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Pathophysiology of complex regional pain syndrome
Journal article   Peer reviewed

Pathophysiology of complex regional pain syndrome

Robert J Schwartzman, Guillermo M Alexander and John Grothusen
Expert review of neurotherapeutics, v 6(5), pp 669-681
May 2006
PMID: 16734515

Abstract

Animals Autonomic Nervous System - physiopathology Complex Regional Pain Syndromes - complications Complex Regional Pain Syndromes - physiopathology Complex Regional Pain Syndromes - therapy Edema - etiology Humans Movement Disorders - etiology
Complex regional pain syndrome (CRPS) most often follows injury to peripheral nerves or their endings in soft tissue. A combination of prostanoids, kinins and cytokines cause peripheral nociceptive sensitization. In time, the Mg(2+) block of the N-methyl-D-aspartate receptor is removed, pain transmission neurons (PTN) are altered by an influx of Ca(2+) that activates kinases for excitation and phosphatases for depression, activity-dependent plasticity that alters the firing of PTN. In time, these neurons undergo central sensitization that lead to a major physiological change of the autonomic, pain and motor systems. The role of the immune system and the sickness response is becoming clearer as microglia are activated following injury and can induce central sensitization while astrocytes may maintain the process.

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Web of Science research areas
Clinical Neurology
Pharmacology & Pharmacy
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