COMPLEX REGIONAL PAIN SYNDROME - Professional Events

COMPLEX REGIONAL PAIN

SYNDROME

Complex Regional

Pain Syndrome

(CRPS)

Dr. Jean Mooney, PhD,

FChS, FCPodS, FCPodMed, FFPM RCPS (Glas), FHEA

Pain is regrettable but normal

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Unpleasant but normal sensory and emotional experience

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Sensory awareness, via afferent neural input to thalamus

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Emotional, via afferent input from thalamus to the limbic system

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Modified by GABA and other inhibitory neurotransmitters

Associated with actual, or the threat of, tissue damage

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Modified by GABA inhibitory descending control mechanisms

Described in terms of ¡®damage¡¯

Normally resolves:

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trauma triggers release of inflammatory mediators + pain

inflammation triggers tissue repair

Inflammation abates (no more inflammatory mediators)

Pain resolves

Persistent Pain (1)

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Pain that persists

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for >3/12

lasts beyond the normal healing time

Pain impulses generated

independently of the initial trigger

event

Pain becomes a self-perpetuating

entity that continues after resolution

of the initiating condition

?

?

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Abnormal synapses form within the dorsal

horn of the spinal cord

Release inflammatory neurotransmitters

in dorsal horn

GABA-dependent descending control

mechanisms no longer effective

Persistent Pain (2)

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Damage to nerve causes

peripheral sensitization and

hyperalgesia

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Damage to peripheral nervous system

? ? activity of peripheral nerves and

neurons within the dorsal root ganglia

of spinal cord

? ? Na+ and Ca2+ channel activity in

peripheral nerves = more action

potentials generated

? tissue sensitization to non-noxious

stimuli

= Causalgia

?

Pain generates pain

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