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Pain Physiology Rdt

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  • 1. PAIN PHYSIOLOGY RDT HOSPITAL, BATHALAPALLI
  • 2. WHAT IS PAIN?
    • In 1968 McCaffery defined pain as
    • “ whatever the experiencing person says it
    • is, existing whenever he/she says it does”
    • In 1979 IASP defined pain as “unpleasant
    • sensory and emotional experience
    • associated with actual or potential tissue
    • damage, or described in terms of such
    • damage.”
    • Pain from poena ---> Latin means punishment.
  • 3. VARIOUS TERMINOLOGIES FUNCTIONAL ABNORMALITY OF NERVE ROOTS RADICULOPATHY ABNORMAL SENSATION PERCEIVED WITHOUT AN APPARENT STIMULUS PARASTHESIA PAIN IN THE DISTRIBUTION OF A NERVE NEURALGIA REDUCED CUTANEOUS SENSATION HYPOASTHESIA INCREASED RESPONSE TO MILD STIMULUS HYPERASTHESIA INCREASED RESPONSE TO NOXIOUS STIMULUS HYPERALGESIA DIMINISHED RESPONSE TO NOXIOUS STIMULUS HYPOALGESIA UNPLEASANT SENSATION WITH OR WITHOUT STIMULUS DYSESTHESIA PAIN IN AN AREA THAT LACKS SENSATION ANESTHESIA DOLOROSA ABSENCE OF ALL SENSATIONS ANESTHESIA ABSENCE OF PAIN PERCEPTION ANALGESIA PERCEPTION OF NON-NOXIOUS STIMULUS AS PAIN ALLODYNIA DESCRIPTION TERM
  • 4.
    • Nociceptive
    • Neuropathic
    • Psychogenic
    CLASSIFICATION OF PAIN
  • 5. TYPES OF PAIN FIBRES DULL ACHE, DIFFUSE   No   1 (slow)   C   SHARP, PRICKING,WELL LOCALIZED    YES 20 (fast) A- DELTA TYPE OF PAIN MELINATED CONDUCTION VELOCITY ( MTS/SEC ) TYPE OF NERVE
  • 6. PAIN PATHWAY
  • 7. SPINALCORD LAMINAE CENTRAL CANAL Aβ X MOTOR HORN Aβ MOTOR IX MOTOR HORN Aβ VIII INTERMEDIOLATERAL COLUMNS SYMPATHETIC VII NUCLEUS PROPRIUS Aβ MECHANORECEPTION VI NUCLEUS PROPRIUS WDR NEURONS Aβ, Aδ, C VISCERAL & SOMATIC NOCICEPTION & MECHANORECEPTION V NUCLEUS PROPRIUS Aβ, Aδ, MECHANORECEPTION IV NUCLEUS PROPRIUS Aβ, Aδ SOMATIC NOCICEPTION MECHANORECEPTION III SUBSTANTIA GELATINOSA C, Aδ SOMATIC NOCICEPTION THERMORECEPTION II MARGINAL LAYER Aδ, C SOMATIC NOCICEPTION THERMORECEPTION I NAME INPUT PREDOMINANT FUNCTION LAMINA
  • 8. PHYSIOLOGY OF NOCICEPTION
    • 1. NOCICEPTORS
    • CUTANEOUS
    • DEEP
    • VISCERAL
    • 2. CHEMICAL MEDIATORS
    • 3. MODULATION OF PAIN
    • PERIPHERAL
    • CENTRAL
  • 9. NOCICEPTORS
    • CUTANEOUS
    • PRESENT IN SKIN AND SUBCUTANEOUS TISSUE
    • CHARACTERIZED BY SHARP AND BURNING PAIN
    • 2. DEEP
    • PRESENT IN BONE, MUSCLES, BLOOD VESSELS
    • CHARACTERIZED BY DULL, ACHING & CRAMPING PAIN
    • LESS SENSITIVE TO NOXIOUS STIMULI THA THE CUTANEOUS NOCICEPTORS BUT EASILY SENSITIZED BY INFLAMMATION
    • VISCERAL
    • PRESENT IN ORGANS & LININGS OF BODY CAVITY
    • CHARACTERIZED BY DIFFUSE, DEEP CRAMPING / STABBING PAIN
    • PAIN IS POORLY LOCALIZED UNLIKE CUTANEOUS NOCICEPTORS
