Sem-3 physiology of pain

7/28/2019 Sem-3 physiology of pain

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WHAT IS PAIN ?

Pain is a complex physical, psychological and social experience.Aristotle described it as a quale: a passion of the soul

Sternbach defined pain as 1) Personal and private sensation of

hurt; 2) A harmful stimulus that signals current or impending tissue

damage; and 3) A pattern of responses that operates to protect theorganism from harm.


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Definition

Fields de fined pain as an unpleasant sensation that is perceived as

arising from a specific region of the body and is commonly produced

by processes that damage or are capable of damaging bodily tissue.

International Association for the Study of Pain (IASP)An unpleasant sensory and emotional experience associated with

actual or potential tissue damage, or described in terms of such

damage.


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BENEFITS OF PAIN SENSATION

Pain is an important sensory symptom. Though it is an unpleasant

sensation, it has protective or survival benefits such

1. It gives warning signal about the existence of a problem or threat

It also creates the awareness of injury

2. It prevents further damage by causing reflex withdrawal of thebody from the source of injury

3. It forces the person to rest or to minimize the activities thus

enabling the rapid healing of the injured part

4. It urges the person to take required treatment to prevent majo

damage.


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AUTONOMICNERVOUS SYSTEM-

maintains visceral

activities of the body

Sympathetic nervous

system- originate in thespinal cord between

T1&L2

Para sympathetic n.s-

>consists of fibers

leaving the CNS through

the cranial nerves

3,7,9,10&2,3,sacral

spinal nerves .


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Afferent (Ascending) transmit impulses from the periphery

to the CNS.

Sensory nerves are afferent nerves.

Efferent (Descending) transmit impulses from the CNS tothe periphery.

Motor nerves are efferent nerves & supplies the muscle or

an exocrine gland.


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A-alpha

myelinated

13-20um 70-120m/sec Somatomotor (a motor),

proprioception.

A-beta

myelinated

6-13um 40-70m/sec Touch and pressure.

A-gamma

myelinated

3-8um 15-40m/sec Motor to muscle spindle.

A-deltamyelinated

1-5um5-15m/sec

Pain, touch, temperature.

Bmyelinated

1-3um 2.5-15m/sec Preganglionic autonomic.

Cunmyelinated

0.5-1um 0.7-1.5m/sec Dorsal root fibres (pain,temperature, etc,, Post-ganglionic

sympathetic.


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A nerve ending is the termination of a nerve fiber in aperipheral structure.

Nerve endings may be sensory (receptor) or motor

(effector).


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RECEPTORS

Receptors are the sensory (afferent) nerve endings that terminate in the

periphery as bare unmyelinated endings or in the form of specializedcapsulated structures.

The receptors give response to the stimulus. When stimulated, receptor

produce a series of impulses which are transmitted through the afferent

nerves.

Actually receptors function like a transducer. Transducer is a device, whi

converts one form of energy into another.

So, the receptors are often defined as the biological transducers whichconvert (transduce) various forms of energy (stimuli) in the environmen

into action potentials in nerve fiber.


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The receptors are located such that they are exposed to the

surrounding external environment. They mostly respondat the conscious level.

Merkels corpuscles Tactile receptors in the submucosa

of the tongue and oral mucosa.

Meissners corpuscles Tactile receptors in the skin.

Ruffinis Sense pressure and warmth.

Krause Sense cold

Free nerve endings Perceive superficial pain and touch


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They are involved with the functioning of ANS. Most

sensations are below consciousness level.1. Muscle spindles Mechanoreceptors sense stretch

(myotactic response)

2. Golgi tendon organs Mechanoreceptors in tendons

signal contraction and stretching are responsible for

nociceptive and inverse stretch reflexes.

3. Pacinian corpuscles Perception of pressure.

4. Periodontal mechanoreceptors

5. Free nerve endings Perceive deep somatic pain.


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Involved with organs of involuntary functioning. They are

sensory receptors located in and transmit impulses fromthe viscera. Function mostly below consciousness level.

1. Pacinian corpuscles Perception of pressure.

2. Free nerve endings Perceive visceral pain.

Associated with all vascular tissue, including endocardium is a

network of sensory receptors derived from myelinated

nerve fibers called endnet, which provides sensory

information from these vessels.


