

The Cartesian Legacy

bull Pain is a Direct Measure of Tissue Damage

bull Brain amp CNS Play a Passive Role

bull No Reason to Look Beyond the Painful Tissues bull In Chronic Pain Tissues are Not Healing and Damage is Ongoing

bull Stopping the Stimulus is the Way to Stop Pain ndash Or Cutting the Wire

bull lsquoMind-Body splitrsquo Pain is Either Physical Or Psychological (Mental Illness)

Pain Management Main CJ et al 2nd Edition 2008 Churchill Livingstone

ldquoIn the past decade scientific evidence has shown that the biomedical model falls short in the treatment of patients with musculoskeletal pain To understand musculoskeletal pain and a patients health behavior and beliefs physical therapists should assess the illness perceptions of their patientsrdquo ldquoThe overall impression was that the assessments of the physical therapists were still bio-medically oriented in these patients with chronic musculoskeletal painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

4

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

ldquoTrust your patient they are telling you the truth it is up to you to find out why If your patient tells you they have widespread pain they do even if

you cannot understand itrdquo

2014

Answers from Neuroscience A Pain Theory Revolution Was Happening

On returning to university (SHU) in 1996 faculty of Biomedical Science I found

bull Pain theory was a hot topic

bull Biomedical model was being overthrown by the lsquoBiopsychosocialrsquo bull A number of landmark discoveries had been made in the 80rsquos

bull Knowledge was largely contained within the academic world of neuroscience

Louis Gifford M App Sc BSc MCSP

httpwwwachesandpainsonlinecomaboutusphp

It is not an exaggeration to say that this book marks a milestone not only for an understanding of pain but also for the maturation of physiotherapy Professor Patrick Wall (1925 ndash 2001) Review 1998

Subsequently adopted as core reading for post graduate and undergraduate training programmes in the UK and abroad

Research Physiotherapist international lecturer Author of the Yearbooks of the Physiotherapy Pain Association (1994) for Chartered Physiotherapists

David Butler M App Sc (NOI)

Physiotherapist international freelance educator senior lecturer at the University of South Australia and a director of the NOI

httpwwwactuariesasnauACS2011ProgramPlenarySpeakersaspx

ldquoI believe the ideal approach in the clinic should be one that encompasses three things the best skills from current therapy the best information from science and the best therapeutic relationship

with a particular patientrdquo

Integrating pain awareness into physiotherapy-wise action for the future In Gifford Topical Issues in Pain 1 1998

Sensory Receptor Afferent Nerve (Axon) C

Mechanoreceptors Touch

Thermoreceptors Cold Warm

Photoreceptors Colour Light

Audioreceptors Sound

Chemoreceptors Taste Smell

Proprioreceptors Position etc body parts

Interoreceptors eg Baroreceptors Osmoreceptors

Nociceptors (Mechano ndash Chemo) Pain

Exteroreceptors enable us to make sense of the External Physical World

Sensation amp Perception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

5

Everything we See Hear Taste and Smell and feel as Touch or Pain Exists in our brains

ldquoWe acknowledge that all the individual features of the world are experienced through our sense organs The information that reaches us through those organs is converted into electrical signals and the individual parts of our brain analyze and process these signals After this interpreting process takes place inside our brain we will for example see a book taste a strawberry smell a flower feel the texture of a silk fabric or hear leaves shaking in the windrdquo

httpwwwsecretbeyondmattercomourbrainstheworldinourbrainshtml

Stimulus Electrical Signal

Meaning

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Nociception

To brain

Zone of Lissauer

Substantia gelatinosa

Dorsal root

DRG

Ventral root

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Pain Cannot Exist Outside of Consciousness

Nociception

Nociception Can Occur Without the Brain

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

bull Damage has Occurred bull It has been Inflicted on the Toe bull Something Needs to be Done

(raise foot hobble utter expletive)

The Brain Decides

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

ldquoIt may feel as if our toe is throbbing but the experience is all contained within a mental projection of the

condition of our toe within our brainrdquo

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

httpgoldsmithsacademiaeduMaxVelmansPapers980457Physical_psychological_and_virtual_realities

Neural Activity (In The Brain) Can Result In Spatially Located

Extended Experiences

ldquoPerceptual processing in the brain can result in experiences that have a subjective location and extension beyond the brain In

Velmans (1990) I have called this phenomenon perceptual projection How spatial encodings and other encodings in the

brain are translated into such spatial phenomenology are matters for scientific researchrdquo Max Velmans

Max Velmans is an Emeritus Professor of Psychology at Goldsmiths University of London

httpwwwspracukexpcmsindexphpsection=87

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

2

Pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply

determined by the magnitude of the painful stimulus but higher cognitive activities can influence perceived intensity and

unpleasantness

Pain can be treated not only by trying to cut down the sensory input but also by influencing the motivational-affective and

cognitive factors as well

Pain is a Multidimensional Experience

Cognitive activities may affect both sensory and affective experience or they may modify primarily the affective-motivational

dimension

Pain in the Absence of Physical Injury is sometimes referred to as

ldquoPhysiological Painrdquo

It Stops as soon as you Withdraw or ldquoEscaperdquo from the Stimulus

Pain in the Presence of Physical Injury (Pathology) is sometimes referred to as

ldquoPathophysiological Painrdquo

Here the stimulus will have a component from the products of Inflammation and Pain Impulses will Bombard the CNS for some

Considerable Time

Physiological amp Pathophysiological Pain

How Do We Treat PatientsrsquoPain

Find the Tissue Lesion

Treat the Lesioned Tissue - to assist healing

Resolution

This is the Traditional Physical Therapy Approach

Understanding amp Treating Pain

Tissue Injury

Nociceptor Firing

CNS

PAIN

Tissue Injury

Nociceptor Firing

CNS

PAIN

Gate

Anxiety Worry

Uncertainty lsquoThreatrsquo

THERAPY Belief Trust

Reassurance (Distraction)

Rubbing Shaking TENS

PathoanatomicalBiomedical Model (Bottom-up) Biopsychosocial Model (Bottom-up and Top-Down)

Professor Eyal Lederman DO PhD is the director of the Centre for Professional Development in Osteopathy and Manual Therapy London

2010

ldquoThe effectiveness of most medical interventions is derived partially from contextual or nonspecific factors commonly referred to as placebo effects These

effects have demonstrated remarkable potency for the alleviation of pain and under certain circumstances placebos have produced effect sizes

indistinguishable from established medications surgeries and other analgesic treatmentsrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

3

ldquoAlthough the effects of manual therapy are classically explained within a biomechanical paradigm research now points to the important role of

neurophysiological processes at both spinal and supraspinal levels in the modulation of nociceptive informationrdquo hellip ldquoin clinical practice manual therapy

articular mobilizations andor manipulations are seldom being used as an isolated interventionrdquohellip ldquocombining various strategies imparts a synergistic

effect on the brain-orchestrated analgesic systemrdquo

2015 Understanding amp Treating Pain

Tissue Injury

Nociceptor Firing

CNS

PAIN

Gate

Anxiety Worry

Uncertainty lsquoThreatrsquo

THERAPY Belief Trust

Reassurance (Distraction)

Rubbing Shaking TENS

Biopsychosocial Model (Bottom-up and Top-Down)

Targets for Treating Pain

1) Tissues Traditional Modalities 2) Gate Non-specific (lsquoplaceborsquo) 3) Consciousness Distraction

ldquoCognitive distraction could be mediated mainly by direct frontal-corticol somatosensory interactions without the engagement of brainstem pain-

control systemsrdquo ldquoPlacebo analgesia does not depend on active redirection of attention and that expectancy and distraction can be combined to maximize

pain reliefrdquo

2012

C Stimulus

Pain is Generated in the Brain

Reneacute Descartes

(1596-1650)

Descartes wrote ldquoThe flame particle jumps from the fire

touches the toe moves up the spinal cord until a little bell goes off in the brain and says lsquoouch It

hurtrsquordquo

Treatise of Man 1662

It is a disturbance which passes along nerve fibres to the brain

Reneacute Descartes ndash Pain is a disturbance that passes along nerve fibres to the brain

The Cartesian Legacy

bull Pain is a Direct Measure of Tissue Damage

bull Brain amp CNS Play a Passive Role

bull No Reason to Look Beyond the Painful Tissues bull In Chronic Pain Tissues are Not Healing and Damage is Ongoing

bull Stopping the Stimulus is the Way to Stop Pain ndash Or Cutting the Wire

bull lsquoMind-Body splitrsquo Pain is Either Physical Or Psychological (Mental Illness)

Pain Management Main CJ et al 2nd Edition 2008 Churchill Livingstone

ldquoIn the past decade scientific evidence has shown that the biomedical model falls short in the treatment of patients with musculoskeletal pain To understand musculoskeletal pain and a patients health behavior and beliefs physical therapists should assess the illness perceptions of their patientsrdquo ldquoThe overall impression was that the assessments of the physical therapists were still bio-medically oriented in these patients with chronic musculoskeletal painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

4

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

ldquoTrust your patient they are telling you the truth it is up to you to find out why If your patient tells you they have widespread pain they do even if

you cannot understand itrdquo

2014

Answers from Neuroscience A Pain Theory Revolution Was Happening

On returning to university (SHU) in 1996 faculty of Biomedical Science I found

bull Pain theory was a hot topic

bull Biomedical model was being overthrown by the lsquoBiopsychosocialrsquo bull A number of landmark discoveries had been made in the 80rsquos

bull Knowledge was largely contained within the academic world of neuroscience

Louis Gifford M App Sc BSc MCSP

httpwwwachesandpainsonlinecomaboutusphp

It is not an exaggeration to say that this book marks a milestone not only for an understanding of pain but also for the maturation of physiotherapy Professor Patrick Wall (1925 ndash 2001) Review 1998

Subsequently adopted as core reading for post graduate and undergraduate training programmes in the UK and abroad

Research Physiotherapist international lecturer Author of the Yearbooks of the Physiotherapy Pain Association (1994) for Chartered Physiotherapists

David Butler M App Sc (NOI)

Physiotherapist international freelance educator senior lecturer at the University of South Australia and a director of the NOI

httpwwwactuariesasnauACS2011ProgramPlenarySpeakersaspx

ldquoI believe the ideal approach in the clinic should be one that encompasses three things the best skills from current therapy the best information from science and the best therapeutic relationship

with a particular patientrdquo

Integrating pain awareness into physiotherapy-wise action for the future In Gifford Topical Issues in Pain 1 1998

Sensory Receptor Afferent Nerve (Axon) C

Mechanoreceptors Touch

Thermoreceptors Cold Warm

Photoreceptors Colour Light

Audioreceptors Sound

Chemoreceptors Taste Smell

Proprioreceptors Position etc body parts

Interoreceptors eg Baroreceptors Osmoreceptors

Nociceptors (Mechano ndash Chemo) Pain

Exteroreceptors enable us to make sense of the External Physical World

Sensation amp Perception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

5

Everything we See Hear Taste and Smell and feel as Touch or Pain Exists in our brains

ldquoWe acknowledge that all the individual features of the world are experienced through our sense organs The information that reaches us through those organs is converted into electrical signals and the individual parts of our brain analyze and process these signals After this interpreting process takes place inside our brain we will for example see a book taste a strawberry smell a flower feel the texture of a silk fabric or hear leaves shaking in the windrdquo

httpwwwsecretbeyondmattercomourbrainstheworldinourbrainshtml

Stimulus Electrical Signal

Meaning

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Nociception

To brain

Zone of Lissauer

Substantia gelatinosa

Dorsal root

DRG

Ventral root

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Pain Cannot Exist Outside of Consciousness

Nociception

Nociception Can Occur Without the Brain

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

bull Damage has Occurred bull It has been Inflicted on the Toe bull Something Needs to be Done

(raise foot hobble utter expletive)

The Brain Decides

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

ldquoIt may feel as if our toe is throbbing but the experience is all contained within a mental projection of the

condition of our toe within our brainrdquo

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

httpgoldsmithsacademiaeduMaxVelmansPapers980457Physical_psychological_and_virtual_realities

Neural Activity (In The Brain) Can Result In Spatially Located

Extended Experiences

ldquoPerceptual processing in the brain can result in experiences that have a subjective location and extension beyond the brain In

Velmans (1990) I have called this phenomenon perceptual projection How spatial encodings and other encodings in the

brain are translated into such spatial phenomenology are matters for scientific researchrdquo Max Velmans

Max Velmans is an Emeritus Professor of Psychology at Goldsmiths University of London

httpwwwspracukexpcmsindexphpsection=87

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

3

ldquoAlthough the effects of manual therapy are classically explained within a biomechanical paradigm research now points to the important role of

neurophysiological processes at both spinal and supraspinal levels in the modulation of nociceptive informationrdquo hellip ldquoin clinical practice manual therapy

articular mobilizations andor manipulations are seldom being used as an isolated interventionrdquohellip ldquocombining various strategies imparts a synergistic

effect on the brain-orchestrated analgesic systemrdquo

2015 Understanding amp Treating Pain

Tissue Injury

Nociceptor Firing

CNS

PAIN

Gate

Anxiety Worry

Uncertainty lsquoThreatrsquo

THERAPY Belief Trust

Reassurance (Distraction)

Rubbing Shaking TENS

Biopsychosocial Model (Bottom-up and Top-Down)

Targets for Treating Pain

1) Tissues Traditional Modalities 2) Gate Non-specific (lsquoplaceborsquo) 3) Consciousness Distraction

ldquoCognitive distraction could be mediated mainly by direct frontal-corticol somatosensory interactions without the engagement of brainstem pain-

control systemsrdquo ldquoPlacebo analgesia does not depend on active redirection of attention and that expectancy and distraction can be combined to maximize

pain reliefrdquo

2012

C Stimulus

Pain is Generated in the Brain

Reneacute Descartes

(1596-1650)

