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Sensory Neurons, Ion Channels, Inflammation and the Onset of Neuropathic Pain

Published online by Cambridge University Press:  02 December 2014

Patrick L. Stemkowski  and
Peter A. Smith
Patrick L. Stemkowski
Affiliation:
Centre for Neuroscience, University of Alberta, Edmonton Alberta, Canada. October 14, 2011 March 1, 2012
Peter A. Smith*
Affiliation:
Centre for Neuroscience, University of Alberta, Edmonton Alberta, Canada. October 14, 2011 March 1, 2012
*
Centre for Neuroscience and department of Pharmacology, 9-75 medical Sciences building, University of Alberta, Edmonton, Alberta, T6G 2h7, Canada. Email: peter.a.smith@ualberta.ca
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Abstract

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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.

Type
Review Article
Information
Canadian Journal of Neurological Sciences , Volume 39 , Issue 4 , July 2012 , pp. 416 - 435
Copyright
Copyright © The Canadian Journal of Neurological 2012

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