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Nerve signal transmitted from one neuron to next through interneuronaljunctionsSYNAPSE

Neuro chemicals transmitting impulses across the synaptic cleft

neurotransmitters

RAPID ACTING (small molecule) NT-acetyl choline, norepinephrine,

glutamate, aspartate, serotonin, GABA, glycine, dopamine, histamine

SLOW ACTING (large molecule)-Substance P, endorphins, bradykinin


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Found in synapses

Bradykinin - Many researchers have suggested that bradykinin

might be the agent most responsible for causing pain following

tissue damage Substance P - thought to be responsible for the transmission of

pain-producing impulses,


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2 types of chemical neurotransmitters that mediate pain

Endorphins - morphine-like neurohormone; thought to pain

threshold by binding to receptor sites

Serotonin - substance that causes local vasodilation & permeability of capillaries

Both are generated by noxious stimuli, which activate the inhibition

of pain transmission


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The transmission of painful impulses in the nervous system1.Nociceptive afferent pain receptors

2.Dorsal horn of spinal cord

3.Ascending spinothalmic tract

4.Thalamus5.Higher brain centres

6.Descending pain modifying pathways


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FIRST ORDER NEURONS Stimulated by sensory receptors End in the dorsal horn of the spinal cord

SECOND ORDER NEURONS The marginal cells and the cells of substantia

gelatinosa form the second order neurons. Fibers from these cells ascend &

terminate in ventral posterolateral nuclei ofthalamus.

THIRD ORDER NEURONS They are the neurons of thalamic nucleus,

reticular formation, tectum and grey matteraround aqueduct of sylvius & terminate onpost central gyrus.


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There are 3 classes of nociceptive afferent neurons which

constitute the 1st order :

1. Mechanothermal afferents Are usually A delta fibers

with a velocity of 12 to 18m/s and respond to intensethermal and mechanical stimuli

2. Polymodal afferents Are C fibers with a velocity of

0.5m/s and respond to mechanical, thermal and chemical

stimuli.3. High threshold mechanoreceptive afferents Are A delta

fibers again which respond to intense mechanical stimuli.


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There are three types of second order neurons.1. Low Threshold Mechanosensitive neurons (LTM)2. Nociceptive specific neurons (NS)

3. Wide Dynamic Range neurons (WDR)

Dorsal horn of spinal cord is subdivided into 6 LaminaeNS and WDR transmit to Laminae I II and VLTM transmits to Laminae III and IV

The region of large number of excitatory interneurons inLaminae II and III is Substantia Gelatinosa of Rolandi.


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Once the impulses have been transferred from the primary

afferents most of the second order neurons cross to the

opposite side of the spinal cord and enter the anterolateral

spinothalamic tract composed of small myelinated andunmyelinated fibers that transmit at 40m/s

Some 2nd order neurons remain on the same side and

ascend by leminscal system and cross over at the level of

medulla. This is composed of large myelinated nerve fibersthat transmit at 30 to 110m/s.


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Anterolateral spinothalamic tract Conducts at a slower rate

and transmits pain, warmth, cold, crude tactile sensations.

Lemniscal tract Immediate response. Pressure, vibration,

touch and proprioception is transmitted through it.

ALT

Neospinothalamic - Adelta

Paleospinothalamic C fibers


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Descending Pain Modulation(Descending Pain ControlMechanism)

Transmit impulses from the brain(corticospinal tract in the cortex) tothe spinal cord (lamina)

Periaquaductal Gray Area (PGA) release enkephalins

Nucleus Raphe Magnus (NRM)release serotonin

The release of theseneurotransmitters inhibit

ascending neurons.


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NOXIOUS

STIMULUS

NOCICEPTORS

PERIPHERAL

NEURALGIC

PATHWAY

CNS

MECHANISMS

PERCEPTION

OF PAIN

PAIN


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Field- described the complex electrical &chemical events involved in the

human pain experience

TRANSDUCTION- noxious stimulus acts upon free nerve endings (pain

receptors) leading to electrical activity-> nerve impulse (action potential)

TRANSMISSION- conveying impulse to CNS

MODULATION-central neural activity controls pain signals

PERCEPTION OF PAIN


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SPECIFICITY THEORY PATTERN THEROY

GATE CONTROL THEORY


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SPECIFICITY THEORY

Classical description provided by Descartes in 1644.