Descartes wrote ldquoThe flame particle jumps from the fire

touches the toe moves up the spinal cord until a little bell goes off in the brain and says lsquoouch It

hurtrsquordquo

Treatise of Man 1662

It is a disturbance which passes along nerve fibres to the brain

Reneacute Descartes ndash Pain is a disturbance that passes along nerve fibres to the brain

The Cartesian Legacy

bull Pain is a Direct Measure of Tissue Damage

bull Brain amp CNS Play a Passive Role

bull No Reason to Look Beyond the Painful Tissues bull In Chronic Pain Tissues are Not Healing and Damage is Ongoing

bull Stopping the Stimulus is the Way to Stop Pain ndash Or Cutting the Wire

bull lsquoMind-Body splitrsquo Pain is Either Physical Or Psychological (Mental Illness)

Pain Management Main CJ et al 2nd Edition 2008 Churchill Livingstone

ldquoIn the past decade scientific evidence has shown that the biomedical model falls short in the treatment of patients with musculoskeletal pain To understand musculoskeletal pain and a patients health behavior and beliefs physical therapists should assess the illness perceptions of their patientsrdquo ldquoThe overall impression was that the assessments of the physical therapists were still bio-medically oriented in these patients with chronic musculoskeletal painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

4

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

ldquoTrust your patient they are telling you the truth it is up to you to find out why If your patient tells you they have widespread pain they do even if

you cannot understand itrdquo

2014

Answers from Neuroscience A Pain Theory Revolution Was Happening

On returning to university (SHU) in 1996 faculty of Biomedical Science I found

bull Pain theory was a hot topic

bull Biomedical model was being overthrown by the lsquoBiopsychosocialrsquo bull A number of landmark discoveries had been made in the 80rsquos

bull Knowledge was largely contained within the academic world of neuroscience

Louis Gifford M App Sc BSc MCSP

httpwwwachesandpainsonlinecomaboutusphp

It is not an exaggeration to say that this book marks a milestone not only for an understanding of pain but also for the maturation of physiotherapy Professor Patrick Wall (1925 ndash 2001) Review 1998

Subsequently adopted as core reading for post graduate and undergraduate training programmes in the UK and abroad

Research Physiotherapist international lecturer Author of the Yearbooks of the Physiotherapy Pain Association (1994) for Chartered Physiotherapists

David Butler M App Sc (NOI)

Physiotherapist international freelance educator senior lecturer at the University of South Australia and a director of the NOI

httpwwwactuariesasnauACS2011ProgramPlenarySpeakersaspx

ldquoI believe the ideal approach in the clinic should be one that encompasses three things the best skills from current therapy the best information from science and the best therapeutic relationship

with a particular patientrdquo

Integrating pain awareness into physiotherapy-wise action for the future In Gifford Topical Issues in Pain 1 1998

Sensory Receptor Afferent Nerve (Axon) C

Mechanoreceptors Touch

Thermoreceptors Cold Warm

Photoreceptors Colour Light

Audioreceptors Sound

Chemoreceptors Taste Smell

Proprioreceptors Position etc body parts

Interoreceptors eg Baroreceptors Osmoreceptors

Nociceptors (Mechano ndash Chemo) Pain

Exteroreceptors enable us to make sense of the External Physical World

Sensation amp Perception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

5

Everything we See Hear Taste and Smell and feel as Touch or Pain Exists in our brains

ldquoWe acknowledge that all the individual features of the world are experienced through our sense organs The information that reaches us through those organs is converted into electrical signals and the individual parts of our brain analyze and process these signals After this interpreting process takes place inside our brain we will for example see a book taste a strawberry smell a flower feel the texture of a silk fabric or hear leaves shaking in the windrdquo

httpwwwsecretbeyondmattercomourbrainstheworldinourbrainshtml

Stimulus Electrical Signal

Meaning

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Nociception

To brain

Zone of Lissauer

Substantia gelatinosa

Dorsal root

DRG

Ventral root

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Pain Cannot Exist Outside of Consciousness

Nociception

Nociception Can Occur Without the Brain

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

bull Damage has Occurred bull It has been Inflicted on the Toe bull Something Needs to be Done

(raise foot hobble utter expletive)

The Brain Decides

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

ldquoIt may feel as if our toe is throbbing but the experience is all contained within a mental projection of the

condition of our toe within our brainrdquo

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

httpgoldsmithsacademiaeduMaxVelmansPapers980457Physical_psychological_and_virtual_realities

Neural Activity (In The Brain) Can Result In Spatially Located

Extended Experiences

ldquoPerceptual processing in the brain can result in experiences that have a subjective location and extension beyond the brain In

Velmans (1990) I have called this phenomenon perceptual projection How spatial encodings and other encodings in the

brain are translated into such spatial phenomenology are matters for scientific researchrdquo Max Velmans

Max Velmans is an Emeritus Professor of Psychology at Goldsmiths University of London

httpwwwspracukexpcmsindexphpsection=87

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

4

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

ldquoTrust your patient they are telling you the truth it is up to you to find out why If your patient tells you they have widespread pain they do even if

you cannot understand itrdquo

2014

Answers from Neuroscience A Pain Theory Revolution Was Happening

On returning to university (SHU) in 1996 faculty of Biomedical Science I found

bull Pain theory was a hot topic

bull Biomedical model was being overthrown by the lsquoBiopsychosocialrsquo bull A number of landmark discoveries had been made in the 80rsquos

bull Knowledge was largely contained within the academic world of neuroscience

Louis Gifford M App Sc BSc MCSP

httpwwwachesandpainsonlinecomaboutusphp

It is not an exaggeration to say that this book marks a milestone not only for an understanding of pain but also for the maturation of physiotherapy Professor Patrick Wall (1925 ndash 2001) Review 1998

Subsequently adopted as core reading for post graduate and undergraduate training programmes in the UK and abroad

Research Physiotherapist international lecturer Author of the Yearbooks of the Physiotherapy Pain Association (1994) for Chartered Physiotherapists

David Butler M App Sc (NOI)

Physiotherapist international freelance educator senior lecturer at the University of South Australia and a director of the NOI

httpwwwactuariesasnauACS2011ProgramPlenarySpeakersaspx

ldquoI believe the ideal approach in the clinic should be one that encompasses three things the best skills from current therapy the best information from science and the best therapeutic relationship

with a particular patientrdquo

Integrating pain awareness into physiotherapy-wise action for the future In Gifford Topical Issues in Pain 1 1998

Sensory Receptor Afferent Nerve (Axon) C

Mechanoreceptors Touch

Thermoreceptors Cold Warm

Photoreceptors Colour Light

Audioreceptors Sound

Chemoreceptors Taste Smell

Proprioreceptors Position etc body parts

Interoreceptors eg Baroreceptors Osmoreceptors

Nociceptors (Mechano ndash Chemo) Pain

Exteroreceptors enable us to make sense of the External Physical World

Sensation amp Perception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

5

Everything we See Hear Taste and Smell and feel as Touch or Pain Exists in our brains

ldquoWe acknowledge that all the individual features of the world are experienced through our sense organs The information that reaches us through those organs is converted into electrical signals and the individual parts of our brain analyze and process these signals After this interpreting process takes place inside our brain we will for example see a book taste a strawberry smell a flower feel the texture of a silk fabric or hear leaves shaking in the windrdquo

httpwwwsecretbeyondmattercomourbrainstheworldinourbrainshtml

Stimulus Electrical Signal

Meaning

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Nociception

To brain

Zone of Lissauer

Substantia gelatinosa

Dorsal root

DRG

Ventral root

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Pain Cannot Exist Outside of Consciousness

Nociception

Nociception Can Occur Without the Brain

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

bull Damage has Occurred bull It has been Inflicted on the Toe bull Something Needs to be Done

(raise foot hobble utter expletive)

The Brain Decides

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

ldquoIt may feel as if our toe is throbbing but the experience is all contained within a mental projection of the

condition of our toe within our brainrdquo

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

httpgoldsmithsacademiaeduMaxVelmansPapers980457Physical_psychological_and_virtual_realities

Neural Activity (In The Brain) Can Result In Spatially Located

Extended Experiences

ldquoPerceptual processing in the brain can result in experiences that have a subjective location and extension beyond the brain In

Velmans (1990) I have called this phenomenon perceptual projection How spatial encodings and other encodings in the

brain are translated into such spatial phenomenology are matters for scientific researchrdquo Max Velmans

Max Velmans is an Emeritus Professor of Psychology at Goldsmiths University of London

httpwwwspracukexpcmsindexphpsection=87

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

5

Everything we See Hear Taste and Smell and feel as Touch or Pain Exists in our brains

ldquoWe acknowledge that all the individual features of the world are experienced through our sense organs The information that reaches us through those organs is converted into electrical signals and the individual parts of our brain analyze and process these signals After this interpreting process takes place inside our brain we will for example see a book taste a strawberry smell a flower feel the texture of a silk fabric or hear leaves shaking in the windrdquo

httpwwwsecretbeyondmattercomourbrainstheworldinourbrainshtml

Stimulus Electrical Signal

Meaning

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Nociception

To brain

Zone of Lissauer

Substantia gelatinosa

Dorsal root

DRG

Ventral root

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Pain Cannot Exist Outside of Consciousness

Nociception

Nociception Can Occur Without the Brain

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

bull Damage has Occurred bull It has been Inflicted on the Toe bull Something Needs to be Done

(raise foot hobble utter expletive)

The Brain Decides

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

When we Stub Our Toe it Hurts But only because Our Brain Says so

INJURY

PAIN

ldquoIt may feel as if our toe is throbbing but the experience is all contained within a mental projection of the

condition of our toe within our brainrdquo

httpwwwwellcomeacukenpainmicrositescience2html

httparchivesciencewatchcomdrfmf201111mayf

mf11mayfmfCrai

AD (Bud) Craig Principal InvestigatorDirector Atkinson Pain Research Laboratory Barrow Neurological Institute Phoenix

httpgoldsmithsacademiaeduMaxVelmansPapers980457Physical_psychological_and_virtual_realities

Neural Activity (In The Brain) Can Result In Spatially Located

Extended Experiences

ldquoPerceptual processing in the brain can result in experiences that have a subjective location and extension beyond the brain In

Velmans (1990) I have called this phenomenon perceptual projection How spatial encodings and other encodings in the

brain are translated into such spatial phenomenology are matters for scientific researchrdquo Max Velmans

Max Velmans is an Emeritus Professor of Psychology at Goldsmiths University of London

httpwwwspracukexpcmsindexphpsection=87

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

6

ldquoThe localisation of pain (and other tactile sensation) is a projection from the brain into 3-dimensional space To facilitate

this the brain makes use of a map of the body surface and lsquoperipersonal spacersquo ldquo

2012

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Perceived Pain in the Tissues is an Illusion Created by the Brain

Somatotopy Somatotopy The correspondence between the position of a receptor in part of

the body and the corresponding area of the cerebral cortex that is activated by it

httpneurocriticblogspotcouk2009_08_01_archivehtml

Penfieldrsquos Somatosensory Homunculus

httpwwwmadscientistblogcamad-scientist-5-

paracelsus-pt-2-paracelsus-homunculus

httpmvameeducationalbrain_areashtml

Neurosurgeon Wilder Penfield (1891ndash1976)mapped the body onto the brain by electrically stimulating the cortex of over 400 conscious epileptic patients and

noting their responses

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

ldquoMicro-electrode stimulation of the somatosensory cortex produces feelings of numbness and tingling which are

subjectively located in different regions of the body not in the brainmdashanother clear case of perceptual projectionrdquo

Max Velmans

2013

Sudden Pain-Related Signals need to be rapidly transformed into External Spatial Coordinates to facilitate defensive reactions and prevent tissue

damage Pain localisation appears to take place in S1 co-localised with touch and in the Insular Cortex where there is more lsquocoarsersquo somatotopic

representation of pain

Insular Cortex

S1 M1

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

7

The Posterior Parietal Cortex houses lsquoExternal Spatial Representationrsquo It Remaps touch from a Somatatopic to a lsquoSpatiotopicrsquo external spatial frame of

reference by integrating touch with proprioceptive information about body posture This area about the body is called lsquoPeripersonal Spacersquo

2010 S1 M1 Important Points ndash Pain Perception

bull Percieved pain is an illusion lsquoprojectedrsquo by the brain

bull Nociception arises in the tissues

bull Nociception can exist without pain

bull Pain can exist without nociception

bull Pain is generated in the brain

bull To the patient the whole pain experience is contained within the tissues

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors High Threshold Gated Ion Channels on Free Nerve Endings

Location

Externally Skin

Cornea Mucosa

Internally Muscles

Joints Bladder Gut etc

httpalexandriahealthlibrarycadocumentsnotesbomunit_6Lec202420Peripheral20mechanismsxml

Nociceptors amp LT Mechanoreceptors

TOUCH

PAIN

Pain amp Touch information travel to the brain in different Tracts ndash Dorsal Columns and Spinothalamic Tracts respectively

Schematic of ion channels in nociceptor function

Mechanical Noxious Cold ndash (lt5C) Protons (Acid-sensing-ion channel) Noxious Heat ndash (gt42C) Serotonin ATP Nerve Growth Factor Chemicals (G-protein-coupled receptors) eg histamine bradykinin prostaglandins

Capsaicin found in ldquoHotrdquo Peppers such as Red Chillies and Jalapenos is able to selectively activate the Trpv1 receptor and thus provides a

means of inducing pain experimentally without tissue damage

C

Stimulators of Nociception

Nociceptor Nociception (Axon)

