pain physiology

May 1, 2023 Dr. Ashok Solanki 1

Pain physiology Nociception Dr. Ashok Solanki )

Everybody experience pain

Sign of underlying disease

Protective phenomenan


Tpes of painyAcute pain may be1.Somatic2.Visceral3.RefferedChronic- long lasting chronic diseases like arthritis.

PAIN - NOCICEPTION

Introduction Types of pain Pain receptors Pain stimulation Fast and slow pain Has dual feeling Path of both types of pain is different. Visceral pain is reffered Lateral spinothalamic tract Through thalamus in V.P.L. PAIN INHIBITORY SYSTEM OF BRAIN Sign of many underlying disease or damage.

a) Types of pain (somatic- fast/slow,muscular or visceral)

b) Pain pathway

c) Visceral pain & Referred Pain

d) Analgesic or pain control system of bDefinition of pain

e) Physiology of pain (properties & reaction) f) rain & spinal cord

g) Clinical

a) Definition of painPain sensation is unpleasant but protective sensation aroused by noxious stimuli that damage or can damage body tissues.

b) Physiology of pain (properties and reaction)Purpose or importance- Protective

Stimulus- noxious (chemicals like- Ach, bradykinin, serotonin, H,K, PGs or mechanical or thermal)

Receptors- free nerve endings (polymodal receptors)

Adaptation- non or slow adopting receptors

Nerve fibers- fast pain is carried by A-delta nerve fibers while slow pain by ’C’ type.

NT-- glutamic acid (at spinal cord) for fast pain, subs P (at spinal cord) for slow pain

Pathway- lateral spinothalamic (neo STT for fast pain paleo STT for slow pain)

Reaction- pain is associated with muscle spasm, withdrawal reflex (SC, fast pain), arousal (RF), unpleasant emotions (limbic system, slow pain) and autonomic changes- nausea, vomiting, pulse and BP changes (hypothalamus, slow pain)

Localization & Intensity discrimination- poor but better for fast pain

c) Pathways of Pain1) From face- by trigeminal nerve (5 cranial nerve)

2) From esophagus, trachea & pharynx- 9 & 10 CN (parasympathetic nerves)

3) From thoracic & abdominal viscera- sympathetic nerves

4) From pelvic region- parasympathetic nerves

5) From skin of rest of the body- by free nerve endings in lateral spinothalamic tract

VBC Of thalamus

thro. post. limb of IC

Primary sensory cortex

dorsal horn of spinal cord, Marginal nucleus for fast pain & Substantia gelatinosa for slow pain

neo STT (fast pain) & paleo STT (slow pain)

Origin, course & crossing

1 order neuronsArise from receptors (free nerve endings) to dorsal hornOf spinal cord, Marginal nucleus (MN) for fast pain &Substantia gelatinosa (SG) for slow pain

2 order neuronsarise from MN & SG, cross to opposite side thro. Ante.commissure & finally ascend in lateral column of SC asneo STT (fast pain) & paleo STT (slow pain) & relay at VBC Of thalamus & nearby st.

3 order neuronsarise from VBC of thalamus (mainly fast & few slow painfibers) & terminate at primary sensory cortex (area 3,1,2)

TerminationAll fast pain fibers & few (20%) slow pain fibers terminateat PSC while majority of slow pain fibers, subcortically atdiffuse nuclei of thalamus, tectal nucleus & RF.

CenterIs PSC but is perceived at the level of thalamus & RF

CollateralsTo RF (aurosal), limbic system (emotion) & hypothalamus(autonomic changes)

Ischemic muscle pain (SN)- During muscle activity Lewis P factor (adenine, K &

lactic acid) pass from muscle to tissue space & clear by blood

- But if level of Lewis P factor becomes high (ex- during exercise) pain starts till it is cleared

Clinical-

i) intermittent claudication (leg pain on walking, when arteries are blocked),

ii) angina pectoris (chest pain on exercise when coronary arteries are blocked )

Visceral pain (SN)Causes- 1. Over distension of hollow viscera (commonest), 2. Ischemia. 3. Obstruction 4. Spasm of hollow viscera.