He conceived of a pain system as a straight- through channel

from the skin to brain. Muller in 19th century postulated that the theory of

information only by way of the sensory nerves.

Late 19th century, Von Frey developed the concept of specific

cutaneous receptors for the mediation of touch , heat, coldand pain.

Free nerve endings were implicated as pain receptors.


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PATTERN THEORY In 1894 Goldscheider was the first to propose that stimulus

intensity and central summation are the critical

determinants of pain. Theory suggested that particular patterns of nerve impulses

that evoke pain are produced by the summation of sensoryinput within the dorsal horn of the spinal column.

Pain results when the total output of the cells exceeds a

critical level.For Example; touch+pressure+heat might add up in such amanner that pain was the modality experienced.


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Melzack & Wall, 1965

Substantia Gelatinosa (SG) in dorsal horn of spinal cord act

as a gate only allows one type of impulses to connect

with the Second order neuron.

If A-beta neurons are stimulated SG is activated whichcloses the gate to A-delta & C neurons

If A-delta & C neurons are stimulated SG is blocked which

closes the gate to A-beta neurons

Gate - located in the dorsal horn of the spinal cord


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Gate located in the dorsal horn of the spinal cord

Smaller, slower nerve carry pain impulses

Larger, faster nerve fibers carry other sensations

Impulses from faster fibers arriving at gate 1st inhibit pain

impulses (acupuncture/pressure, cold, heat, chem. skin

irritation).


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THRESHOLD AND INTENSITY.If the intensity of the stimulus is below the threshold

pain is not felt.

As the intensity increases more and more pain is feltmore and more and the pain sensation spreads.

However if the mind is distracted the threshold ofpain increases.


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ADAPTATION

Pain receptors show no adaptation and so the pain continues

as long as the receptors continue to be stimulated.

LOCALIZATION OF PAIN

Pain sensation is somewhat poorly localized. Superficial pain is

comparatively better localized than the deep pain.


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EMOTIONAL ACCOMPANIMENT.

Pain sensations are commonly accompanied by emotions.

These emotions as a rule are unpleasant.

INFLUENCE OF THE RATE OF DAMAGE ON THE INTENSITY OF

PAIN

If the rate of tissue injury is high, intensity of pain is also high

and vice versa. Eg: cancer in the beginning are mostlypainless.


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BEHAVIOURAL

This includes crying, moaning, whining. In long standing pain

frustration, mental irritation or depression can develop.

MUSCULAR

Spasm of the skeletal muscles in the affected region develops.

It causes immobilization or ischemia.


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CHANGES IN THE ANS.

Somatic pain is usually accompanied by signs of sympathetic

over activity eg: rise of BP, tachycardia and pupillary dilation

Conversely in visceral pain there is often fall of BP andvomiting.

REFLEX RESPONSE.

A painful stimulus is usually associated with somatic reflexeseg: pin prick and withdrawal of hand.


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Clinical vs. experimental pain: Pain as presented by patientsi.e. the pathologic or clinical pain is different from the

experimental pain that is induced and is studied in a

laboratory.

They are explained by different mechanisms, it is likely that

the emotional significance embodied in clinical pain is the

real determinant.

Acute vs chronic pain:


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Acute vs. chronic pain:

Acute pain It is caused by an injury to the body. It can develop slowly or quickly. It can last for a few minutes to six months and goes away

when the injury heals.

Chronic pain

Persists long after the trauma has healed (and in somecases, it occurs in the absence of any trauma). It usually lasts longer than six months

There is a definite relationship between duration and intensity


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There is a definite relationship between duration and intensityof pain. The higher the intensity, the shorter the period thepain can be tolerated by the sufferer. Low-intensity pain canbe sustained for about 7 hours, whereas pain of maximum

intensity can hardly be sustained for a few seconds.

Primary vs. secondary pain: The site where pain is felt may ormay not identify the location of the source of the pain. If thepain does emanate from the structures that hurt then it

constitutes a primary nociceptive input.If however the true source of pain is located elsewhere, thearea of discomfort represents secondary pain, secondarypains are called heterotopic pain.