Brain

Nociceptor Activators Mechanical pressure Thermal stimuli (gt42C lt5C) Chemical (inflammatory mediators or products of damaged cells) Potassium ions ATP Protons (acidity hypoxia) Histamine Serotonin Bradykinin

Nociceptor Sensitisers Chemical (released from damaged tissue or axon reflex) Prostaglandins Cytokines Substance P CGRP

Transduction Pain Conduction

Neuropeptides

CGRP = Calcitonin Gene Related Peptide

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

8

Axon Reflex ndash Neurogenic Inflammation Neuropeptides (eg Substance P CGRP) and Inflammation

Action potentials in branches of an afferent nociceptor can move

peripherallyThis is called the axon reflex The release of substance P and CGRP (sensitises) increases inflammation by causing histamine

release and dilation of blood vessels

httpcourseswashingtoneduconjsensorypainhtm

Mechanisms Associated with Peripheral Sensitisation to Pain

After an injury occurs there is a time-dependent expansion in the area of sensitivity as tissue that is not damaged becomes increasingly sensitive to any sort of stimulus that is applied This is called HYPERALGESIA

wwwpagesdrexeledu~mab337Pain20Lectureppt

C Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Peripheral Sensitisation (Hyperalgesia)

If there is tissue injury diffusion of the lsquoinflammatory souprsquo activates adjacent nociceptors causing the painful tender area to

expand The barrage of nociception is then the source of pathophysiological pain

Injury

A Critical Number of Open Sensors will Start the Response

Acute_Pain_Normal

httptriactionpotentialblogspotcom

Movie Clip ndash Key Points

Injury

Inflammatory Reaction

Electrical Signal - Fast Ad and Slow C Fibre Nociceptors

Dorsal Horn

Spinothalamic Tract

Thalamus

Cortex Frontal Lobe Limbic System

PERCEPTION - Texture amp Intensity Emotional Impact Link to Memory Meaning

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

9

Fast Ad Fibre Pain bull Sharp and well localised bull Nociceptive impulses synapse in the dorsal horn initiate withdrawal reflexes and travel to the sensory cortex via the thalamus

Slow C Fibre Pain bull Diffuse more burning and unpleasant ndash lingers bull Nociceptive impulses synapse with interneurons in the dorsal horn then travel to

1) Sensory cortex and insular cortex 2) Limbic System ndash memory and emotion 3) Hypothalamus (ANS) and brain stem

Only C fibres respond to Chemical stimulation

Fast amp Slow Acute Pain

Bear MF et al Neuroscience exploring the brain

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Can be Referred to as Projection Neurons

Dorsal Horn Neurons 2nd Order Neurons

httpwwwrnceuscomagesnociceptivehtm

They arise from Lamina 1 as Nociception

Specific (NS) neurons and Lamina V as Wide Dynamic

Ranging (WDR) neurons

NS

WDR

How Mechanoreceptor Activity Can Decrease Nociceptive Processing

(Why Movement and Rubbing Decreases The Perception of Pain)

Melzack and Wallrsquos Pain Gate Theory was the first real challenge to the Pathoanatomical model It postulated that nociception could be lsquomodulatedrsquo at the dorsal horn

and that some lsquointegrationrsquo of nociceptive and other sensory

information could occur

httppublicationsmcgillcaheadwaymagazine

the-king-of-understanding-pain-qa-with-ronald-melzack

naturecom

Ronald Melzack Patrick Wall

1965

R Melzack PD Wall Pain mechanisms a new theory Science 1965150971ndash979

Neurons That Conduct Nociception (Pain Impulses) to the Brain

Many interneurons and interconnections within

the dorsal horn allow integration of different sensory channels Eg Inhibitory interneurons

can be activated by touch and propriceptive input to deep laminae to lsquogatersquo NS

output from lamina 1

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

As Wall himself wrote evaluating the gate theory in the light of further experiments lsquolsquoThe least and perhaps the best that can be said for the 1965

paper is that it provoked discussion and experimentrsquorsquo

2014

Free Access httpwwwsciencedirectcomscience

articlepiiS0306452214007830

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

10

Neurons That Conduct Nociception (Pain Impulses) to the Brain

httpwwwrnceuscomagesnociceptivehtm

NS

WDR

NS neurons are more associated with the emotional suffering

dimension of pain Also autonomic motivational

amp homeostatic responses

WDR neurons are mainly associated with the

sensory discriminative dimension of pain ndash location amp intensity

Spinal Polysynaptic Interneurons (PSINs) (Eg Flexor amp Crossed Extensor Reflex)

httpalexandriahealthlibrarycadocumentsnotesbomunit_6lec2025_moo_spinreflexxml

Withdrawal reflexes are mainly initiated by Ad fibres and involve

interneurons that cross the midline

Other cord level responses effected by nociceptors and interneurons include altered muscle tone and sympathetic effects (sweating vasoconstrictiondilation) via links to the preganglionic cell bodies in the lateral horn

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Experiment to Demonstate Secondary Hyperalgesia with Capsaicin induced Nociception

Nerve Block (local anaesthetic)

Nerve Block

Capsaicin

Amplification

R L R L

C Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Mental Projection

Amplifier

Injury

Discovery of the dorsal horn amplifier proved that the pain circuitry exhibits lsquoactivity-dependent-synaptic-plasticityrsquo It is not

hard-wired

Clifford Woolf Discovered central sensitization whilst researching at University College London alongside Patrick Wall and published his findings in 1983 (Woolf CJ Evidence for a central component of post-injury pain hypersensitivity Nature 1983 306686-8)

ldquo pain does not simply reflect the presence intensity or duration of specific lsquopainrsquo stimuli in the periphery but also changes in the

function of the central nervous systemrdquo

Woolf CJ Central sensitization ndashuncovering the relation between pain and plasticity Anesthesiology 2007106864-7

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

11

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Central Sensitisation

Mental Projection

Amplifier

Transduction

C

C

C C

C C

C

C

C C

C C C

C

C C C

C

Peripheral amp Central Sensitisation Stimulus

Injury + Inflammation

Dorsal Horn Amplification

Amplification In The Brain

PNS CNS

C

C

C

C C C

C Peripheral amp Central Sensitisation

As Inflammation Resolves Peripheral Sensitisation dies down but Central Sensitisation

sometimes persists to be the cause of Chronic pain

lsquoNormallyrsquo ndash Pain goes

lsquoPathologicalrsquo ndash Pain becomes Chronic Brain continues to generate pain Cortical Reorganisation

Dorsal Horn Amplifier stays on High Gain

PAIN

Important Points ndash Pain Sensitisation

bull Peripheral sensitisation drives central sensitisation

bull Secondary hyperalgesia (central sensitisation) gives additional warning of the need to protect the injured anatomy whilst it is inflamed thus assisting healing

bull Perceived worsening pain and an often massive spread of tenderness into multiple tissues is mainly on account of central sensitisation These tissues are not all injured

bull Pain circuitry is not hard-wired

bull Spreading pain is lsquobeyond dermatomesrsquo

Glutamate amp NMDA Receptors Main Neurotransmitter Released by C Fibres

During prolonged excitation the sum of EPSPs lowers the membrane potential sufficiently for the NMDA channels to expel their magnesium molecule allowing an influx of Ca2+ This triggers the release of retrograde messengers that stimulate the

release of more glutamate from the pre-synaptic membrane This all leads to a greater response from the secondary nerve

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Glutamate normally opens only AMPA channels because NMDA channels are blocked by a magnesium molecule

Substance P Sensitising Neuropeptides Also Released by C Fibres

Subtance P and CGRP sensitise the secondary nerve to glutamate Within the dorsal horn these can diffuse around several levels of the spinal cord sensitising

other secondary nerves (dorsal horn neurons) in the process

What was previously an innocuous stimulus may now be perceived as pain and pain may be perceived at a seemingly unrelated anatomical site

Substance P

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

12

Long Term Potentiation ndash Remodelling (Activity Dependent Plasticity)

Bliss TVP amp Cooke SF Long-term potentiation and long-term depression a clinical perspective Clinics 201166(S1)3-17

bull Glutamate release binds to bull AMPAR Na+ influx and bull NMDAR (blocked by Mg2+) bull If depolarisation sufficient a) Mg2+ plug removed b) NMDAR Ca2+ influx bull Ca2+ signals coincidence and activates enzymes a) Enhance AMPARs b) Increase AMPAR number c) Retrograde nitric oxide pre-synaptic glutamate bullCa2+ -more than a few hours a) Signals to cell nucleus b) Altered gene expression c) Structural changes d) Sprouting of dendrites e) Inhibitory interneuron f) Enhanced transmission

Long Term Potentiation ndash Remodelling Activity-Dependent Synaptic Reconfiguration

Ever Increasing Calcium Influx into the Secondary Neuron can cause More Permanent Synaptic (Neuroplastic) Changes Known as

Remodelling or Structural Changes

bull Increase release of retrograde messenger induces greater glutamate release bull Glutamate reaches levels that are toxic to inhibitory interneurons at the dorsal horn and so causes their destruction lsquoPruningrsquo bullDorsal horn may grow new nerves and connections so that innocuous sensation feeds into the pain system lsquoSproutingrsquo

Long-Term Potentiation (LTP) bull Defn A long-lasting enhancement in signal transmission

between two neurons that results from stimulating them synchronously bull One of several phenomena underlying synaptic plasticity the ability of chemical synapses to change their strength bull Memories are encoded by modification of synaptic strength LTP is widely considered one of the major cellular mechanisms that underlies learning and memory

Cells that fire together wire togetherldquo Hebbrsquos Rule Donald Hebb 1949

Synaptic Remodelling

Sensitisation starts as functional electrochemical changes that are reversible

Remodelling (Structural Changes) can make pain amplification more Permanent

ldquoEffective pain control can prevent these changes but it is much more difficult reverse themrdquo

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Healthy Tissue Feels Injured

Peripheral amp central sensitisation can make healthy tissue feel painful amp hypersensitive

Allodynia Painful to Touch

Hyperalgesia Extra Painful to Noxious Stimulation

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

13

2009

httpwwwncbinlmnihgovpmcarticlesPMC2852643

2009

Cellular and molecular mechanisms of pain Basbaum AI et al Cell 2009139(2)267-84

Somatosensory cortex Physical location quality intensity

Insular cortex Feeling

unpleasantness suffering

Cingulate cortex Evaluates context for

behavioural response Eg Escape

What is Pain

ldquopain is both a specific sensation and a variable emotional staterdquo ldquopain normally originates from a physiological condition of the body that

automatic (subconscious) homeostatic systems alone cannot rectifyrdquo

2003

ldquoChanges in the mechanical thermal and chemical status of the tissues ndash stimuli that can cause pain ndash are important for homeostatic maintenance of

the bodyrdquo

2003

Bud Craig argues we form an image of all of the bodys unique homeostatic

sensations in the brains primary interoceptive cortex located in the

insular cortex which is modulated by input from cognitive affective and reward-related circuits It embodies conscious awareness of the whole

bodys homeostatic state

Pain A Homeostatic (Primordial) Emotion

Homeostatic emotions such as pain hunger thirst and fatigue are attention-demanding feelings evoked by body states that drive behaviour (withdrawal

eating drinking or resting in these examples) aimed at maintaining homeostasis

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

14

Insular Cortex ndash lsquoHow we Feelrsquo The limbic-related insular cortex plays

a role in a variety of homeostatic functions related to basic survival

needs such as taste visceral sensation and autonomic control

The insula controls autonomic functions through the regulation of

the sympathetic and parasympathetic systems

The insula represents homeostatic integration of the condition of the body and all regions of the brain associated with feelings It is also activated by the emotions displayed by others - empathy It represents how we feel and integrates this with homeostatic motor function At any moment in time it represents awareness of

ourselves others and our environment ndash consciousness itself

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

(ACC)

(PAG)

WHERE WHAT

The sensory-discriminative and affective-emotional components of pain are processed in different

parts of the brain They are integrated with other

information - from memory stores and from the situation at hand etc to assess lsquothreatrsquo value future implications etc All this is blended as the

unified unpleasant experience we call pain

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

CNS Ascending Pain Pathways

parabrachial nucleus

NS (lamina I) and WDR (lamina V) neurons form the

Spinothalamic Tract

This gives off branches to other centres eg

Spinohypothalamic Pathway (subconscious autonomic)

Spinomesencephalic Tract (Parabrachial nucleus to

insula amygdala ACC amp PAG)

Thalamus sends fibres to somatosensory cortex

(ACC)

(PAG)

WHERE WHAT

The Brain

bull The brain weighs about 3lbs

bull The brain contains about 100 billion neurons and many more support cells

bull Each neuron is capable of connecting to thousands of others

httpwwwuheduenginesepi2821htm

The Brain ndash Frontal Lobe

bull This is the most recent evolutionary addition

bull It makes up 20 of the human brain

bull Its development is not complete until we are in our 30s

bull At the forefront of the frontal lobe is the prefrontal cortex (PFC)

bull The PFC facilitates our most complex cognitive reasoning behavioural and emotional capabilities

httpwwwwiredtowinthemoviecommindtrip_xmlhtml

The Neuromatrix of Pain There is No Single lsquoPain Centrersquo

When you are experiencing pain the activity of many specific areas of your brain is altered These areas are interconnected and form a network that some neuroscientists call the pain matrix Different areas are often associated with different aspects of pain

httpwwwdentalumarylandedudentaldeptsneural_pain_sciencesseminowiczhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

15

Thalamus amp Ascending Nociception

The thalamus is terminus for ascending nociceptive fibres It acts like a giant switchbox