  • 10. CHEMICAL MEDIATORS INHIBITORY GLYCINE INHIBITORY A.B GABA INHIBITORY 5-HT SEROTONIN INHIBITORY A1 ADENOSINE INHIBITORY Α2 NOREPINEPHRINE INHIBITORY µ, δ, κ B- ENDORPHIN INHIBITORY µ, δ, κ ENKEPHALIN INHIBITORY M1 Ach INHIBITORY SOMATOATATIN EXCITATORY P1, P2 ATP EXCITATORY NMDA ASPARTATE EXCITATORY NMDA GLUTAMATE EXCITATORY CALCITONIN EXCITATORY NK – 1 SUBTANCE P EFFECT ON NOCICEPTION RECEPTOR NEUROTRANSMITTER
  • 11. PAIN MODULATION
    • CAN EITHER INHIBIT OR FACILITATE PAIN
    • MODULATION CAN BE OF TWO TYPES
    • PERIPHERAL
    • CENTRAL
    • PERIPHERAL MODULATION
    • TISSUE INJURY
    • RELEASE OF SUBBSTANCE-P CHEMICAL MEDIATORS OF
    • AND GLUTAMATE INFLAMMATION
    • STIMULATE NOCICEPTORS IN
    • THE PERIPHERY
  • 12. PAIN MODULATION
    • CENTRAL MODULATION
    • FACILITATION
    • THREE MECHANISMS ARE RESPONSIBLE
    • WIND-UP & SENSITIZATION OF 2 ND ORDER NEURONS
    • ( WDR NEURONS )
    • RECEPTOR FIELD EXPANSION
    • HYPEREXITABILITY OF FLEXION REFLEXES
    • INHIBITION
    • NOCICEPTIVE INPUT CAN BE INHIBITED BY
    • SEGMENTAL INHIBITION
    • SUPRASPINAL INHIBITION
  • 13. PAIN MODULATION
    • SEGMENTAL INHIBITION
    • GATE- CONTROL THEORY ( WALL AND MELZACK 1965 )
    • ACTIVATION OF LARGE AFFERENT FIBRES ( A-BETA ) INHIBITS WDR NEURONS & ST TRACT ACTIVITY
    • ACTIVATION OF NOXIOUS STIMULI IN NON-CONTIGUOUS PART OF THE BODY INHIBITS WDR NEURONS IN OTHER LEVELS
    • GLYCINE AND GABA AMINO ACIDS
    • FUNCTION AS INHIBITORY NEUROTRANSMITTERS IN THE SPINAL CORD
    • THEY INHIBIT FACILITATION OF WDR NEURONS
    • ADENOSINE
    • MODULATES NOCICEPTIVE ACTIVITY IN THE DORSAL HORN
    • IT IS MEDIATED BY A1 RECEPTOR ACTIVITY WHICH INHIBITS ADENYLCYCLASE WHICH IN TURN MEDIATES ANTI-NOCICEPTIVE ACTION
  • 14. PAIN MODULATION
    • GATE CONTROL THEORY
    • (WALL AND MELZACK 1965 )
  • 15. PAIN MODULATION
    • SUPRASPINAL INHIBITION
  • 16. ACUTE Vs CHRONIC
    • 1. Nociceptive and has 1. No biologic value
    • Biologic function
    • 2. Acts as warning and 2. Detrimental effects
    • indicates tissue injury
    • 3. Recent onset & finite 3. Persists beyond acute
    • duration-weeks to days
    • Illness or injury-months
    • 4. Remits when underlying 4. Chronic pathological
    • pathotlogy resolves process & can recur
  • 17. REFERRED PAIN
  • 18. PHYSIOLOGICAL EFFECTS OF PAIN Hyperglycemia Sodium & water retention Protein catabolism Endocrine system HTN Tachycardia Myocardial Ischemia Cardiac Dysrhythmia CVS(SNS Stim) Atelectasis Ventilation perfusion mismatch Arterial hypoxemia Hypercarbia pneumonia Pulmonary (Dec lung volume)
  • 19. PHYSIOLOGICAL EFFECTS OF PAIN Urinary retention Genitourinary system Ileus GI system Increased platelet adhesiveness Decreased fibrinolysis Hypercoagulation DVT Coagulation system Decreased immune function Immune system
  • 20. THANK YOU