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

Unpleasant but normal sensory and emotional experience

Sensory awareness, via afferent neural input to thalamus

Modified by GABA inhibitory descending control mechanisms

Emotional, via afferent input from thalamus to the limbic system

Modified by GABA and other inhibitory neurotransmitters

Associated with actual, or the threat of, tissue damage

Described in terms of `damage'

Normally resolves:

trauma triggers release of inflammatory mediators + pain inflammation triggers tissue repair Inflammation abates (no more inflammatory mediators) Pain resolves

Persistent Pain (1)

Pain that persists

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

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)

Damage to nerve causes peripheral sensitization and hyperalgesia

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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