Sensory neurons, ion channels, inflammation and the onset of neuropathic pain.
Neuropathic pain often fails to respond to conventional pain management procedures. here we review the aetiology of neuropathic pain as would result from peripheral neuropathy or injury. We show that inflammatory mediators released from damaged nerves and tissue are responsible for triggering ectopic activity in primary afferents and that this, in turn, provokes increased spinal cord activity and the development of 'central sensitization'. Although evidence is mounting to support the role of interleukin-1β, prostaglandins and other cytokines in the onset of neuropathic pain, the clinical efficacy of drugs which antagonize or prevent the actions of these mediators is yet to be determined. basic science findings do, however, support the use of pre-emptive analgesia during procedures which involve nerve manipulation and the use of anti-inflammatory steroids as soon as possible following traumatic nerve injury.
Centre for Neuroscience, University of Alberta, Edmonton Alberta, Canada.
Patrick L
PL
Stemkowski
Peter A
PA
Smith
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D007473:Ion Channels / Q000502:physiology*; D009437:Neuralgia / Q000150:complications* / Q000473:pathology*; D011984:Sensory Receptor Cells / Q000502:physiology*
D007473:Ion Channels