Stimulus evoked vs spontaneous pain: Most primary


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Stimulus evoked vs. spontaneous pain: Most primary

somatic pains result form stimulation of neural structures at

the site. The clinical characteristics displayed by stimulus

evoked pain relates to the location, timing, and intensity ofthe stimulus.

Neuropathic pain maybe felt spontaneously along the

distribution of the affected nerve. Heterotopic pain occursspontaneously as far as the site of pain is concerned.

SOMATIC PAIN


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SOMATIC PAIN Noxious stimulation of somatic structures, sensory

nervous system. It can be Superficial or Deep- musculoskeletal.

NEUROPATHIC PAIN Chronic state due to a series of changes in the nervous

system. CNS has been sensitized by repetitive direct or indirect

injury.

PSYCHOGENIC PAIN individual feels pain but cause isemotional rather than physical

REFERRED PAIN


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REFERRED PAIN

Visceral pain is often referred ,that is pain is not felt over the

area where the viscus is situated but is felt somewhere else.

l f f d i


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examples of referred pain

Cardiac pain is fell al the inner part of left arm and left

shoulderPain in ovary is referred to umbilicus

Pain from testis is felt in abdomen

Convergence


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Convergence

The sympathetic afferent fiber carrying the pain sensation emerges from

the viscus and via the dorsal root ganglion ends at the posterior horn of

the spinal cord. Afferent somatic nerve, emerging from the pain receptor,

of the corresponding dermatome of this viscus, enters the same segmentand terminates on the very same cell where the sympathetic nerve is

terminating, i.e. these two different neurons converge on the same next

order neuron. Therefore, when the next order neuron is stimulated the

impulse reaches the brain and the person feels pain, but he feels as if

the pain is coming from the dermatome (not the viscerotome).

Subliminal fringe effect


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g

The afferent sympathetic nerve bringing pain sensation from the

viscus terminates on the second order neuron; but at the same time

it also, via collateral, stimulates another second order neuron. thislast named second order neuron is synapsing with the somatic

neuron of the corresponding derma tome. Therefore, when the pain

is felt by the patient, he feels as if the pain is coming from the

corresponding dermatome.


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Increased catabolic demands: poor wound

healing, weakness, muscle breakdown

Decreased limb movement:

Respiratory effects: shallow breathing, tachypnea,

cough suppression increasing risk of pneumonia

Tachycardia and elevated BP


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Negative emotions: anxiety,depression

Sleep deprivation

Existential suffering: may lead to

patients seeking active end of life.


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In the assessment of pain intensrating scale techniques are often

used. The most commonly usedforms are

. The Visual Analogue Scales (VA(e.g. 10 cm line with anchor poinat each end). The VAS has beenshown to be more sensitive tochange and is therefore morewidely used.

Wong-Baker FACES Pain Rating Scale


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Verbal pain scale.

Uses vast array of words commonly used to describepain empirically.Items 1-10 ,18 &19-character or sub-modality of pain 11-16 and 20- indicate affective (emotional ) pain

components 17-concerns localization PPI- patients pain intensity rating accompanying symptoms
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Turk and Rudy have developed the Multiaxial Assessment of
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Pain (MAP) classification. Their assessment included a 61-

item questionnaire West Haven-Yale Multidimensional Pain

Inventory (WHYMPI), which measures adjustment to painfrom a cognitive behavioral perspective.

Dworkin, LeResche and collegues have developed a method

for assessing dysfunctional chronic pain as a part of

classification system, the Research Diagnostic Criteria.

They used:


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a) The Graded Chronic Pain severity scale,

b) Depression and vegetative symptom scale,

c) Jaw disability checklist.

One of the other scales that can be used to measure pain is

Pictorial representation of illness and self measure or

(PRISM).


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Pain at the angle Cardiac ischemia

New onset, localized, headache, superficialtemporal a. swelling, transient visual

abnormalities, systemic symptoms

Temporal arteritis.

New onset of headache in adult life, nausea,

vomiting, nocturnal occurrence, neurologic

signs

Intracranial tumor

Earache, trismus, altered sensation in the

mandibular branch distribution.