Somatosensory cortex

httpthebrainmcgillcaflashdd_03d_03_crd_03_cr_doud_03_cr_douhtml

Many WDR fibres synapse in the lateral thalamus whose cells are arranged

somatotopically Neurons from them pass to the somatosensensory cortex for

analysis regarding location and intensity

Some NS fibres synapse in the medial thalamus forming connections to many centres (including forebrain and limbic areas) that collectively represent the emotional (aversive) quality of pain

Limbic System - Seat of our Emotions

httpcwxprenhallcombookbindpubbooksmorris5chapter2custom1deluxe-contenthtml

Amygdala (Almond-shaped structure)

Hippocampus (Seahorse-shaped structure)

Limbic System ndash Memory amp Emotion Hippocampus

bull Storage and Retrieval of Long-term lsquoExplicitrsquo Memories such as Facts Pieces of Information bull The Amygdala lsquoTagsrsquo incoming information with an Emotional Value The more Intense the Emotion the Deeper the information is Etched into Memory bullWhen we Recall a Memory (from the Hippocampus) we also Recall the Emotion Associated with it

Limbic System ndash Memory amp Emotion Amygdala

bull Storage and Retrieval of Long-term lsquoImplicitrsquo Memories such as Procedural Skills Emotional Memories

bull Vital for the Expression and Interpretation of Emotion

bull Sets the Emotional Tone of any experience

bull It is our FEAR and ANXIETY Centre It can set off an lsquoalarmrsquo reaction (like a panic button) very quickly before you know it and activate the HPA

httppotrehabcomcannabis-reduces-perception-of-threat

The amygdala lets us react almost instantaneously to the presence of danger So rapidly that often we lsquostartlersquo first and realize only

afterward what it was that frightened us

The subconscious ldquoshort routerdquo provides only crude discrimination of potentially threatening situations It is the cortex that provides the confirmation a few fractions of a second later via the ldquolong routerdquo as to whether danger is actually present Those fractions of a second could be fatal if we had not already begun to react to the danger

httpthebrainmcgillcaflashdd_04d_04_crd_04_cr_peud_04_cr_peuhtml

Amygdala ndash Fear Reaction

300ms

20ms

Amgydala ndash Fear Reaction (The Amygdala Never Forgets)

httpwaitingcomblog200811paranoia-on-the-rise-experts-sayhtml

httpamygdalanet

Through life the amygdala remembers the things you felt saw and heard each time you had a painful or threatening experience Even subliminal hints of these can trigger lsquoknee jerkrsquo flight or fight responses Such fear responses to real or lsquoperceivedrsquo threats can become overwhelming

A fear of pain can lead to avoidance of the situation where it arose and avoidance of

movement or activities that cause only mild discomfort ndash fear of (re)injury

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

16

httpmedics4uwebscomeconepidemiopsychologyhtm

Taming the Amygdala Habits emotional responses and behavioural patterns are implicit memories Conditioned fears (for example) can be unconscious mediated by sub-cortical pathways that connect thalamus to amygdala

Systematic Desensitisation Graded exposure to (irrational) fearful stimuli repeated over time can generate a new memory for safety

Hypothalamus

ldquoThe hypothalamus tunes the body to facilitate whatever the personrsquos intentions and emotions

demandrdquo

The pain modulatory system is a part of this

Other effects are mediated by the Sympathetic Nervous System and Hypothalamus-Pituitary-Adrenal (HPA) Axis

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Referred Pain - lsquoBrain Gets it Wrongrsquo Pain perceived at a location other than the site of the

painful stimulus

Neuropathic Arising from lesion of the nervous system

eg Compressed peripheral nerve (Now includes pain caused by functional changes of

the nervous system arising from neuroplasticity)

Visceral or Somatic Arising from Convergence of nociceptors

eg Viscerally referred pain trigger point pain

Neuropathically Referred Pain

Peripheral Nerve Injury

X

(Abnormal Impulse Generating Site) ldquoAIGSrdquo

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

httpwwwhumanneurophysiologycomsensorypathwayshtm

C

Nociceptor

Peripheral Nerve

Transduction

Conduction Spinal Nerve

Transmission C

Localisation Interpretation

Meaning

C

Spatial Projection

Convergence of Sensory Information bull Loss of Discrimination bull Referred Pain bull Referred Tenderness bull Very Few Spinal Neurons are Dedicated to

Transmission of Visceral Nociception

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

17

httpwwwamicusvisualsolutionscom

Viscerally Referred Pain Convergence of Nociceptive Input From the Viscera and the Skin

Our Brain Can Generate Misleading Illusions Or Be A Source of Pain Itself

Important Points ndash Referred Pain

bull Pain is said to be referred if is perceived to be at a location other than the source ndash brain lsquoprojectsrsquo to the wrong place

bull Referred pain can arise as a result of a) Convergence (visceral myofascial somatic) a) Injury to nerves in the pain circuitry (neuropathy) b) Dysfunction of pain circuitry (central sensitisation) d) Phantom

bull All pain is referred from the brain

bull Pain is said to be local if it is perceived to be at the source

bull Parts of our anatomy can hurt when therersquos nothing wrong

CNS lsquoFeedbackrsquo Can Modulate Pain Signals

Descending Pain Modulation

httpwwwccaccaenCCAC_ProgramsETCCModule1007html Phase_of_Nociceptive_Pain

Brain Stem

Central sensitisation is opposed (or

sometimes enhanced) by nerves that descend down from the brain to

exert their influence at the dorsal horn

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Descending Modulation can Turn the Amplifier Down ndash Reducing Nociceptive Transmission Or Turn the Amplifier Up ndash Facilitating Nociceptive Transmission

Descending Modulation of Nociception Schematic view of the

interrelationship between cerebral structures involved in the

initiation and modulation of descending controls of

nociceptive information

PAG Periaqueductal grey NTS nucleus tractus solitarius PBN parabrachial nucleus DRT dorsoreticular nucleus RVM rostroventral medulla NA noradrenaline 5-HT serotonin

httpmeagherlabtamueduM-Meagher20Health20Psyc20630Readings20630Pain20mech20readMillan2002pdf

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

18

Mark J Millan Progress in Neurobiology200266355ndash474

Descending Control of Nociception

PAG-RVM-Spinal cord pathways are subject to

ldquoBottom Uprdquo feedback inhibition

ldquoTop Downrdquo (from cortex) control (eg Cognitive and emotional regulation) PAG (amp RVM nuclei) also send projections to higher pain-related centres of the brain (eg thalamus and frontal lobes) to effect central modulation of pain

PAG-RVM-Spinal Cord Pathway

Handbook of Clinical Neurology Vol81 (3rd series Vol3) 2006 Endogenous pain modulation Ch13 Descending inhibitory systems Pertovaara A and Almeida A

Midbrain (3) PAG (Periaqueductal Gray) Medulla (5) RVM (Rostral-Ventral Medulla) Contains Raphe Nuclei Locus Coeruleus

Descending Control of Nociception

Stimulation of the PAG causes analgesia so profound that surgery can be performed

wwwpagesdrexeledu~mab337Pain20Lectureppt

RVM

Periaqueductal Gray

The PAG is the main relay station for descending modulation of nociception

It send projections to other relays lower in the brainstem such as the Raphe situated within the Rostral-Ventral Medulla (RVM) These then send

projections down to dorsal horn neurons

The activation sequence for the descending pathways involve brain structures such as the DLPFC (an area involved in predictions based

on beliefs) which through synaptic connections using opioids communicates with the ACC This structure then via limbic centres activates the

PAG and then the raphe nuclei and other nuclei in the brainstem Complex modulations

occur at each of these sites

Descending Control of Nociception

Opioids (opiates)are the main neurotransmitters used within the brain Opioid receptors are found

particularly within the DLPFC ACC PAG and also the spinal cord

Receptors for Enkephalins are known as delta receptors d

Receptors for Endorphins are known as mu receptors m

Receptors for Dynorphins are known as kappa receptors k

There are three well-characterized families of opioids produced by the body

Enkephalins Endorphins and Dynorphins

Neurotransmitters Involved in Pain Suppression Opioids

Hypothalamus Projection neurons use dopamine

RVM

Neurotransmitters Involved in Pain Suppression Serotonin amp Nor-Adrenaline

Descending projection neurons from the RVM to the dorsal horn do not use opioids

Raphe Magnus Projection neurons use serotonin

Locus Coeruleus (A6) Projection neurons use nor-adrenaline

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

19

ldquothe hypothalamus is the principle source of descending dopaminergic pathwaysldquo ldquo the dopaminergic descending pathway has an antinociceptive

effect via D2-like receptors on SG neurons in the spinal cordrdquo

2011

httpthalamuswustleducoursebodyhtml

Pain Modulation Dorsal Horn Serotonin (5-HT) from the

Raphe amp Noradrenaline (NA) from the LC are released at

the dorsal horn

They can prevent the primary afferent from passing on its signal

by blocking neurotransmitter release

They can inhibit the secondary afferent so it does not send the

signal up to the brain

Activate inhibitory interneurons containing enkephalin GABA or

glycine

Important Points ndash Descending Modulation

bull Resting tone is anti-nociceptive (descending analgesia)

bull Responds to lsquoperceivedrsquo threat inhibitory or facilitatory In acute situations can suppress massive nociception or can result in massive pain for very little nociception In chronic situations can contribute to lsquohabituationrsquo or lsquosensitisationrsquo ndash the latter significant in chronic pain bull Provides a plausible (neurobiological) mechanism for many lsquotherapiesrsquo some previously catagorised as placebo

bull Operates subconsciously

bull Can be tapped into in multiple ways during our treatments

Descending Pain Control - Further Reading

1) Descending control of pain Millan MJ Progress in Neurobiology2002355ndash474

2) Endogenous Pain Modulation Ch13 Descending Inhibitory Systems 2006

Pertovaara A amp Almeida A Handbook of Clinical Neurology Vol81 Pain

3) Descending control of nociception specificity recruitment and plasticity Heinricher

MM et al Brain Research Reviews 200960(1)214-225

Brain lsquoFeedbackrsquo Can Modulate Pain Signal

Pain Modulation

Emergence of the Bio-Psycho-Social Model of Pain Pain is a Multidimensional Phenomenon

End of the Patho-Anatomical Model which assumes that

Pain Circuitry is Hard-Wired and that Somatic Pain is Proportionate to Tissue Pathology

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons in the brain can Regroup and Remodel (sprout new branches) according to Incoming Information

With Repetition it becomes Easier for them to Fire Again in the Same Pattern in the Future ndash Breeds Habits

Only by Regular Usage does a neuronal pathway Remain Strong and Healthy ndash Long-term Potentiation (LTP)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

20

The Brain ndash Activity Dependent Plasticity Essence of Learning

Neurons that lsquofirersquo together lsquowirersquo together

Neurons that lsquofirersquo apart lsquowirersquo apart Out of synch ndash lose the link

lsquoSynaptic Pruningrsquo

Mental practice alone contributes to rewiring the brain

The Brain ndash Activity Dependent Plasticity Essence of Learning

Activity dependent plasticity starts by reconfiguration of the electrochemical relationship between neurons then

later the genes within the neurons are turned on to enhance this

Brain-Derived-Neurotrophic-Factor (BDNF) production is activated by glutamate It enhances neuronal growth and

vitality If sprinkled onto neurons in a petri dish they sprout new branches

lsquoMiracle Growrsquo

Cortical Plasticity

During most of the 20th century the general consensus among neuroscientists was that brain structure is

relatively immutable after a critical period during early childhood This belief has been challenged by new

findings revealing that many aspects of the brain remain plastic into adulthood

httpenwikipediaorgwikiNeuroplasticity

Cortical Plasticity amp Chronic Pain

ldquoPain syndromes are likely to involve changes of cortical representation These changes may form a

lsquopain memoryrsquo that can be triggered by stimuli that are not necessarily painful in themselvesrdquo

Hubert van Griensven

Pain In Practice 2005 Elsevier Ltd

httpnewsbbccouk1hihealth7219344stm

Consultant Physiotherapist

Pain In Practice Hubert van Griensven 2005 Elsevier Ltd

Cortical Processing of Pain

1) Forebrain Pain Mechanisms Neugebauer V et al httpwwwncbinlmnihgovpmcarticlesPMC2700838

2) Forebrain mechanisms of nociception and pain Analysis through imaging Casey KL httpwwwncbinlmnihgovpmcarticlesPMC33599

References

3) Chronic non-specific low back pain ndash sub-groups or a single mechanism Benedict M Wand and Neil E OConnell httpwwwbiomedcentralcom1471-2474911

Biomedical Pain amp Placebo

According to the Biomedical Model bull Pain we feel should Always be Proportionate to the Stimulus (because the pain circuitry is hard-wired not plastic) bull There is no other lsquoPlausiblersquo Mechanism

bull If Pain is Disproportionate to lsquoPathologyrsquo the Patient is at Fault Hysterical Imagining Psychosomatic Malingerer Liar etc

bull Anything that Affects Pain (but has no essential Efficacy) attracted the label lsquoPLACEBOrsquo C

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

21

There are now known to exist physiological mechanisms whereby pain

can fluctuate according to our mood

attention and expectation A mechanism for Placebo Analgesia

Summary

Placebo - Latin ldquoI will pleaserdquo

Placebo Historically Associated With Trickery Dishonesty Fake Sham or

just lsquoQuackeryrsquo

Definition A substance or procedurehellip that is objectively without specific activity for the

condition being treated

ttpwwwwiredcommedtechdrugsmagazine17-

09ff_placebo_effectcurrentPage=all

Placebo is a Real Neurobiological Phenomenon

Dr Fabrizio Benedetti MD PhD professor of physiology and

neuroscience University of Turin Medical School

ldquothe placebo effect is a real neurobiological phenomenon where something happens in the patientrsquos brainrdquo

