Pain: Underlying Mechanisms,

Rationale for Assessment

Jessie VanSwearingen, Ph.D, PT

Associate Professor
Department of Physical Therapy
University of Pittsburgh School of
Health and Rehabilitation Sciences
 PAIN

an unpleasant sensory and emotional

experience.primarily associate with
tissue damage or describe in terms of
such damage or both.
Intl. Assoc. for Study of Pain
 The Report of Pain
3 components of the patients experience:

sensory discriminative (localize, quality)

motivational / affective (emotional)
cognitive / evaluative (meaning)
 The Report of Pain

Relation of pain and tissue damage:

not consistent or constant

All pain is truly experienced

(-- a helpful clinician belief)
 Terminology of Pain

Nocioception neural response related to

potentially tissue damaging
stimuli

Pain conscious experience of

nocioception
 Terminology of Pain
Experience of pain
dysthesia - experience abnormal noxious
sensation
paraesthesia - abnormal nonpainful
sensation;
hyperpathia- exaggerated pain response to
noxious or nonoxious stimuli)
allodynia - perception of nonoxious stimuli
as painful
 Terminology of Pain
hyperalgesia increased pain response
to painful stimuli
hypoalgesia - decreased sensitivity to
noxious stimuli
hyperesthesia and hypoesthesia -
increase or decrease, respectively, in
sensitivity to nonnoxious stimuli
 Characteristics of Pain

Nocioceptive pain - directly related to the

activation of peripheral nocioceptors

somatic - aching , squeezing, stabbing

visceral - cramping, knawing, rise and fall

 Characteristics of Pain
Neuropathic - pain assumed to be related to
aberrant sensory processing (PNS or CNS)

Deafferentation- sympathetic maintained

alterations in peripheral transmission or
central representation

burning, lancinating, electrical

 Characteristics of Pain
Idiopathic - pain persisting without
identifiable organic basis or excessive
pain for organic processes
(presumes some clinical correlation)

(psychogenic - no clinical observations

correlating with the pain)
 Nocioceptive Pain
Activation of nocioceptors by tissue-damaging stimuli.
Mechanisms:
neurogenic inflammation - vasodilation; inflammatory
cells; antidromic (polymodal) nocioceptor release of
Substance P and others from nerve terminals
endogenous substances - directly activate nocioceptors -
histamine, Subs. P, bradykinin, ACH, serotonin, K+
prostoglandins - sensitize nocioceptors: produce lower
thresholds for noxious stimuli (also: serotonin, ADP, NE,
interleukin, NGF); role in development of chronic pain
 Neuropathic Pain

Peripheral tissue injury leading to aberrant

somatosensory
processingpathophysiologic changes,
which sustain a pain experience.
Mechanisms:
peripheral generators
sympathetic maintained
central (mechanism) generators
 Neuropathic Pain Example:
Axonal Injury
1) multiple axon sprouts neuroma
2) axon sprouts spontaneous activity (peripheral generator)
pain
3) neuromas sensitive - tenderness mechanical and
chemical sensitivity
chronic pain
4) ephases - spread of impulses in juxtaposed nerve fibers;
incl sympathetic nerves (sympathetic maintained)
5) ectopic generation of impulses in DRG, transmitter
releasedorsal horn neurons expand receptive fields
(hyperalgesa)
Neuropathic Pain:CNS Activity
Increased activity in spinal cord,
thalamus, cortex following peripheral
nerve injury:

central sensitization of neurons

abnormal feedback (sympathetic
outflow stimulate peripheral
nocioceptors)
 Clinical Events of Pain
Hyperalgesia
1 -site of injury: peripheral nocioceptor
sensitization
2 -surrounding region: peripheral and
central mechanisms
central - hyperexcitable neruon
activated by nocioceptor
Pain episodes with the same phenomena may
not have the same mechanism
 Referred Pain
Phenomena:
stimulation of peripheral nerve fascicles, report of
pain throughout the extremity
pain from muscle or visceral injury accompanied
by cutaneous hyperalgesia

convergence-projection theory
convergent input of nocioceptors from different
sources on to the same projection neurons or
central neurons
 Basis for Joint and Bone Pain:
Joint Nocioceptors
1. nocioceptors - polymodal cutaneous receptor; c-
fiber, unmyelinated (capsule, type IV)
2. free- nerve endings - A -delta nocioceptors in intl
and extl joint ligaments
3. Synovium - small diameter, neuropeptide
containing fibers

