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Dr. S.

Umesh
PAIN

Definition:
“An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or
described in terms of such damage” – (Merskey 1990)
(The International Association for the Study of Pain)

Benefits of pain (sensation)


Though pain is an unpleasant sensation, it has protective or survival benefits such as:
1. It gives warning signal about the existence of a problem or threat
2. It creates awareness of the injury.
3. It prevents further damage by causing “Reflex Withdrawal” of the body from the source of the injury
4. It forces the person to rest or to minimize the activities thus enabling the rapid healing of the injured part.

PAIN ANATOMY & PHYSIOLOGY


Pain arises from the stimulation of specialized peripheral free nerve endings called “NOCICEPTORS”.
Types: (MPT) – Mechanical, Polymodal, Thermal

PNS - NERVE FIBER TYPES / ASSIFICATION (Afferent)


Sensory Axon diameter Conduction Innervation
axons/fibers (µm) velocity m/s
Ia A-alpha large diameter 65-130m/s Muscle spindles (annulospiral endings)
(12-22µm) Fast transmitting
myelinated
Ib A-alpha large diameter 65-130m/s GTOs
(12-22µm) Fast transmitting
myelinated
II A-beta large diameter 20-90m/s Pressure, temperature, vibration, (flower spray endings)
(5-15µm) Fast transmitting
myelinated
III A-delta Smaller diameter 6-45m/s FAST PAIN (sharp pain), Temperature,
(2-10µm) Fast transmitting Mechanoreceptors, thermal.
myelinated
IV - C Smallest diameter 0.2-2m/s SLOW PAIN, (dull/aching) visceral, temperature, crude
(0.2-1.5µm) Slow transmitting touch, Mechanoreceptors & Chemoreceptors
unmyelingated
Efferent – Motor neurons
Interneurons – Connect Afferent and Efferent

PATHWAYS OF PAIN SENSATION

1st ORDER NEURONS:


These are the cells in the post. Nerve root ganglia.
These neurons receive impulses of pain sensation from the pain receptors through their dendrites & their axons
carry the pain impulses to the spinal cord.
Aδ fibers synapse with marginal cells & C type with substantia gelatinosa in the posterior gray horn.

2nd ORDER NEURONS:


The marginal cells & the cells of substantia gelatinosa form the 2nd order neurons.
Fibers from these cells ascend in the form of the lateral spinothalamic tract.

3rd ORDER NEURONS:


The 3rd order neurons of pain pathway are the neurons of thalamic nucleus, reticular formation, tectum
& gray matter around aqueduct of sylvius.
Axons from these neurons reach the sensory area of cerebral cortex.
Some fibers from reticular formation reach hypothalamus.
Spinal Cord Transmission Pathways
1. Spinothalamic tract
2. Spinoreticular tract
3. Spinomesencephalic tract
4. Dorsal column-medial lemniscal system

The Neurochemicals of Pain


Pain Initiators Pain Inhibitors
Glutamate - Central Serotonin
Substance P – Central Endorphins
Brandykinin - Peripheral Enkephalins
Prostaglandins- Peripheral Dynorphin