Trigeminal neuralgia


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Throbbing, unilateral,frontal, temporal, young

with history

Throbbing intense ache,periorbital,20-50yrs,smoking

habit

Throbbing with burningache, area of artery,>50

yrs

1-2days,Episodic

Visual, GI, cold

extremities,

Min-hrs, cluster of days to

weeks, lacrimation,

perspiration no prodrome

Hrs-days, tender swollen

artery, fever, malaise

Diet,hypoglycaemia,stress, alcohol

alcohol, vasodilators Continuous

stress, estrogen

imbalance

Stress, tension, vasodilators Lying position,

mastication

Vasoconstrictors,

holding head still

Vasoconstrictors, distractors Pressure in artery,

upright position

Family history, relief

with ergot

Brought on by sublingual

nitroglycerin, family history

Inflammation-

biopsy,>ESR

MIGRAINE CLUSTER ARTERITIS

Quality

Duration

Precipitate

Aggravate

Alleviate

Key diagnostics


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Ache, steady, head, neck,shoulders . Steady ache, in ear, periauricular

Constant, nonprogressive, all

ages, limited movement,

tenderness,

Fluctuates, all ages limited

motion, crepitus clicking

Stress, bruxism, trauma,occlusion, jaw opening

Aging, trauma

Exercise, cold weather, systemic

disorders, stress

Movement, chewing, yawning,

occlusal disharmony

Massage ,heat, exercise Rest, heat, cold

Palpation of muscle trigger point,

referral, injection historyExamine, radiograph, associated

with myofascial pain

MUSCULAR TMJ

Quality

Duration

Precipitate

Aggravate

Alleviate

Determinants


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Pain may occur because of progression of thedisease, treatment procedures, recurrence of

uncontrolled disease following treatment

Stimulation of mucosal & sub mucosal nerve

endings, tumor infiltration of peripheral nerves,

ulceration & infection

Pain may be felt at the primary site, referred to

another site or both


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Modified WHO Analgesic Ladder


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PainStep 1

NonopioidAdjuvant

Pain persisting or increasing

Step 2Opioid for mild to moderate pain

Nonopioid Adjuvant

Pain persisting or increasing

Pain persisting or increasingStep 3

Opioid for moderate to severe painNonopioid Adjuvant

Invasive treatments

Opioid Delivery

Quality of LifeProposed 4th Step

The WHO

Ladder


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Decrease the frequency and / orseverity of the pain

General sense of feeling better

Increased level of activity

Return to work

Elimination or reduction inmedication usage


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1. Removing the cause Desirable method

Affects pain perceptionElimination of cause

No more excitation of free nerveendings

No more impulses

2. Blocking the pathway of painful impulses

Most widely used method in dentistry

ff


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Affects pain perception

LA injected into tissues in proximity to nerve

Prevents depolarization of nerve fibers

Conduction blockade

3.Raising the pain threshold


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g p Pain perception is reduced at first synapse. Pain threshold is increased to limited degree only, depending

upon the type of drug. E.g. NSAIDs & Opioids Opioids are able to raise pain threshold to a greater degree

than NSAIDs. Certain drugs also act on cortical & subcortical areas &

reduces fear, anxiety & apprehension.


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4. Preventing the pain reaction by cortical depression

Cortical depression causesa. Loss of all sensations, especially painb. Sleep (unconsciousness) & amnesiac. Immobility & muscle relaxationd.

Abolition of reflexes E.g. general anesthetic agents

5 Using psychosomatic methods


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5.Using psychosomatic methods

Affects both pain perception & pain reaction Have honesty & sincerity towards the patient Keep the patients well informed about the procedure Avoid surprises & rapid movements. Patients central control mechanism aids in pain control

Better than pharmacologic method with no side effects.


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1. Burkets Textbook of Oral Medicine 10th edition.2. James R Fricton and Kate M Hathaway, TMJ and Orofacial

Pain.3. Bells Orofacial pains Jeffery P Okeson.4. Concise medical physiology Chaudhuri.5. Essentials of Medical Pharmacology- K.D.Tripathi6. Principles of anatomy and physiology. Eleventh edition.

Gerard J Tortora, Bryan Derrickson.

Sem-3 physiology of pain

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