Pain:%20Underlying%20Mechanisms,%20Rationale%20for%20Assessment

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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

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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

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The Report of Pain

• 3 components of the patients experience
• sensory discriminative (localize, quality)
• motivational / affective (emotional)
• cognitive / evaluative (meaning)

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The Report of Pain

• Relation of pain and tissue damage
• not consistent or constant
• All pain is truly experienced
• (-- a helpful clinician belief)

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Terminology of Pain

• Nocioception neural response related to
  potentially tissue damaging stimuli
• Pain conscious experience of nocioception

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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

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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

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Characteristics of Pain

• Nocioceptive pain - directly related to the
  activation of peripheral nocioceptors
• somatic - aching , squeezing, stabbing
• visceral - cramping, knawing, rise and fall

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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

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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)

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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

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Neuropathic Pain

• Peripheral tissue injury leading to aberrant
  somatosensory processing?pathophysiologic
  changes, which sustain a pain experience.
• Mechanisms
• peripheral generators
• sympathetic maintained
• central (mechanism) generators

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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 release?dorsal horn neurons expand
  receptive fields (hyperalgesa)

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Neuropathic PainCNS Activity

• Increased activity in spinal cord, thalamus,
  cortex following peripheral nerve injury
• central sensitization of neurons
• abnormal feedback (sympathetic outflow? stimulate
  peripheral nocioceptors)

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Clinical Events of Pain

• Hyperalgesia
• 1º -site of injury peripheral nocioceptor
  sensitization
• 2 º -surrounding region peripheral and central
  mechanisms
• central - hyperexcitable neruon activated by
  nocioceptor

Pain episodes with the same phenomena may not
have the same mechanism
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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

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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

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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

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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)

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Basis for Joint and Bone Pain Spinal Cord
Mechanisms

• Dorsal horn neurons
• nocioceptive specific (NS)
• wide dynamic range (WDR)

articular inputs

• Basis for arthritic pain being
• poorly localized
• poorly discriminated
• Basis for referred pain and hyperalgesia

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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

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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

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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)

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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

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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

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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

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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

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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

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Clinical Assessment of Joint and Bone Pain

• Looking for
• anatomic origin - define the tissue damage
• mechanisms of pain production
• associated disease

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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.
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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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