PAIN THEORIES

 Pre-Cartesian:
 Cartesian model
 Post - Cartesian development

Theory Author/year Summary


1. Intensive/ Erb – 1874 - Based on Aristotle concept
Summation Goldscheid - That pain resulted from excessive stimulation of the sense of touch (1840).
Theory er (1894) Erb said “Every stimulus was capable of producing pain if it reached
sufficient intensity.” Further Goldscheider (1894) who described both about
Stimulus Intensity & Central Summation as critical determinants of pain.
2. Specificity Von Fery States that “Free nerve endings are pain receptors & other 3 types or
theory 1895 receptors are specific to a sensory experience”. Physical damage is not the
only component of pain perception; rather psychological components are also
part of pain perception.
3. Strong’s Strong “Pain is an experience based on both the noxious stimulus & the psychic
theory 1895 reaction or displeasure provoked by sensation”.
4. Pattern Nafe 1934 “All cutaneous qualities are produced by spatial & temporal patterns of
theory nerve impulses rather than by separate, modality-specific transmission
routes”
5. Central Livingson Intense stimulation resulting from nerve & tissue damage --- activate fibers
summation 1943 that project to neuron pools in the spinal cord. --- Abnormal reverberating
theory circuits are created, with self activating neurons. --- Prolonged abnormal
activity bombards cells in the spinal cord --- information projected to the brain
for pain perception.
6. The Fourth Hardy, Supporting & expanding Strong’s theory, it states that pain has 2 components:
theory of Wolff & 1. Perception of pain 2. The Reaction one has to it. Reaction- is a complex
pain Goodell physiopsychological process involving cognitive functions the individual,
1940 influenced by past experiences, culture & various psychological factors that
produce great variation in the “Reaction pain Threshold”.
7. Sensory Noordenbo Described two systems of transmission of pain & other sensory information
integration s 1959 with a fast & slow system. Slow system- small, unmyelinated fibers, slow
theory conducting which conduct somatic & visceral afferents.
Fast system- large, myelinated fibers, fast conducting which inhibit
transmission of small fibers.
8. Gate Melzack & The essence of this theory is that pain perception is regulated by a ‘gate’
control Wall1965 (substantia gelatinosa) in the dorsal horn at each segmental level of the spinal
theory cord. This may be opened or closed by means of other inputs from peripheral
nerves or from the CNS, thus increasing or decreasing the pain perceived.
Stimulation of large diameter fibers closes the gate, inhibits the release of
substance P & pain sensation is suppressed. Larger fibers reduces nociceptive
traffic; smaller fibers increases nociceptive traffic.
PAIN ASSESSMENT:
It includes:-
Demographic data:
Pain history:
Pain measurement:
Client evaluation:
Treatment:

DEMOGRAPHIC DATA: name, age, sex, occupation, handedness, ht, wt…

PAIN HISTORY:
“PAIN – format”
Pattern: onset & duration
Area: location of pain
Intensity: level or severity
Nature: description of pain

“OPQRST – format”
Onset: sudden/insidious/gradual…
Provocation/precipitating factors: any particular posture/activity or others
Quality of pain: aching (impingement), burning (nerve irritation), sharp (acute injury), radiating (nerve root)
Relieving factors: what makes intensity of pain less/absent?
Site: of pain (anatomical location)
Temporal variation: when does pain occur morning/evening/ or after activity / all time

PAIN MEASUREMENT:
Measuring pain intensity:
1. Visual analog scale-
The client rates the pain on a continuum that begins with ‘no pain’ & ends with ‘max pain tolerable’.

No pain Maximum pain tolerable


VAS has been proved to be a reliable & valid scale. Ref:

2. b)Simple Descriptive pain scale:


The client rates the pain on scale that is subdivided into, no pain, mild, moderate, severe & maximum pain tolerable.

3. Pain estimate:
0 100
4. Numerical pain rating scale:

5. Faces pain scale:

6. Pain diary:
Localizing pain symptoms:
Pain Drawings

Describing pain quality:


One of the most popular scales to rate pain quality is the “McGill Pain Questionnaire”
It includes 20 categories of descriptive words covering the sensory (no. 1 - 10), affective (11 -15), & evaluative
(16) pain properties.
Sensory measurements include temporal, thermal, spatial & pressure descriptors.
Affective properties are measured using fear, tension, & autonomic descriptors.
Evaluative properties are measured using pain experience descriptors.

CLIENT EVALUATION:
Inspection:
Palpation:
Movements: Active/Passive
End feel:
ROM – analysis:
Manual muscle testing:
Resisted isometric testing:
Special tests: as relevant
Assessment of neurological function:
Investigations: as required

MANAGEMENT

There are 3 broad avenues of interventions for pain management: P-C-B


Physical interventions
Cognitive strategies
Behavioral manipulations

Reference:
1. Pain textbook for therapists: Jenny Strong, Patrick Wall.
2. Umphred DA. Neurological Rehabilitation.
3. O’Sullivan: Physical Rehabilitation
4. Low Ann Reed: Electrotherapy Explained. Principles & Practice

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