WHAT IS PAIN?
• In 1968 McCaffery defined pain as“whatever the experiencing person says itis, existing whenever he/she says it does”
• In 1979 IASP defined pain as “unpleasantsensory and emotional experienceassociated with actual or potential tissuedamage, or described in terms of suchdamage.”
• Pain from poena ---> Latin means punishment.
VARIOUS TERMINOLOGIES TERM DESCRIPTION
ALLODYNIA PERCEPTION OF NON-NOXIOUS STIMULUS AS PAIN
ANALGESIA ABSENCE OF PAIN PERCEPTION
ANESTHESIA ABSENCE OF ALL SENSATIONS
ANESTHESIADOLOROSA
PAIN IN AN AREA THAT LACKS SENSATION
DYSESTHESIAUNPLEASANT SENSATION WITH OR WITHOUT
STIMULUS
HYPOALGESIA DIMINISHED RESPONSE TO NOXIOUS STIMULUS
HYPERALGESIA INCREASED RESPONSE TO NOXIOUS STIMULUS
HYPERASTHESIA
INCREASED RESPONSE TO MILD STIMULUS
HYPOASTHESIA
REDUCED CUTANEOUS SENSATION
NEURALGIA PAIN IN THE DISTRIBUTION OF A NERVE
PARASTHESIAABNORMAL SENSATION PERCEIVED WITHOUT AN APPARENT STIMULUS
RADICULOPATHY
FUNCTIONAL ABNORMALITY OF NERVE ROOTS
• Nociceptive
• Neuropathic
• Psychogenic
CLASSIFICATION OF PAIN
TYPES OF PAIN FIBRES
TYPE OF NERVE
CONDUCTION VELOCITY ( MTS/SEC )
MELINATED TYPE OF PAIN
A- DELTA 20 (fast) YES SHARP, PRICKING,WELL LOCALIZED
C 1 (slow) No DULL ACHE, DIFFUSE
PAIN PATHWAY
SPINALCORD LAMINAELAMIN
A PREDOMINANT FUNCTION
INPUT NAME
ISOMATIC
NOCICEPTIONTHERMORECEPTION
Aδ, C MARGINAL LAYER
IISOMATIC
NOCICEPTIONTHERMORECEPTION
C, AδSUBSTANTIA
GELATINOSA
IIISOMATIC
NOCICEPTIONMECHANORECEPTION
Aβ, AδNUCLEUS
PROPRIUS
IV MECHANORECEPTION Aβ, Aδ, NUCLEUS
PROPRIUS
V
VISCERAL & SOMATIC NOCICEPTION & MECHANORECEPTION
Aβ, Aδ, C
NUCLEUS PROPRIUS
WDR NEURONS
VI MECHANORECEPTION AβNUCLEUS
PROPRIUS
VII SYMPATHETICINTERMEDIOLATER
ALCOLUMNS
VIII Aβ MOTOR HORN
IX MOTOR Aβ MOTOR HORN
X Aβ CENTRAL CANAL
PHYSIOLOGY OF NOCICEPTION
1. NOCICEPTORS• CUTANEOUS• DEEP• VISCERAL
2. CHEMICAL MEDIATORS
3. MODULATION OF PAIN• PERIPHERAL• CENTRAL
NOCICEPTORS
1. 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
3. VISCERAL• PRESENT IN ORGANS & LININGS OF BODY CAVITY• CHARACTERIZED BY DIFFUSE, DEEP CRAMPING / STABBING
PAIN• PAIN IS POORLY LOCALIZED UNLIKE CUTANEOUS
NOCICEPTORS
CHEMICAL MEDIATORS NEUROTRANSMITTER
RECEPTOR
EFFECT ON NOCICEPTION
SUBTANCE P NK – 1 EXCITATORY
CALCITONIN EXCITATORY
GLUTAMATE NMDA EXCITATORY
ASPARTATE NMDA EXCITATORY
ATP P1, P2 EXCITATORY
SOMATOATATIN INHIBITORY
Ach M1 INHIBITORY
ENKEPHALIN µ, δ, κ INHIBITORY
B- ENDORPHIN µ, δ, κ INHIBITORY
NOREPINEPHRINE Α2 INHIBITORY
ADENOSINE A1 INHIBITORY
SEROTONIN 5-HT INHIBITORY
GABA A.B INHIBITORY
GLYCINE INHIBITORY
PAIN MODULATION
• CAN EITHER INHIBIT OR FACILITATE PAIN• MODULATION CAN BE OF TWO TYPES1. PERIPHERAL2. CENTRAL
1. PERIPHERAL MODULATION TISSUE INJURY
RELEASE OF SUBBSTANCE-P CHEMICAL MEDIATORS OF
AND GLUTAMATE INFLAMMATION
STIMULATE NOCICEPTORS INTHE PERIPHERY
PAIN MODULATION
2. CENTRAL MODULATION
A. FACILITATION
THREE MECHANISMS ARE RESPONSIBLE• WIND-UP & SENSITIZATION OF 2ND ORDER NEURONS
( WDR NEURONS )• RECEPTOR FIELD EXPANSION• HYPEREXITABILITY OF FLEXION REFLEXES
B. INHIBITION
NOCICEPTIVE INPUT CAN BE INHIBITED BY • SEGMENTAL INHIBITION• SUPRASPINAL INHIBITION
PAIN MODULATION
1. SEGMENTAL INHIBITION
A. 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
B. GLYCINE AND GABA AMINO ACIDS• FUNCTION AS INHIBITORY NEUROTRANSMITTERS IN THE SPINAL
CORD• THEY INHIBIT FACILITATION OF WDR NEURONS
C. 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
PAIN MODULATIONGATE CONTROL THEORY
(WALL AND MELZACK 1965 )
PAIN MODULATION
2. SUPRASPINAL INHIBITION
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
REFERRED PAIN
Pulmonary(Dec lung volume)
AtelectasisVentilation perfusion mismatchArterial hypoxemiaHypercarbiapneumonia
CVS(SNS Stim)
HTNTachycardiaMyocardial Ischemia Cardiac Dysrhythmia
Endocrine system
HyperglycemiaSodium & water retentionProtein catabolism
PHYSIOLOGICAL EFFECTS OF PAIN
Immune system
Decreased immune function
Coagulation system
Increased platelet adhesivenessDecreased fibrinolysisHypercoagulation DVT
GI system Ileus
Genitourinary system
Urinary retention
PHYSIOLOGICAL EFFECTS OF PAIN