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ANALGESIA

Pathophysiology of Peripheral Neuropathic Pain: Immune Cells and Molecules

Michael A. Thacker, MSc, Grad Dip Phys^*, Anna K. Clark, BSc^*, Fabien Marchand, PhD^*, and Stephen B. McMahon, PhD^*

From the *Neurorestoration group, Wolfson Centre for Age Related Diseases; Academic Department of Physiotherapy, Kings College London; and London Pain Consortium, London, UK.

Address correspondence and reprint requests to S.B. McMahon, Kings College London, Neurorestoration group, Wolfson Centre for Age Related Diseases, Wolfson Wing, Hodgkin Building, Guys Campus, London, SE1 1UL, UK. Address e-mail to stephen.mcmahon{at}kcl.ac.uk.

Abstract

Damage to the peripheral nervous system often leads to chronic neuropathic pain characterized by spontaneous pain and an exaggerated response to painful and/or innocuous stimuli. This pain condition is extremely debilitating and usually difficult to treat. Although inflammatory and neuropathic pain syndromes are often considered distinct entities, emerging evidence belies this strict dichotomy. Inflammation is a well-characterized phenomenon, which involves a cascade of different immune cell types, such as mast cells, neutrophils, macrophages, and T lymphocytes. In addition, these cells release numerous compounds that contribute to pain. Recent evidence suggests that immune cells play a role in neuropathic pain in the periphery. In this review we identify the different immune cell types that contribute to neuropathic pain in the periphery and release factors that are crucial in this particular condition.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999