It is triggered not by the ingredients of the placebo itself but by what it symbolises In a clinical setting there are

many symbolic factors which Benedetti refers to collectively as the lsquopsychosocial contextrsquo

httpwwwincamresearchcaindexphpid=195540010

Power of Placebo

Real Placebo

Active Drug

Spontaneous

Remission

etc

Apportionment of patient benefits for

antidepressant drug use in the treatment of major depression

according to analysis of 19 double blind clinical

trials

Kirsch I amp Sapirstein G Listening to Prozac but hearing placebo A meta-analysis of antidepressant medication Prevention and Treatment 1998Vol1(2)June

Conclusion In this controlled trial involving patients with

osteoarthritis of the knee the outcomes after

arthroscopic lavage or arthroscopic debridement were no better that those

after a placebo procedure

Power of Placebo 2002 Power of Placebo

ldquo the more impressive the procedure the more powerful the placebo effect Skilled manipulation and surgery are good examplesrdquo ldquoSurgery has the most potent placebo effect that can be exercised in medicinerdquo Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

1998

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

22

Placebo ndash Different Mechanisms

ldquoThere is not a single mechanism of the placebo effect and not a single placebo effect ndash but many

So we have to look for different mechanisms in different medical conditions and in different

therapeutic interventionsrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

Placebo is an Inextricable Part of

httppowerstatescomtagnocebo

To what extent are the benefits our patientsrsquo

experience attributable to placebo

Any Therapeutic Intervention

Pain is Especially Responsive to Placebo

ldquoPain is a subjective experience that undergoes

psychological and social modulation more than any other conditionrdquo

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

httpwwwincamresearchcaindexphpid=195540010

2009

ldquoWith clearly defined neurobiological and psychological underpinnings the placebo analgesic response is one of the most well-understood models of

placebordquo

2014

ldquoThe brain has been selected to ensure that evolved responses (such as fever sickness behaviour fatigue pain etc) are deployed only when the cost benefit

is biologically advantageous To do this the brain factors in a variety of information sources including the likelihood derived from beliefs that the body will get well without deploying its costly evolved responses One such source of

information is the knowledge the body is receiving care and treatmentrdquo

The placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of getting well so that it

selects not to deploy an evolved self-treatment[101

ldquoThe placebo effect in this perspective arises when false information about medications misleads the health management system about the likelihood of

getting well so that it selects not to deploy an evolved self-treatmentrdquo

2011

Health Governor

What Evolutionary Advantage is Placebo

Humphrey N amp Skoyles J The evolutionary psychology of healing A human success story Current Biology 2012 2217695-8

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

23

Placebo Analgesia

Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

Placebo analgesia is effected by

bull Inhibition of Ascending Nociceptive Pathways

bull Modulation (Decreased Processing) of Forebrain and Limbic Pain-Generating Circuits

Benedetti F et al Effects of placebo on the activation of μ-opioid receptor-mediated neurotransmission J Neurosci 20052510390-10402

Placebo Analgesia Activates the Same Opioid Using Brain Regions

as Descending Modulation

2005

Pain Placebo and Endorphins Landmark Discoveries

bull The discover of Endorphins (Natural lsquoMorphinesrsquo or Opioids) provided Avenues of Research into Placebo

bull In 1978 it was discovered that Placebo Responses could be produced by lsquoPsychological Expectationrsquo and (partially) Blocked by Naloxone

bull In 1982 researches discovered that there were both Endorphin-Based and Non-Endorphin-Based mechanisms in Placebo Analgesia bull In 2002 Brain Imaging Studies showed that the same Pain-Processing Regions of the Brain are similarly activated by either a Placebo or an Opioid Drug

Placebo ndash Expectation Induced Analgesia

Placebo works on the basis of our Expectations

Cognitive Expectation Triggers the Biochemical Placebo Response

Placebo ndash Expectation Induced Analgesia

Two Psychological Mechanisms are Particularly Important

Suggestion amp Conditioning

httpbloglibumnedumeriw007myblog201202the-placebo-effecthtm

Placebo ndash Suggestion amp Conditioning

Suggestion Someone introduces an idea into someone elsersquos brain and they accept it This conscious thought

then induces Real Physiological Changes

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

24

Placebo ndash Suggestion amp Conditioning

Conditioning A form of learning by which we acquire beliefs attitudes and associations that subconsciously

modify our responses and behaviours associated with a stimulus or lsquosituationrsquo

Eg Pavlovrsquos Dogs Bell becomes a Conditioning Stimulus Salivation elicited by the bell is a Conditioned Response

Suggestion and Conditioning (which can be very deep rooted) can be Additive and difficult to separate

its all in your head

ldquoFor decades the placebo effect has existed basically as a nuisance so far as the medical profession is concerned Some people benefit from being

given a sugar pill instead of an actual drug This remarkable result cannot be marketed however It doesnt fall within the ethics of medicine to

prescribe fake drugs Therefore a doctor in practice whose training has drummed into him that real medicine means drugs and surgery will shrug off the placebo effect as psychosomatic or its all in your headldquo

Deepak Chopra

httpwwwsfgatecomopinionchopraarticleI-Will-Not-Be-Pleased-Your-Health-and-the-3798901php

httpenwikipediaorgwikiDeepak_Chopra

Dr Deepak Chopra is a physician and writer He has taught at the medical schools of Tufts University Boston University and Harvard University

Placebo Liberates the Therapist

ldquoThe discovery that a therapy depends on a placebo response should be welcomed with relief because it liberates the therapist

into a positive area to explore the economics and the precise nature of the placebo component of the therapyrdquo

Patrick Wall 1998 (In Gifford Topical Issues in Pain 1

Patrick David Pat Wall was a leading British neuroscientist described as the worlds leading expert on pain and best known for the Gate control theory of pain Wikipedia

Naturecom

1998

Placebo Analgesia Wager TD amp Fields H Placebo analgesia

In Wall PD amp Melzack Textbook of Pain

ldquoIn clinical situations the enthusiasm and belief of the physician and what is verbally communicated to the patient are criticalrdquo ldquoThe more ineffective treatments a patient receives the more likely it is that future treatments will failrdquo ldquoIt is important that patients believe that they can improverdquo ldquoIt is important for the person who is providing the treatment to communicate to the patient why a particular therapeutic approach is being usedrdquo ldquoIf the practitioner doubts the efficacy of the treatment and this doubt is communicated to the patient it may negatively impact treatmentrdquo

Placebo Analgesia

The scheme shows how psychosocial signals including conditioning verbal and

observational cues are detected by the brain interpreted and translated into

neural inputs crucial to form expectations and placebo

responses resulting in behavior and clinical changes

(adapted from Colloca and Miller 2011a)

The placebo effectadvances from different methodological approaches Meissner K et al The Journal of Neuroscience 20113116117-16124

2011 Placebo amp lsquoNon-Specific Factorsrsquo

httpthebrainmcgillcaflashaa_03a_03_pa_03_p_doua_03_p_douhtml2

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

25

Expectation of analgesia can be directed via attentional mechanisms to different spatial loci of the body

Somatotopic organization of the PAG

Somatotopic Activation of Opioid Systems by Target-Directed Expectations of Analgesia

Four body parts simultaneously injected with capsaicin Specific expectations of analgesia were induced by applying a placebo cream on one of these body parts and by telling the subjects that it was a powerful local anaesthetic A placebo analgesic response occurred only on the treated part whereas no variation in pain sensitivity was found on the untreated parts

Benedetti F et al Somatotopic activation of opioid systems by target-directed expectations of analgesia The Journal of Neuroscience 1999193639-48

1999

Nocebo - Latin ldquoI will harmrdquo

httpboingboingnet20120814nocebo-now-available-withouthtml

Opposite of the Placebo Effect Worsening of symptoms

because of Negative Expectations

httpbloglibumneduvanm0049psy1001section09spring2012201203the-nocebo-effecthtml

Nocebo-Effect Noncompliance When Telling The Patient Enough May Be Too Much

httpalignmapcom20081126clinicians-can-choose-how-not-if-they-influence-patient-compliance

Nocebo Effects

What we do know suggests the impact of nocebo is far-reaching Voodoo death if it exists may represent an extreme form of the nocebo phenomenon says anthropologist Robert Hahn of the US Centers for Disease Control and Prevention in Atlanta Georgia who has studied the nocebo effect

httpcurrentcomshowsupstream90045865_the-science-of-voodoo-the-nocebo-effecthtm

Can Nocebo Kill

Nocebo Hyperalgesia is Mediated by Cholecystokinin (CCK)

Nocebo Hyperalgesia only occurs as a result of Anxiety due to

Anticipation of Pain Attention is Focussed on the Impending Pain

Other extreme Anxiety Producing Situations induce Analgesia Here Attention is Focussed Not on Pain but on some

Environmental Stressor

CCK has Pronociceptive and Anti-Opioid actions that are effected particularly via the PAG and RVM CCK causes tolerance to opioid drugs CCK receptors can be Blocked by the drug Proglumide

ldquoCholecystokinin (CCK) has been suggested to be both pro-nociceptive and anti-opioid by actions on pain-modulatory cells within the rostral ventromedial

medulla (RVM) ldquo ldquoProstaglandins such as PGE2 are known to function as important mediators in the development of central sensitization and when

applied to the spinal cord produce an allodynic and hyperalgesic staterdquo

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

26

Within the RVM two distinct cell types modulate spinal nociceptive signalsmdash on cells and off cells Tonic activation of off cells is thought to inhibit

nociceptive signals in the dorsal horn whereas activation of on cells supports hyperalgesic states

2013

Nocebo induces anxiety which in turn activates two different and independent biochemical pathways bull A CCK-ergic facilitation of pain and bull The Hypothalamic-Pituitary-

Adrenal (HPA) axis raising plasma ACTH and cortisol

The anti-anxiety drug diazepam prevents both hyperalgesia and HPA activation

The CCK antagonist proglumide inhibits hyperalgesia but not HPA activity

Nocebo Hyperalgesia

F Benedetti Placebo Effects understanding the mechanisms in health and disease Oxford University Press 2009

Placebo amp lsquoNon-Specific Factorsrsquo ldquoWhilst some clinicians are natural walking placebos others

may have to work hard at patientrelationship issues There is a placebonocebo component or percentage in all we do as

cliniciansrdquo Louis Gifford

Listen to the Patient Show Caring

Understanding Empathy

Placebo ndash Further Reading 1) Benedetti F et al Neurobiological mechanisms of the placebo effect The Journal of

Neuroscience 20052510390-10402

2) Scott DJ et al Placebo and nocebo effects are defined by opposite opioid and

dopaminergic responses Archives of General Psychiatry 200865220-231

3) Benedetti F et al How placebos change the patientrsquos brain

Neuropsychopharmacology 201136339-354

4) Wager TD amp Fields H Placebo analgesia In Wall PD amp Melzack Textbook of Pain

httpwagerlabcoloradoedufilespapersWager_Fields_Textbookofpain_tosharepdf

5) Schweinhardt P et al The anatomy of the mesolimbic reward system a link between

personality and the placebo analgesic response The Journal of Neuroscience

2009294882-4887

6) Lidstone SC et al The placebo response as a reward mechanism Seminars in pain

medicine 2005337-42

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain may persist because the original inciting stimulus is still present andor because changes to the nervous system have occurred

making it more sensitive to painrdquo

Lee YC et al Arthritis Research amp Therapy 2011 13211

2011

Chronic Pain

Traditional Definition

Pain Persisting for at least 3 ndash 6 months

ldquoChronic pain has been a mystery because we were just looking at the tissues and joints

while ignoring the nervous system and the brain But It is in the brain and the nervous

system that the action happensrdquo

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

27

ldquoArising from these data is the striking argument that chronic pain is a disease of the nervous system which distinguishes this phenomena from acute pain that is

frequently a symptom alerting the organism to injury rdquo

2015 In Clinical Practice What Does Pain Tell Us

ldquoSensitisation of Ad and C fibre nerve endings rarely outlast the primary cause for pain ndash thus peripheral sensitisation may be considered as always adaptiverdquo

ldquoIn contrast central changes in the processing of nociceptive information may potentially outlast their

trigger events for days months or even years ndash and may spread to sites remote from the primary cause of painrdquo

Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

In Clinical Practice What Does Pain Tell Us

ldquoWhen the location the duration or the magnitude of pain hyperalgesia and allodynia has become maladaptive rather than protective then the pain is no longer a meaningful homeostatic factor or symptom of a disease but rather a disease in its own rightrdquo Clifford J Woolf

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Central Sensitisation

Definition Enhanced Responsiveness of Nociceptive Neurons in the CNS to their Normal Afferent Input IASP

(Umbrella Term for All Changes in the CNS which Enhance Pain Perception)

Includes

Wind-up and Long Term Potentiation of Dorsal Horn Neurons

Malfunction of Descending Anti-Nociceptive Mechanisms

Altered Sensory Processing in the Brain ndash Cortical Plasticity

Jo Nijs holds a PhD in rehabilitation science and physiotherapy He is a

researcher and assistant professor at the Vrije Universiteit Brussel (Brussels

Belgium) and the Artesis University College Antwerp (Belgium) and he is a

physiotherapist at the University Hospital Brussels His research and clinical interests are patients with chronic painfatigue He has (co-)

authored more than 100 peer reviewed publications and served over

40 times as an invited speaker at national and international meetings

httpbodyinmindorgprimary-care-physical-therapy-treatment-of-fibromyalgia

Dr Jo Nijs

Practice Guidelines by Jo Nijs for the treatment of chronic musculoskeletal pain are being adopted

worldwide within Physical Therapy and

Manual Therapy

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

28

lsquoPathologicalrsquo Central Sensitisation

Frequently Present in Chronic Musculoskeletal Pain Disorders

ldquo implies an increased complexity of the clinical picture (ie an increase in unrelated symptoms and hence a more difficult clinical reasoning process) as

well as decreased odds for a favourable rehabilitation outcomerdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010 Central Sensitisation amp Acute Traumatic Injury

