EVERY PAIN IS NEEDED TO TREAT

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IS EVERY PAIN REQUIRES TREATMENT ?:

IS EVERY PAIN REQUIRES TREATMENT ? DR.S.SREENIVASARAO MD,C.C.P.P.M, ASSIST PROFESSOR, DEPT.OF ANAESTHESIA, S.V.R.R.G.G.H.&S.V.M.C, TIRUPATI

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“ An unpleasant sensory and emotional experience associated with actual or potential damage or described in terms of such damage ” -International Association for the Study of Pain, 1979

PROPHYLACTIC TREATMENT:

PROPHYLACTIC TREATMENT EVERY PERSON TALKS ABOUT P’ TO ATHEROSCLROSIS P’ TO M.I, P’ TO D.M, P’ TO HTN etc BUT NOT P’ TO PAIN …………..?

REASONS FOR NOT TO TALK ARE……:

REASONS FOR NOT TO TALK ARE…… WE ARE GIVING LESS IMP TO PAIN OR WE ARE TREATING WHEN IT IS MORE DISTURBING LACK OF AWARENESS REGARDING PAIN CONSEQUENSES

QUALITY OF LIFE………:

QUALITY OF LIFE……… MAN STARTED USE LEGS---HORSE---BICYCLE---MOTOR BIKE---CAR---AEROPLANE…………… EVERY TIME HE SEARCHES HIS COMFORT CAN HE ENJOYS HIS LIFE WITH PAIN ?

PAIN CONSEQUENSES:

PAIN CONSEQUENSES MODULATION OF PAIN AT PERIPHARY LEVEL PRIMARY HYPERLAGESIA SEC. HYPERLAGESIA AT SPINAL LEVEL CANTAL SENSITIZATION AT SUPRASPINAL LEVEL

NOCICEPTORS :

NOCICEPTORS FUNCTION DETECTION & TRANSDUCTION&TRANSMISSION OF NOXIOUS STIMULI TYPES 1.EXTEROCEPTORS—SKIN SURFACES 2.INTEROCEPTORS—VISCERAL WALLS DEEP BODY STRUCTURES

ERLANGER & GESSER CLASSIFICATION:

ERLANGER & GESSER CLASSIFICATION FUNCTION SIZE SPEED A ALFA BET GAMA DELTA MOTOR&PROPRIOCEPTION TOUCH &PRESSURE MUSCLE SPINDLE PAIN 1--20 MICRO METRE 5-20 M/SEC B POSTGANDLIONIC SYMPATHETIC & VISCERAL AFFERENTS <3 MICRO METRE 3—14 M/SEC C PAIN&PREGANGLIONIC AUTONOMIC

TABLE 55-1 Somatosensory Receptors:

TABLE 55-1 Somatosensory Receptors RECEPTOR SENSATION PERCEIVED Nerve fibers on hair follicles Touch Merkel's disks Touch Meissner's corpuscles Touch Free nerve endings (nociceptors) Pain Krause's end bulbs Cold Ruffini's endings Heat Pacinian corpuscles Pressure Golgi-Mazzoni endings Pressure

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Serotonin, noradrenaline

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Chemical Excitation of Non-nociceptors beta

Recruitment:

Recruitment Neuroanatomical Reorganisation Recruitment to adjacent segments Nerve injury + recruitment of nerves outside site of injury State of Hyperalgesia - Primary and secondary

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NERVE INJURY DRG NEUROCHEMICAL ANATOMICAL INCREASE IN SURVIVAL FACTORS CELL DEATH ALTERATION OF TROPHIC FCTR EXPRSN SYMPATHETIC SWITCH IN EXITATORY PEPTIDES SPROUTING INCREASE OF INHIBITORY PEPTIDES CHANGE IN RECEPTOR EXPRESSION INCREASE IN NITRIC OXIDE SYNTHASES CHANGE IN ION CHANNEL ALL THE ABOVE LEADS TO PHYSIOLIGICAL CHANGES LIKE REDUCTION IN PRESYNSPTIC INHIBITION ECTOPIC DICHARGES

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NERVE INJURY DORSAL HORN NEUROCHEMICAL ANATOMICAL REDUCTION IN GABA RECEPTORS TERMINAL ATROPHY REDUCTION IN OPIOD RECEPTORS CELL LOSS GLIA CELL ACTIVATION APOPTOSIS INCREASE IN CYTOKINES INCREASE IN IMMEDIATE EARLY GENES INCREASE IN TRANSCRIPTION SIGNALS ALL THESE ABOVE CHANGES CAUSES INCREASED WINDUP ,LONG TERM POTENTIATION REDUCED INHIBITORY CONTROLE IN DORSAL HORNS

Mechanisms of Neuropathic Pain:

Mechanisms of Neuropathic Pain Chemical Excitation of non-nociceptors Recruitment of nerves outside the site of injury Excitotoxicity Excess Sodium channels Ectopic discharge De-afferentation Central sensitization maintained by peripheral input Sympathetic involvement Ephaptic cross talk

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Glutamate Substance P Excessive Sodium channels Excessive Calcium channels Decreased Potassium channels Nerve Growth Factor, Nitric-oxide Present mainly in Dorsal Horn Cells Increased Stimulation causes ‘Wind up’ Phenomena Increased Excitation leads to Persisting pain Agents which increase NMDA Receptor activity: Central Sensitisation - Role of NMDA Receptor

Ectopic Discharge :

Ectopic Discharge Discharge of impulses from Areas of nerve which normally should not be discharging

CONSEQUENSES:

CONSEQUENSES Peripheral Sensitisation & Recruitment Central Sensitisation & “Wind up” Somatic - Neuropathic interphase Reflex responses Genetic changes

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