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