Nociception arising from traumatic injury that has a high lsquoPhysical Threatrsquo andor lsquoPsychological Distressrsquo value is particularly potent at inducing central sensitisation Whiplash injury is a classic example A high percentage of victims who suffer minor whiplash injury (Grade 1 or 2) lapse into chronic pain syndromes or even fibromyalgia This is virtually unknown in those who sustain similar injury on fairground rides

The speed of onset and lsquocontextrsquo of injury is pivotal

httpwwwaddonheadrestcomneckpainhtml

Pain Memories

ldquoA reasoned understanding of pain mechanisms validates the reality of ongoing unrelenting and often

untreatable chronic post-whiplash painrdquo

ldquoAdequate management in the acute stages that recognises the biopsychosocial and hence

neurobiological impact of injuries like whiplash is probably the best hope at this timerdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Volume 384 Issue 9938 12ndash18 July 2014 Pages 109ndash111

ldquoCentral sensitisation in patients with chronic whiplash-associated disorders warrants

treatment of cognitive emotional factors like pain catastrophising hypervigilance and maladaptive beliefs

about illnessrdquo

2014

Chronic whiplash-associated disorders to exercise or not NijsJ and Ickmans K

Soft Tissue Injury

Soft Tissue Healing Review Tim Watson (2009)

(Tissue Healing)

2 Days

3 to 4 Weeks

Soft Tissue Healing Phases amp Timescales

ldquoAn important and ongoing source of pain is required before the process of peripheral sensitisation can establish central

sensitisationrdquo ldquoPain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread painrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Chronic Pain

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

29

Butler D Moseley GL Explain Pain Adelaide NOI Group Publishing 2003

Chronic Pain

ldquo appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent

evolvement from an acute localised problem to more complex clinical cases characterised by chronic widespread pain rdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Memories

ldquoMemories are hard to get rid of and if ongoing pain has a large memory component it may be beyond any tooltherapy we

presently haverdquo Louis Gifford

ldquo many probably all ongoing pains have a major component of their pain source within the central nervous system in the form of

a somatosensory memory or imprintrdquo ldquothe roots are in the biology of memory and synaptic efficacyrdquo

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

1998

Pain Memories

ldquoMemories can be put into subconsciousness but dragged back up if given the right cues Some memories and experiences may if

given great significance stay continuously in our consciousness rather like an annoying tune or nagging worry tends tordquo

ldquothere has been a gross error in reasoning in the past with the insistence that all pain should have a tissue sourcerdquo

Louis Gifford

httpwwwachesandpainsonlinecom

aboutusphp

Louis Gifford (Topical Issues in Pain 1) 1998

Pain_Chronic

1998 Important Questions for Patients with Acute Musculoskeletal Pain

Have you had pain like this before

Was the original injury emotionally charged

Their present pain experience may be largely on account of reawakening of a pain memory Any

present physical injury may be much less than the perceived level of pain suggests

Pathological Central Sensitisation

ldquoThere is now enough evidence available indicating that chronic pain syndromes such as low back pain whiplash and fibromyalgia share the same pathogenesis namely sensitization of pain modulating systems in the central

nervous system ldquo

van Wilgen CP amp Keizer D The sensitization model to explain how chronic pain exists without tissue damage Pain Management Nursing 201213(1)60-5

2012

Pathological Central Sensitisation

ldquoWhy some of these chronic pain disorders remain localized to few body areas whereas others become

widespread is unclear at this time Genetic environmental and psychosocial factors likely play an

important rolerdquo

Staud R Evidence for shared pain mechanisms in osteoarthritis low back pain and fibromyalgia Current Rheumatology Reports 201113(6)513-20

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

30

Fibromyalgia ndash Pain Processing Disease

httpdardipaincliniccomfibromyalgiaphp

Location of the 18 tender points that make

up the criteria for identifying fibromyalgia

Patient must feel pain in

at least 11 of these points when a pressure of 4Kgcm2 is applied

Patient must also have

had pain in all 4 quadrants of the body for at least 3 months

Fibromyalgia amp Central Sensitisation

ldquoThe precise etiology and pathogenesis of fibromyalgia syndrome remains undefined and there is no definite curerdquo ldquoFMS is

characterised by sensitisation of the central nervous system which explains the majority of if not all symptomsrdquo Central sensitisation is ldquothe sole feature of FMS pathophysiology that is no longer in debaterdquo

Jo Nijs et al

Nijs J et al Primary care physical therapy in people with fibromyalgia opportunities and boundaries within a monodisciplinary setting Physical Therapy 2010901815-22

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

httpwwwfmcfsmecomresearchers_spotlightphp

ScienceDaily (June 25 2007) mdash Fibromyalgia a chronic widespread pain in muscles and soft tissues accompanied by fatigue is a fairly

common condition that does not manifest any structural damage in an organ Twenty-five years ago Muhammad B Yunus MD and

colleagues published the first controlled study of the clinical characteristics of fibromyalgia syndrome

Further Legitimization Of Fibromyalgia As A True Medical Condition

Yunus MB Fibromyalgia and overlapping disorders the unifying concept of central sensitivity syndromes Seminars in Arthritis and Rheumatism 200736(6)339ndash356

Fibromyalgia 2007

Without question Muhammad Yunus is the father of our modern view of fibromyalgiardquo

John B Winfield MD (accompanying editorial)

ldquoThere is now significant evidence that fibromyalgia is part of a much larger continuum that has been called many things including functional somatic

syndromes medically unexplained symptoms chronic multisymptom illnesses somatoform disorders and perhaps most appropriately central pain or central

sensitivity syndromes ldquo

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

Together these advances have led to an emerging recognition that chronic central

pain itself is a ldquodiseaserdquo and that many of the underlying mechanisms operative in these

heretofore ldquoidiopathicrdquo or ldquofunctionalrdquo pain syndromes may be similar no matter

whether the pain is present throughout the body (eg in FM) or localized to the low

back the bowel or the bladder httpwwwsciencedailycomreleases200706070625095756htm

2011

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia

The notion that fibromyalgia and related syndromes might represent biological amplification of all sensory stimuli has

significant support from functional imaging studies that suggest that the insula is the most consistently hyperactive region This

region has been noted to play a critical role in sensory integration fibromyalgia patients also display a low noxious

threshold to auditory tones httpwwwsciencedailycomreleases200706070625095756htm

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

31

Fibromyalgia

ldquo in FM the stress response system notabably the HPA axis and the sympathetic

nervous system is deregulatedrdquo this can ldquofoster pathological immune activation with

release of pro-inflammatory cytokines provoking a so-called lsquosickness responsersquo

(lethargy and malaise social withdrawal flu-like symptoms concentration difficulties) and generalised pain hypersensitivity)rdquo

httpwwwsciencedailycomreleases200706070625095756htm

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201125141-154

Fibromyalgia amp ldquoFibromyalgia-nessrdquo

httpwwwsciencedailycomreleases200706070625095756htm

many patients with chronic pain disorders have variable degrees of

ldquofibromyalgia-nessrdquo When this occurs we need to treat both the peripheral and

central elements of pain along with other somatic symptoms The era of

evidence-based individualized analgesia in chronic pain is upon us

2011

Fibromyalgia Treatment Considerations

ldquoManual therapists unaware of or ignoring the processes involved in the development and maintenance of chronic

widespread painFM may cause more harm than benefit to the patient by triggering or sustaining central sensitisationrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice Manual Therapy 2009143-12

ldquoFor some therapists central sensitisation remains a theoretical concept that is unlikely to occur in the patients they are treatingrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

httpbestfibromyalgiatreatmentnetpage_id=4

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoClinicians should be aware of the consequences of central sensitisation (ie marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly

Any therapeutic interventions triggering more pain will serve as a new source of nociceptive barragerdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httplakescenterchirocomchiropractic-carefibromyalgia

ldquoSoft-tissue mobilisation is required to free up restrictions and restore local blood flow However it is important not to increase pain during treatment Starting superficially with well-tolerated

strokes along the length of the muscle fibres and progressing towards deeper strokes that go perpendicular to the soft-tissue

fibres is recommendedrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Fibromyalgia Treatment Considerations

httpbestfibromyalgiatreatmentnetpage_id=4

ldquoAggressive ways of treating trigger points (eg by using ischaemic pressure) are not usually well tolerated and therefore

not recommendedrdquo ldquoSensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movementrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

32

Fibromyalgia Treatment Considerations

Exercise

ldquoPain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-

exercise This is the result of endogenous opioid release and related activation of several (supra)spinal anti-nociceptive

mechanisms such as adrenergic and serotinergic pathwaysrdquo ldquoA constant or decreased pain threshold during and following

exercise suggests malfunctioning of anti-nociceptive mechanisms and hence central sensitisationrdquo

Nijs J et al Recognition of central sensitisation in patients with musculoskeletal pain application of pain neurophysiology in manual therapy practice

Manual Therapy 201015135-141

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2010

Exercise-induced Analgesia

In Healthy Individuals Exercise Stimulates Brain Release of Opioids Pituitary Release of Peripherally Acting Opioids (b-endorphins) Hypothalamus Release of Centrally Acting Opioids (b-endorphins) Eg Via projections to PAG

Also Peripherally Increased Ab fibre input to dorsal horn (Gate Control) and DNIC from muscle ischaemia and lactate accumulation

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Brain centres involved in pain modulation are believed to be stimulated by arterial baroreceptors in response to increasing blood pressure

2012

Fibromyalgia Treatment Considerations

Exercise

Suitable exercises and activities are low-intensity (aqua)aerobics gentle stretching relaxation sessions etc Any post-exertional pain soreness or malaise should be responded

to by cutting back Else very gradual pacing-up may be beneficial in improving exercise and activity tolerance

httpwwwlivestrongcomarticle324688-relaxation-exercises-for-

fibromyalgia

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Central Sensitisation amp Chronic Inflammatory States

Research studies of pain patients with RhA and OA (traditionally considered as peripheral or

nociceptive pain states) indicate that the pain has an important central component

The evidence comes from mechanistic studies (ie experimental pain testing functional neuroimaging and genetic studies) and

therapeutic trials

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

OA like nearly all other chronic pain states is likely a ldquomixed pain staterdquo with individual variability in the relative balance of peripheral (ie nociceptive) and

central elements of pain

httpwwwbuzzlecomarticlesarthritic-fingershtml

Central Sensitisation amp Chronic Inflammatory States

2012

ldquoAs a consequence of their training and education the majority of musculoskeletal therapists are educated in the biomedical model of pain This

traditional model of pain assumes that there is a direct link between the amount of local tissue damage (ie structural joint degeneration) and the pain

experienced by the patient ldquoHowever chronic OA-related pain does not always adhere to this biomedical model of pain It is common to observe a

discordance between the degree of structural joint damage and the amount of symptoms experienced by the patientrdquo

2015

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

33

Phillips K amp Clauw DJ Central pain mechanisms in chronic pain states ndash maybe it is all in their head Best Practice amp Clinical Rheumatology 201225141-154

Central Sensitisation amp Chronic

Inflammatory States

It has been evident for some time that peripheral factors can at

best only partially explain the pain and other symptoms suffered by individuals with OA Population-based studies consistently

show a poor relationship between the degree of ldquopathologyrdquo in OA and reported pain intensity In fact in population-based

studies approximately 30 ndash 40 of knee OA patients with the most severe forms of radiographic knee OA have no pain

httpwwwmendmeshopcomkneeknee_osteoarthritis_diagnosisphp 2012

C

Nociceptor

Peripheral Nerve Conduction

Spinal Nerve Transmission C

Localisation Interpretation

Meaning

Pain is Generated in the Brain

Spatial Projection

Amplifier

Transduction Descending Modulation

Threat

Pain Pathology(injury)

OA and RhA Generate Chronic Nociception

Habituation vs Sensitisation

2011

ldquoRheumatologists often consider pain a peripheral entity but there is great discordance between pain severity and purported peripheral causes of pain such as inflammation and structural joint damage - for example cartilage degradation erosionsrdquo ldquoThe relationship between inflammation psychosocial factors and

peripheral and central pain processing are intricately entwinedrdquo

Pain Treatment for Patients With

Osteoarthritis and Central Sensitization

Enrique Lluch Girbeacutes Jo Nijs Rafael Torres-Cueco Carlos

Loacutepez Cubas

Physical Therapy Volume 93 Number 6 June 2013

ldquoNonsteroidal anti-inflammatory drugs can be beneficial in initial stages but in time they become inefficient and the administration of other medications such

as amitriptyline or gabapentin is more advisable This phenomenon might be related to the fact that chronic pain in people with OA is related more to

neuroplastic changes in the nervous system than to an inflammatory condition of the jointrdquo

2013

ldquoWhy do studies repeatedly show gross abnormalities like disc bulges spinal stenosis herniations meniscus tears and so on in 20-70 of people who have no history of painrdquo

ldquoitrsquos not the signals that go to the brain from the body that matters itrsquos what the brain decides to do with these signals that mattersrdquo

Anoop Balachandran

Pain = Pathology

Balachandran A A revolution in the understanding of pain and treatment of chronic pain 2011

httpworkout911comp=3709

2011 Important Points - Central Sensitisation amp Chronic Inflammatory States

bull OA amp RhA develop slowly with minimal acute stress

bull Brain facilitates lsquoHabituationrsquo

bull Central Sensitisation is minimised ndash until realisation of lsquothreatrsquo

bull The disease can be quite advanced but asymptomatic

bull Natural course of disease will involve ROM limitation (partly C fibre mediated hypertonicity)