A-delta and C-fibers innervate joint nocioceptors;

? Also sensitive mechanical and chemical stimuli
Basis for Joint and Bone Pain:
Joint Mechanoreceptors
1. Large diameter, fast-conducting afferents,
serving..
2. Corpuscular receptors - low-threshold,
dynamic receptors; capsule outer layer -type
I, subsynovial layer - type II, dynamic
receptors on surface of joint ligaments
3. Mechanically Insensitive Afferents (MIAs) -
C-fiber afferents, become sensitive to
mechanical stimuli only with inflamed joint
Basis for Joint and Bone Pain:
Sleeping Nocioceptors (MIAs)
insensitive to pain or mechanical stimuli
become spontaneously active
active during non-noxious movement
enlarged receptive fields
(central targets unknown)
 Basis for Joint and Bone Pain:
Spinal Cord Mechanisms
Dorsal horn neurons:
nocioceptive specific (NS)
wide dynamic range (WDR)

articular visceral Cutaneous muscle

inputs afferents
afferents
Basis for arthritic pain being:
poorly localized
poorly discriminated

Basis for: referred pain and hyperalgesia

Basis for Joint and Bone Pain:
Spinal Cord Mechanisms
Noxious joint inputs reach cortical targets.
inputs from inflamed joints appear to take
paths to widespread supraspinal targets

With persistent nocioceptive input, dorsal

horn neurons in sensitivity
enhanced responsiveness
enlarged receptive fields
Basis for Joint and Bone Pain:
Spinal Cord Mechanisms
With acute joint inflammation,
(sensitivity)
1) dorsal horn neurons with little response to
movement show large response
(enhanced receptive fields)
2) respond to stimuli remote from the site of
inflammation
3) become spontaneously active
 Basis for Joint and Bone Pain:
Somatosensory Cortex
Chronic inflammation
receptive field changes
increased background activity
prolonged response to non-noxious stimuli

(reduced inhibition of pain afferents in the dorsal

horn - decreased descending inhibitory pain
projections with inflammation)
 Neurogenic Inflammation
Example: axon reflex
- localized vasodilation and exudation in
response to an irritant
- intact sensory innervation
- mediated by release of neuropeptides from
C-fiber terminals
change in vascular tone and permeability
production of inflammatory cells; immune
response
 Neurogenic Inflammation
Partially attenuated by Substance P
depleter (eg capsaicin)

In Rheumatoid Arthritis, reduced

neuropeptide Y (vasoconstrictor) in the
sympathetic nerve terminals no
stop to the inflammatory response
 Summary of Pathophysiology
of Joint and Bone Pain
Chemical Nocioception
pain activation of nocioceptors
primary hyperalgesia - sensitization of
nocioceptors
swelling, vascular response to
neuropeptide release
Summary of Pathophysiology
of Joint and Bone Pain
Mechanical Nocioception
(joint bomechanics) mechanical
nocioceptors activated
primary hyperalgesia, sensitized
mechano - nocioceptors
mechanoreceptors, incl remote
musculotendinous site receptors,
induce dorsal horn plasticity
 Summary of Pathophysiology
of Joint and Bone Pain
Secondary Hyperalgesia / Neuropathic Model
altered central pathways with chronic arthritis
(both altered dorsal horn neurons responding
and the pattern of the response)
changes in threshold for response
changes in projection targets
changes in the responsiveness
referred pain to: other joints; cutaneous areas
and deeper tissues
 Clinical Assessment of Joint
and Bone Pain
Looking for:
anatomic origin - define the tissue
damage
mechanisms of pain production
associated disease
 Clinical Assessment of Joint
and Bone Pain
Finding a hyperalgesic joint in the region of pain
- likely to be the origin
- other signs: crepitus, swelling (implies
nocioceptors activated)
but in osteoarthritis: mechanoreceptors could
elicit mechanical nocioception and sensitize
primary afferents..
Joints which dont move and
joints that move properly can be
painful.
 Clinical Assessment of Joint
and Bone Pain
Recognizing Bone pain:
(causes: vascular, infection, neoplastic, metabolic)
not influenced by posture or movement
worse at night
well localized, over the painful site (eg
vertebra)
(eg. Osteonecrosis; osteoporotic fracture)

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