Pathway- from via type C autonomic nerves to lateral STT.

Properties- -cause referred and radiating pain (like viscera toperitoneum).

-more commonly associated with muscle guarding,

-associated with unpleasant emotions and autonomic changes (nausea, vomiting, low pulse and low BP.)

-localization & intensity discrimination is poor

-Visceras insensitive to pain-

Parenchyma of liver, brain tissue and alveoli of lungs are insensitive to pain.

But liver capsule, bronchi, parietal pleura & meninges are very sensitive to pain.

Referred Pain (SN)

Referred Pain is the pain that is felt away from the damaged tissue.

Dermatome rule-

visceral pain is often referred to embryonic corresponding dermatome. The dermatome and the visceral are innervated by the nerves arising from the same spinal segment.

Example-

- Cardiac pain is referred to inside of the left arm.- Pain of Appendix & ovary is referred to umbilicus,- Diaphragm to rt. shoulder

1)convergence theory of referred pain

sensory nerve carrying pain sensation from the visceraand the sensory nerves carrying pain sensation thedermatome converge on to same second order neuron.

2) Facilitation theory of referred pain

sensory nerve carrying pain sensation from the visceravia branches (collaterals) stimulate sensory nervecarrying pain sensation from the dermatome. (producesubliminal fringe effect)

a) Analgesic or pain control system of brain and spinal cord Or

Mesenchephalic descending pain suppressing pathway

1. Periaqueductal grey area These fibers cause release of encephalin & stimulates neurons in raphe nucleus

2. The raphe magnus nucleus These fibers cause release of serotonin & stimulates neurons in spinal cord

3. Local neurons present in dorsal horns of spinal cord. These fibers cause release of encephalin.

& encephalin causes presynaptic inhibition of pain fibers entering into dorsal horn of spinal cord.

Stimulants ofAnalgesic system

-fibers from limbicSystem,hypothalamus

-Stress, psychological

-Collaterals from painpathway,

-Brain opiate system(endorphins andencephalin)

The raphe magnus nucleus in pons (serotonin)

Local neurons present in dorsal horns (encephalin)

Periaqueductal grey area in midbrain (encephalin)

presynaptic inhibition of pain fibers in dorsal horn

b) Gait control theory of pain (dorsal horn of SC)in the dorsal horn A beta, fine touch fibers cause pre-Synaptic inhibition of pain fibers & closes the date forpain sensation.

Role of brain in gate controlTerminals of pain fibers at dorsal horn have opiate receptors, here descending cortical fibers can also inhibitpain fibers & close the gate by secreting opiates

Clinical

Hyperalgesia- increase sensitivity to pain is known as hyperalgesia. It may be due to:

1) primary hyperalgesia- increase sensitivity of receptors

2) secondary hyperalgesia increase sensitivity of pathway. (thalamic overreacton)

Hypoalgesia- is decrease sensitivity to pain while

Paralgesia is abnormal pain sensation

Acute pain (good pain) & chronic pain (bad pain)


Two components of pain

Fast pain is acute- 0.1 secSharp pain

pricking acute pain burning pain

Only on superficial part Short duration Highly localized

Slow pain 1 sec later Slow burning Aching pain Throbbing pain Chronic pain Prolongrd Tissue damage or organ Poory localized


Common causes of painRise in body temp above 45 Some chemical –bradykininTissue ischemia- lack of oxygenMuscular spasm Inflammation5 Cardinal signs of inflammation Heat,

swelling, redness, tenderness, loss of function.Pain has psychological aspects.