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

34

Habituation (Learning to ignore a stimulus that lacks meaning)

Defn Progressively Smaller Responses elicited by

Repeated Stimuli

In habituation repeated presentation of the same stimulus produces a progressively smaller response

Stimulus number

Habituation to Nociception (Learning to ignore a stimulus that lacks lsquothreatrsquo)

ldquoRepetitive nociceptive stimuli in healthy subjects lessens the pain experience over time and causes

habituation This process is in part mediated by the antinociceptive systemrdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The context group (n _ 22) was told that repeated pain over several days will increase the pain sensation overtime eg from day to

day This was the conditioning stimulus ndash applied just once verbally at the start of the study

Identical painful heat stimuli (not enough to cause tissue damage) were applied to the forearm and the subject asked to rate the pain on a 0-100 VAS Repeated for 8 consecutive days

Ten blocks of heat stimuli each consisting of 6 heat applications (60 per session)at 48rsquoC were given Subjects were asked to rate the sensation after each 6 applications

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

The control group habituated as expected - the context group did not ldquoExpectation alone can shape the outcomerdquo ldquoUncareful nocebo information may have significant consequences at a much later time pointrdquo

ldquoA negative expectation raised verbally by a doctor only once in a clinical context may cause changes of the patientrsquos perception in the futurerdquo

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010

Habituation to Nocicepeption (With amp Without a Single lsquoThreateningrsquo Conditioning Stimulus)

Donrsquot give your patientsrsquo Negative Expectations (nocebo conditioning stimuli)

Functional brain imaging showed a difference between

the two groups in the right parietal operculum ndash a part of

the insular cortex

Rodriguez-RaeckeR et al Insular Cortex Activity Is Associated with Effects of Negative Expectation on Nociceptive Long-Term Habituation The Journal of Neuroscience August 201030(34)11363-11368

2010 Careful What You Say

Negative verbal suggestions induce anticipatory anxiety about the impending pain increase and this verbally-

induced anxiety triggers pain facilitation

httpmindblogdericbowndsnet2007_07_01_archivehtml

Always be positive and optimistic stress the gains of treatment Avoid words like lsquoarthritisrsquo lsquospondylosisrsquo lsquodamagersquo or lsquodegenerationrsquo Use

words like lsquostiffnessrsquo lsquotightnessrsquo or lsquodeconditionedrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

35

ldquoSimilar to placebo effects nocebo effects have been shown to be especially large when verbal suggestions (of increased pain) are combined with

conditioning Therefore it is likely that the efficacy of future pain treatments may be enhanced if both positive and negative experiences with treatments

are addressed in pain patientsrdquo

2014 Careful What You Say If the patient thinks we disbelieve or blame them they will feel

angry betrayed and misunderstood Even a lsquopull yourself togetherrsquo tone of voice will heighten sensitivity defensiveness and distrust and likely break any existing therapeutic alliance

Examples of Words to Avoid Use Instead Disease ndash infers serious Problem Behaviour ndash associated with lsquobadrsquo Habit Avoidance ndash could infer lsquoblamersquo Tend to Avoid Fear ndash is only for lsquowimpsrsquo Apprehension Conditioning ndash trickery or manipulation (rats in lab) Learning Should and Must ndash judgemental May or Could Medical terms ndash arrogant condescending frightening

Primary amp Secondary Hyperalgesia

Primary Hyperalgesia Only

Nerve Block

R L

Recognising Central Sensitisation

ldquoThe notion that lsquorealrsquo pain can exist that is not activated by noxious stimuli (but which has almost precisely the same lsquosymptomrsquo profile to that found in many clinical conditions) was generally not very well received initially particularly by physiciansrdquo

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain

Pain 2011152(3 Suppl)S2-15

2011

Physicians ldquobelieved that pain in the absence of pathology was simply due to individuals seeking work or insurance-

related compensation opioid drug seekers and patients with psychiatric disturbances ie malingerers liars and hysterics

That a central amplification of pain might be a ldquorealrdquo neurobiological phenomena seemed to them to be unlikely

and most clinicians preferred to use loose diagnostic labels like psychosomatic or somatiform disorder to define pain

conditions they did not understandrdquo

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

2011

Woolf CJ Central sensitisation implications for the diagnosis and treatment of pain Pain 2011152(3 Suppl)S2-15

httparchivesfocushmsharvardedu2002Oct11_2002neurosciencehtml

Recognising Central Sensitisation

ldquoBecause we cannot directly measure sensory inflow and because peripheral changes can contribute to sensory

amplification as with peripheral sensitisation pain hypersensitivity by itself is not enough to make an irrefutable

diagnosis of central sensitisationrdquo

Some 30 years on central sensitisation and the biopsychosocial model of pain are firmly

established and health professionals are being actively retrained

However clinical diagnosis still presents problems

2011

ldquoThe first and obligatory criterion entails disproportionate pain implying that the severity of pain and related reported or perceived disability are

disproportionate to the nature and extent of injury or pathology (ie tissue damage or structural impairments) The 2 remaining criteria are 1) the

presence of diffuse pain distribution allodynia and hyperalgesia and 2) hypersensitivity of senses unrelated to the musculoskeletal systemrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

36

Recognising (lsquoDysregulatedrsquo) Central Sensitisation

bull Pain persisting beyond expected healing times bull Widespread diffuse pain bull Widespread tissue tenderness to palpation bull Bizarre symptoms disproportionate unpredictable bull Excessive post-treatment soreness bull Exercise exacerbates pain bull Previous similar pain episodes or past traumatic associations bull Anxietyworryangerdepression negative emotions bull Unhelpful beliefs or expectations bull History of failed (manual) treatments ndash or made worse by bull Hypersensitivity to bright light noise highlow temperatures bull Presence of trigger points bull Poor response to analgesics such as NSAIDs respond to TCAs

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

lsquoCognitive-emotional sensitisationrsquo activates forebrain areas that exert powerful influences on various

brainstem nuclei including those identified as the origin of descending pain facilitatory pathways This in

turn sustains the process of central sensitisation

Psychosocial Prevention amp Treatment of lsquoDysregulatedrsquo Central Sensitisation

Introducing CBT

Cognitive-behavioral therapy is an action-oriented form of psychosocial therapy that assumes that maladaptive or faulty thinking patterns cause maladaptive behavior and negative emotions (Maladaptive behavior is behavior that is counter-productive or interferes with everyday living) The treatment

focuses on changing an individuals thoughts (cognitive patterns) in order to change his or her behavior and emotional state

FreeOn-LineDictionary

Cognitive-Behavioural Therapy Should we be giving psychological treatment

ldquoDespite the fact that physiotherapists do not receive CBT training they still may apply some of its principles within their treatmentrdquo

ldquoThis does not suggest that physiotherapists should become

amateur psychologists but be much more aware that psychological factors are involved and that physiotherapists are in a position to influence those factors related to physical fitness and functionrdquo

Louis Gifford

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoThus we demonstrate that central sensitization can be modified volitionally by altering pain-related thoughtsrdquo

2014 Cognitive-Behavioural Therapy

In practice a patient with musculoskeletal type pain symptoms will consult a lsquophysical therapistrsquo If the physical therapist lacks

biopsychosocial understanding of pain he will try to rationalise and treat the problem according to the old Pathoanatomical Model -

and miss important psychosocial barriers to recovery

httpwwwachesandpainsonlinecom

aboutusphp

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

37

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising

2) Fear-Avoidance Syndrome

3) Disuse or Deconditioning Syndrome

4) Hypervigilance

Worried or Anxious thinking generated within the Human Cortex (from Real or Perceived Threat) can Persist over Long Periods

Common Clinical Findings

Cognite-Behavioural Therapy

For patients with low back pain studies have shown that ldquocatastrophising has been found to be seven times more

powerful than any other predictor in predicting the transition from acute to chronic painrdquo ldquofear also appears

to play a rolerdquo

Dr Sean Mackey Associate Professor amp Chief of the Pain Management Division at Stanford University 2011

httpnewsstanfordedunews2006january11med-rein-011106html

Dr Sean Mackey

State of Mind Can Turn Acute Pain to Chronic

2011

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

1) Catastrophising The injury is worse (or worse consequences) than it is

I canrsquot work because of the pain therefore

bull I canrsquot earn any money bull I canrsquot pay the mortgage bull I will lose my house bull My family will leave me bull I have nothing to live for bull There is no point in trying

Therapists Role Be on the lookout for this type of thinking Question as to its origin Offer appropriate explanation and reassurance

httpchipurcom20110801catastrophizing-finding-a-sense-of-peace

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

2) Fear-Avoidance Syndrome Fear of pain and consequent withdrawal from activity in the

belief that even a small amount will cause injury or re-injury

bull Limits activities bull Limits treatment compliance bull Becomes self-perpetuating bull Lessening activity promotes deconditioning amp disability

Therpists Role This usually starts soon after the injury and should be easy to recognise Common in cases of recurring injury Need to

identify movements or activities that are being avoided and confront them with lsquopacedrsquo exercise

httpgoalisticscom201106chronic-pain-management-fear-avoidance-disability

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

3) Disuse or Deconditioning Syndrome Result of Inactivity

bull Tissue weakness Pain increased fatigue decreased function bull Altered patterns of movement and muscle function bull Learned responses and protective habits bull Leads to accelerated degenerative changes

Therpists Role Similar approach as in fear-avoidance Need to identify movements or activities that are being avoided and

confront them with lsquopacedrsquo exercise

httpwwwmerlinochiropracticclinic

comnew-chronic-painhtml

Cognitive-Behavioural Therapy Psychosocial Barriers to Recovery

4) Hypervigilance

bull Excessive preoccupation with their problem bull Excessive attention to bodily sensations bull Obssessional search for a lsquocurersquo (therapists tests) bull Always lsquoat the doctorsrsquo

Therapists Role Need to show empathy and give reassurances Prescribe exercises or encourage activities as a distraction

httpwwwanxietytreatment2com

hypervigilance-and-anxietyhtml

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

38

Cognitive-Behavioural Therapy Pain - Fear it or Confront it

Vlaeyen amp Geert Fear amp Pain Pain Clinical UpdatesXV6

httpwwwsportsphysionorthsydneycomauchronic_low_back_painphp

Cognitive-Behavioural Therapy

Gifford L Topical Issues in Pain 1Physiotherapy Pain Association Yearbook 1998-1999

httpwwwachesandpainsonlinecom

aboutusphp

ldquoSuccessful cognitive behavioural approaches to pain management stear patients away from a focus on pain

and pain related behaviour and towards positive functional achievementsrdquo

Louis Gifford

CBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT

changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to increased access to executive regions for

reappraisal of pain

ldquoCBT led to increased activations in the ventrolateral prefrontallateral orbitofrontal cortex regions associated with executive cognitive control We suggest that CBT changes the brainrsquos processing of pain through an altered cerebral loop between pain signals emotions and cognitions leading to

increased access to executive regions for reappraisal of painrdquo

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

Pathoanatomical beliefs about pain ie that it must have some lsquoproportionatersquo cause in the tissues may

constitute a psychological barrier to recovery

ldquoPlacebo effects in pain treatment can be enhanced by informing the patients about placebo mechanisms and by explaining their effects to them Such an

educational informative approach ought to explain the placebo effect based on the models of classical conditioning and expectancy but also its neurobiological

bases without overstraining the patientrdquo

2014

ldquoThe course of CBT led to significant improvements in clinical measures of pain and self-efficacy for coping with chronic painrdquo ldquoCBT is a valuable

treatment option for chronic painrdquo

2014

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

39

When to Use CBT Introducing lsquoPain Physiology Educationrsquo

ldquoPain Physiology Education is indicated when

1) The clinical picture is characterised and dominated by central sensitisation

2) Maladaptive pain cognitions illness perceptions or coping strategies are present

Both indications are prerequisites for commencing pain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

2011 When to Use CBT

Introducing lsquoPain Physiology Educationrsquo

ldquoIt is important for clinicians to recognise that pain cognitions such as fear of movement and

catastrophizing are not only of importance to chronic pain patients but may even be crucial at

the stage of acutesubacute musculoskeletal disordersrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2009

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011 When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

Examples of Maladaptive pain cognitions illness perceptions or coping strategies

1) Moderate hip OA Cartilage is eroding away any exercise will accelerate 2) Chronic whiplash Convinced of severe damage lsquoinvisiblersquo to scans 3) Fibromyalgia patient Convinced she has an undetectable lsquonewrsquo virus

Initiating a treatment such as paced exercise is unlikely to be successful in these patients

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

When to Use CBT Introducing lsquoPain Physiology

Educationrsquo

ldquoIt is crucial to change the patientrsquos maladaptive illness perceptions and maladaptive pain

cognitions and to reconceptualise pain before initiating the treatment This can be accomplished

by patient education about central sensitisation and its role in chronic pain a strategy frequently

referred to as lsquopain physiology educationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

Pain Physiology Education

ldquoDetailed pain physiology education is required to reconceptualise pain and to convince the patient that hypersensitivity of the central nervous system

rather than local tissue damage is the cause of their presenting symptomsrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

40

Pain Physiology Education

ldquoPhysiotherapists or other health care professionals are required to provide tailored education to

address individual needsrdquo ldquoface-to-face sessions of pain physiology education in conjunction with

written educational material are effectiverdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

ldquoThe education is presented verbally (explanations by the therapist) and visually (summaries

pictures and diagrams on computer and paper) During the sessions patients are encouraged to ask questions and their input should be used to

individualise the informationrdquo

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Pain Physiology Education

Nijs J et al How to explain central sensitization to patients with lsquounexplainedrsquo chronic musculoskeletal pain Practice guidelines

