Chronic pain

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Chronic pain

Usually defined as pain that has not resolved in the normal time for tissues to heal. Acute pain functions as a waring system, whereas in those with chronic pain, the pain no longer serves as a warning system. The effects of chronic pain (eg reflexes; altered muscle action; muscle spasm) may be the main reason for the painful condition. Affects ~10% of the population

Mechanisms by which acute pain becomes chronic :
Chronic sensitisation of nociceptors:
if sensitising substances continue to affect nociceptors over a longer period of time  may get persistence of sensitisation
Changes in innervation density:
may get increase in density of nerve fibres. If develop increased density of nerve fibre, noxious stimulus  excite more nerve endings  more pain
Vicious cycles including the CNS:
‘vicious’ cycle (positive feedback loop) is believed to be set up: Pain  reflex  muscle spasm  more pain
widely held assumption, but largely unproven mechanism
Neuroplasticity:
nociceptive inputs  long term functional changes in synaptic processes (similar to learning processes). Neurons are then thought to increase their excitability to stimuli.
Disturbance of the antinociceptive system:
processing of input from deep nociceptors in spinal cord is normally inhibited by input from supraspinal centres. There may be a dysfunction of this system.
Psychosomatic interactions:
pain perception is modulated by psychological factors; mechanisms controversial (many factors present prior to pain experience)
Aggravating and perpetuating factors:
mechanical (eg head forward posture; leg length; pronated foot)
systemic (eg anaemia; nutritional disturbances)

Taxonomy of chronic pain:
• nocioceptive pain
• neuropathic pain
• psychogenic pain

Nocioceptive/inflammatory pain:
• pain related to ongoing stimulation of nocioceptive pathways
• pain originates in tissues other than CNS and PNS
• may have somatic (described as aching, throbbing, stabbing) or visceral (described as dull or crampy) origin
• may be physiological (due to non-tissue damaging stimulus) or pathological (due to a tissue damaging stimulus)
• most acute and chronic pain is associated with some degree of tissue damage
• pain tends to be localised and respond predictably (eg certain movement)
• improves with simple analgesics and NSAID’s

Neuropathic pain:
precipitated by neuronal damage  dysthaesias and paraesthesias
• can be:
• 1) Deafferentation pain
• caused by activity in central neurons
• may follow any type of injury to the somatosensory nervous system
• eg phantom limb pain, thalamic pain
• peripheral therapeutic mechanisms fail (pathogenesis is in CNS)
• 2) Sympathetically mediated pain (SMP)
• caused by abnormal efferent function of the sympathetic nervous system
• pain is non-dermatomal and usually burning in sensation
• group of disorders with disorders of local autonomic function and local trophic changes  usually associated with other symptoms (eg colour and temperature changes)
• eg complex regional pain syndrome; reflex sympathetic dystrophy
• 3) Peripheral pain
• caused by ongoing activity in a peripheral focus of efferent neuroactivity
• peripheral therapeutic mechanism (eg nerve block) successful (pathogenesis is local)
• eg compression neuropathies
• tends be distributed in an anatomical region
• usually described as burning, sharp, shooting
• often have allodynia, dysaesthesia and/or parathesias
• poor response to NSAID’s and analgesics

Psychogenic pain:
May or may not have evidence of an associated organic process.
If have pathologic process, complaints of pain are out of proportion to extent of lesion.
Tended to be over-diagnosed in the past in those with severe pain.

Peripheral Sensitisation:
Important in up regulation of nociceptive system after injury  increased sensitivity to a subsequent stimulus following tissue damage (as a result of release of chemical mediators in the injured tissues and changes in pH)  threshold of afferent receptors is reduced

Central Sensitisation:
Important mechanisms of up regulation of nociceptive system after tissue injury.
Pain tends to be widespread with a non-anatomical distribution
Often have hyperalgesia and allodynia- pain and sensations are amplified
NSAID’s and analgesics ineffective
Inconsistent response to clinical tests

Central Sensitivity Syndromes (CSS):
Similar and overlapping group of conditions that have the mechanism of central sensitisation in common
• fibromyalgia, chronic headaches, irritable bowel syndrome, chronic fatigue syndromes, myofascial pain syndromes, restless legs syndrome, periodic limb movement disorder, multiple chemical sensitivity

Common features- female more common; fatigue; poor sleep; hyperalgesia/sensitivity to stimuli; no structural pathology

New paradigm for consideration of this group of syndromes

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