Nociceptirs- and their stimulation

Free nerve endingsWidespreadStimuli- mechanical, electrical, chemical.Permanent or short duration.Slow adaptation natureProtective Rate of tissue damage


Pain has dual pathways

1. The sharp fast pain pathway2. Slow – chronic pain pathway.3. Fast by small type A delta fiber4. Slow by type C fibers– 0.5 to 2 m/sec5. Stimulus gives double sensation 6. Terminates on dorsal horns7. Carried to the brain

THE ANALGESIA SYSTEMPREAQUEDUCTAL GRAYRAPHE MAGNUS NUCLEUSPAIN INHIBITORY COMPLEX IN

DORSAL HORNS


Referred Pain – why away from the site of origin?

Dermatomal Rule- embriological devlopment of embriyo.

plasticity in the CNS coupled with convergence of peripheral and visceral pain fibers on the same second-order neuron that projects to the brain.


Dorsal Column–MedialLemniscal System

1. Touch sensations requiring a high degree of localization of the stimulus

2. Touch sensations requiring transmission of fine gradations of intensity

3. Phasic sensations, such as vibratory sensations

4. Sensations that signal movement against the skin

5. Position sensations from the joints 6. Pressure sensations having to do with fine

degrees of judgment of pressure intensity


Area S1

AnterolateralPathwayAnteriorandLateralDivision

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Characteristics of Transmission in the Anterolateral Pathway

the velocities of transmission are only one third the degree of spatial localization of signals is

poor; the gradations of intensities are also far less accurate the ability to transmit rapidly changing or rapidly repetitive signals is poor. is a cruder type of transmission system than the

dorsal column–medial lemniscal system.

Dr. Ashok Solanki

PAIN CONTROL (ANALGESIA)

THE ANALGESIA SYSTEMTHE BRAIN’S OPIATE SYSTEM INHIBITION OF PAIN BY TACTILE

STIMULATIONTREATMENT OF PAIN BY ELECTRICAL

STIMULATIONREFERED PAIN

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Distribution of Referred Pain

Dr. Ashok Solanki 36

Monday, May 1, 2023 37


Structurally distinct areas, called Brodmann’s areas, of the human

cerebral cortex.DIVISIBLE INTO 50 AREAS.


Referred Pain

Not at the site but superficial part of skin.Deep somatic pain may also be referredcardiac pain to the inner aspect of the left

arm tip of the shoulder caused by irritation of

the central portion of the diaphragm Important clinical sign for clinician.Follows the Dematological rule.

Three major pathways carry sensoryinformation– Posterior column pathway– Anterolateral pathway– Spinocerebellar pathway


Role of Formation, Thalamus, Cerebral Cortex

cortex plays an especially important role in interpreting pain quality

strong arousal effecta cordotomy in the thoracic region of the

spinal cord often relieves the paincauterize specific pain areas in the

intralaminar nuclei in the thalamus


Transmission of Less CriticalSensory Signals in theAnterolateral Pathway

Carries following sensationsPain heat,Coldcrude tactileTickle Itchsexual sensations


PALEOSPINOTHALMIC TRACTfor transmitting slow- chronic pain

Slow –chronic type C fibersLamina 2 and 3 of dorsal hornsJoined by lamina 5.To anterior commissureTo the opposite side of the cordTo the brain through anterolateral pathwaySubstance P – the NT.


Pain Suppression


Neospinothalamic tractTerminate mainly in lamina 1.Fast A delta fibersCross immediately opposite side.To anterior commissureUpwards passing to brainCalled anterolateral column.Glutamate – the NT.


Projection of the Paleospinothalamic Pathway

terminates widely in the brain stem Only one tenth to one fourth of the fibers pass all the way

to the thalamus most terminate in one of three areas (1) the reticular nuclei of the medulla, pons, and

mesencephalon (2) the tectal area of the mesencephalon (3) the periaqueductal gray region surrounding the

aqueduct of SylviusThen upward to the thalamus and hypoyhalamus


Some Clinical Abnormalitiesof Pain

HyperalgesiaHerpes Zoster (Shingles)Tic DouloureuxBrown-Séquard Syndrome

pain physiology

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