Manual Therapy 201115413-418

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquoPain physiology education is typically followed by various components of a biopsychosocial-orientated rehabilitation

program like stress management graded activity and exercise therapy It is important for clinicians to introduce

these treatment components during the educational sessions and to explain why and how the various treatment

components are likely to contribute to decreasing the hypersensitivity of the central nervous systemrdquo

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2011

Use of Exercise Motor Control Training

httpwwwricorgaboutusmediacenterpress2010painmedicinenews2010

ldquo manual therapy aimed at improving motor control in symptomatic regionsjoints is likely to have its place in the

prevention of chronicityrdquo Indeed a sustained mismatch between motor activity and sensory feedback is able to

serve as an ongoing source of nociception inside the CNSrdquo ldquoIn case of inaccurate execution of movements due to

deconditioning or joint tissue damage (and consequently altered proprioception) an incongruence is likelyrdquo

Nijs J amp Houdenhove BJ From acute musculoskeletal pain to chronic widespread pain and fibromyalgia application of pain neurophysiology in manual therapy practice

Manual Therapy 2009143-12

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html 2009

ldquoIn acute musculoskeletal pain the main focus for treatment is to reduce the nociceptive trigger Such a focus on peripheral pain generators is often effective

for treatment of (sub)acute musculoskeletal pain In patients with chronic musculoskeletal pain ongoing nociception rarely dominates the clinical

picturerdquo hellip ldquoThe goal of cognition-targeted exercise therapy is systematic desensitization or graded repeated exposure to generate a new memory of

safety in the brain replacing or bypassing the old and maladaptive movement-related pain memoriesrdquo

2015 Use of Exercise

Prescribing of home exercises is extremely useful where there is fear-avoidance deconditioning movement or postural lsquofaultsrsquo

hypervigilance etc to improve function and to serve as a distraction from pain Attention to pain will expand itrsquos cortical representation

Exercise should always be lsquopacedrsquo ie intensity and duration

increased gradually (eg 10 per week) starting from a lsquobasersquo level that is initially comfortably attainable by the patient Warn about the

possibility of lsquoflare-upsrsquo especially if pacing is exceeded but not to worry about it if it happens

If patient says they lsquocanrsquotrsquo do something gently explain that there

are always degrees of lsquocanrsquo

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

41

Use of Exercise in Chronic Pain Patients

Guidelines by Jo Nijs

Exercise is good for all chronic pain sufferers But fibromyalgia and CFS (and also chronic whiplash) are particularly associated with dysfunctional endogenous analgesia in response to aerobic and

local muscle exercise LBP OA and RhA sufferers are more tolerant For more details see paper below

Nijs J et al Dysfunctional endogenous analgesia during exercise in patients with chronic pain to exercise or not to exercise Pain Physician 201215ES203-ES213

httpwwwmeresearchorgukinformationpublicationsconferencesnewhorizons2008html

2012

httpphysical-therapyadvancewebcomArchivesArticle-ArchivesPassion-and-Purposeaspx

dailymailcouk

Use of Exercise

Goals of Pain Therapy

Acute Pain1

bull Provide rapid and effective Analgesia bull Treat the Cause

Chronic Pain2

bull Reduce Pain bull Address Functional Impairment and Depression bull Address Psychosocial Issues 1 Fields HL et al InHarrisonrsquos Principles of Internal Medicine 199853-58 2 Marcus DA Postgraduate Medicine 200311349-66

httpwwwmedscapeorgviewarticle487064

Chronic Pain Induced Cortical Remodelling

Evidence from Brain Imaging Studies

Cortex amp Pain

httpenwikipediaorgwikiPain

Recent advances in brain imaging

technology have vastly increased our

ability to see how the brain processes

pain

Cortical Plasticity

Real time brain scanning (eg fMRI PET) has revealed that

people with chronic pain syndromes show greater

activity in areas of the brain that generate pain and lesser activity in areas that suppress pain than do healthy controls

when subjected to experimental pain

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

42

Cortical Processing of Pain (Neural Plasticity by Joe Muscolino)

httpwwwlearnmusclescomoriginalsmtj20Fall20201120-20neural20faciliationpdf

2011 Brain Gray Matter Loss in Chronic Pain is a Consistent Finding

Brain Areas Affected Varies with the Condition

a and b show imaging capability

These images can be subject to statistical analysis to identify regions of lesser gray matter density or thickness

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2009

ldquoFibromyalgia patients have abnormal brain gray matter lossrdquo ldquoGray matter loss occurred mainly in regions related to stress and pain processingrdquo

2007

Fibromyalgia Patients Show Reduced Gray Matter amp Brain Volume

Fibromyalgia shows as accelerated loss of gray matter and total brain volume compared to

healthy controls

Kuchinad A Et al Accelerated brain gray matter loss in fibromyalgia patients premature aging of the brain The Journal of Neuroscience 2007 274004-4007

2007

Cognitive Performance Tests

Psychomotor Performance (Simple motor test)

Memory

(Memory test)

Executive Function (Attention switching mental

flexibility)

Jongsma MJA et al Neurodegenerative properties of chronic pain cognitive decline in patients with chronic pancreatitis PLoS One 20116(8)e23363 Epub 2011 Aug 18

Longer Pain Durations are associated with Greater Declines in Cognitive Performance

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

43

Chronic Low Back Pain (CLBP) Patients Show Particular Loss of Gray Matter

(Cortical Thinning) in the DLPFC

DLPFC is Associated With bull Pain Modulation bull Placebo Analgesia bull Perceived Pain Control bull Pain Catastrophising bull Pain disengagement

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

DLPFC is Abnormally Thin in Untreated Chronic Low Back Pain (CLBP)

Abnormal Recruitment of DLPFC and Impaired Disengagement from pain Negatively Affects Task-Related Activity

Result Pain-Related Disability (Reduced Physical Ability)

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011

A Cortical Dysfunction Model of Chronic Non-Specific Low Back Pain

BMC Musculoskelet Disord 2008 9 11

Abbreviations LTP = Long Term Potentiation DLPFC = Dorsolateral Prefrontal Cortex mPFC = medial Prefrontal Cortex

Central Sensitisation

2011

CLBP Study Design A group of 14 CLBP Sufferers (pain for gt 1yr) were Treated with Either Spinal Surgery or Facet Joint Injection(nerve block) 11 reported Improvements in Pain and Pain-Related Disability 6 months later (lsquoRespondersrsquo) whilst 3 reported they were Worse This was confirmed by Questionnaires All Patients Initially had Significant Thinning of DLPFC as expected After 6 months all lsquoRespondersrsquo to treatment had Increased Thickness of DLPFC None of the non-responders showed this The extent of Thickening was Proportional to Both Improvements in Pain and in Pain-Related Disability

Seminowicz DA et al Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function The Journal of Neuroscience 2011 31 7540-7550

2011 Cortical Thickness Changes in Patients 6 months After Effective Treatment

Seminowicz D A et al J Neurosci 2011317540-7550 copy2011 by Society for Neuroscience

All 11 Responders showed increased gray matter thickness in the DLPFC 2 Non-responders are also shown

2011

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

44

2008

ldquo we have shown that treating chronic pain with CBT leads to increased GM in several brain areas including prefrontal and parietal regions and that decreased pain catastrophizing is associated with increased GM in

prefrontal and parietal areas Our data suggest that the GM changes following standard 11-week group CBT parallels clinical improvements in

coping with pain and overall mental healthrdquo

2013

Treatment of Refractory Pain

Non-Invasive Neurostimulation Therapy 1) Transcutaneous Electrical Nerve Stimulation (TENS) 2) Transcranial Magnetic Stimulation (TMS) 3) Transcranial Direct Current Stimulation (TDCS)

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory pain Discovery Medicine 2012 Jul14(74)21-31

2012

httpcourseswashingtoneduconjsensorypainhtm

Conventional TENS (70 ndash 100Hz) Pain Inhibition ndash Gate Control

Applied to the skin near the site of pain in order to stimulate the Ab fibres

and reduce the flow of pain information to the brain

Considered most useful for (sub)acute

pain states

ldquoAcupuncture-Like TENS (AL-TENS) (1-4Hz)

httpcourseswashingtoneduconjsensorypainhtm

Thought to activate anti-nociceptive systems via the PAG Effects at least

partly blocked by naloxone

Potentially of more use in treatment of chronic pain A recent RCT showed both real and sham TENS produced similar effects over a 1 year period

suggesting long-lasting placebo effects

Oosterhof J et al Pain Practice 2012 Sep12(7)513-22 The long-term outcome of transcutaneous electrical nerve stimulation in the treatment for patients with

chronic pain a randomized placebo-controlled trial

2012

Potential pathways activated by low-

frequency (LF) or high-frequency (HF) transcutaneous electrical nerve

stimulation (TENS) and receptors known to be

involved in the analgesia produced by

TENS

TENS for Hyperalgesia amp Pain

DeSantana JM et al Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain Current Rheumatol Reports 2008 Dec10(6)492-9

LF lt 10Hz HF gt 50Hz

2008

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

45

Transcranial Magnetic Stimulation

Mode of action is thought to be by disruption or

inhibition of ongoing processing in the stimulated regions

TMS

Transcranial Magnetic Stimulation

ldquoTranscranial magnetic stimulation (TMS) and transcranial direct

current stimulation (tDCS) are two noninvasive brain stimulation techniques that can modulate

activity in specific regions of the cortexrdquo

ldquoThere is clear evidence that these tools can reduce pain and modify neurophysiologic correlates of the

pain experiencerdquo

Allyson C Rosen et al Curr Pain Headache Rep 2009 February 13(1) 12ndash17

Patient receiving an outpatient rTMS session for refractory neuropathic pain

Nizard J et al Non-invasive stimulation therapies for the treatment of refractory

pain Discovery Medicine 2012 Jul14(74)21-31

2009

Treatment of Refractory Pain

Biofeedback - Sean Mackey

Brain_Controls_Pain

httpnewsstanfordedunews2006january11med-rein-011106html

Associate Professor Stanford University Pain Management Centre Neuroimaging expert

Sean Mackey has found that chronic pain sufferers can use real-time fMRI to reduce their pain while

viewing images of their own live brains

ldquoHypnoanalgesia has proved to be very effective in the treatment of pain which includes chronic oncological pain HIV neuropathic pain pain during extraction of molars pain associated to physical trauma pain in surgical

procedures pain associated to temporomandibular joint disorder phantom limb fibromyalgia pain in amyotrophic lateral sclerosis acute pain in

children lumbago and pain in childbirthrdquo

2014

ldquoDifferent changes in brain functionality occurred throughout all components of the pain network and other brain areas The anterior

cingulate cortex appears to be central in modulating pain circuitry activity under hypnosis Most studies also showed that the neural functions of the prefrontal insular and somatosensory cortices are consistently modified

during hypnosis-modulated painrdquo

2015 Participant Enjoying a Virtual Reality Game

Li A et alVirtual Reality and pain management current trends and future directions Pain Management March 2011147-157

Virtual Reality Analgesia has

proven efficacy during painful

medical procedures and is thought to

work by distraction of attention and a

sense of lsquotransportedrsquo

presence

2012

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time

Pain Theory for Therapists Alan P Smith BSc MSc DO ebmseminars 2015

46

First (Biopsychosocial) Consultation Video Clip ndash Key Points

Therapist Should Show

Empathy Listening Putting at Ease

Therapist Should Explore Patientrsquos

Beliefs Expectations Goals

First_Consultation

Whatrsquos the Problem

Brain Cord Periphery

Acute Physiological

Pain (eg Stub toe)

Acute Pathophysiological

Pain (eg Muscle strain)

Chronic Pathophysiological

Pain (eg OA)

Chronic Pathological

Pain (eg Fibromyalgia)

Patientrsquos Pain Complaint

ldquoThe pain started here in my low back but now itrsquos spreading down both legs and travelling up towards my neckrdquo ldquoMy back pain comes and goes It went away all yesterday afternoon whilst I was painting the garden fencerdquo ldquoMy neck pain started after a minor whiplash over a year ago But now itrsquos into my shoulders and I get headaches most days My GP says therersquos nothing wrong with merdquo ldquoThe pain in my leg only comes on when I hear an ambulancerdquo

Potential Painkillers Via Enhanced Belief and Expectation Reduced Anxiety Uncertainty lsquoThreatrsquo

Pre-Conditioning Why Consult You Belief (Trust) in you Clinic Reputation Recommendation Qualifications

About lsquoYoursquo Your Appearance Your Manner Good Listening Caring Attention Empathy Interest Friendliness Positivity Commitment Body Language Voice

Your Initial Interview Thorough Medical History History to lsquoProblemrsquo lsquoAttitudersquo to Problem

Your Diagnosis amp Prognosis Explain in some depth Use lsquonon-threateningrsquo words Discourage Excessive Rest Encourage lsquoPacedrsquo Activity Explain Pain lsquoPost Treatment Sorenessrsquo

About Your Clinic Welcome Certificates Clinic Ambience Warmth Calmness

Your Physical Examination Thorough Explanation During No lsquoRed Flagsrsquo Reassure

Summary ndash Treating Patientsrsquo Pain bull Remember pain is in the brain ndash not in the tissues

bull Try and apportion the contribution of central sensitisation

bull Search for psychosocial issues that increase lsquothreatrsquo or anxiety

bull Always show empathy and give reassurance Be careful not to alarm

bull Take every opportunity to exploit lsquoplaceborsquo opportunities

bull Use CBT to address unhelpful or negative lsquothoughtsrsquo

bull Use pain physiology education if negative thoughts are associated with pathoanatomical beliefs such as pain being proportional to some pathology

Question Time