Articles
Vol. 1 No. 1 (2010): January-March 2010
Pathophysiological Mechanisms and Therapeutic Drug Targets for Complex Regional Pain Syndrome – Type I
Department of Anesthesia, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec
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Author Biography
Department of Anesthesia, McGill University, 3655 Promenade Sir William Osler, Montreal, Quebec, H3G 1Y6, Canada
Alan Edwards Centre for Research on Pain, McGill University, 740 Dr. Penfield Ave, Montreal, Quebec, H3A 1A4, Canada
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Author Biography
1) Alan Edwards Centre for Research on Pain, McGill University, 740 Dr. Penfield Ave, Montreal, Quebec, H3A 1A4, Canada 2) Department of Psychology, McGill University, 1205 Dr. Penfield Ave, Montreal, Quebec, H3A 1B1, Canada 3) McGill University Hospital Centre Research Institute, 2155 Guy St, Montreal, Quebec, H3H 2R9, Canada
Abstract
Reflex sympathetic dystrophy (RSD), also known as complex regional pain syndrome type I (CRPS-I), is a disabling neuropathic pain syndrome. It is characterized by regional disabling pain, increased sensitivity to tactile stimuli, swelling, vasomotor and sudomotor abnormalities, and impairment of motor function. The disorder usually develops after minor trauma (contusions, sprains, and fractures) or surgery. Pathophysiologically, there is evidence for functional changes within the central nervous system and for involvement of peripheral inflammatory processes, the signs of which are very much evident at the early stage of the disorder. The sympathetic nervous system plays a key role in maintaining pain and autonomic dysfunction in the affected extremity. Accordingly, in the chronic stages of the disease, patients present with a cold-affected extremity and atrophy of skin, muscles, and bones. Increased vasoconstriction, tissue hypoxia, and consequently metabolic tissue acidosis have all been demonstrated in the affected extremity. As for therapeutic drug targets, various modalities of drug action have been extensively studied, which include targeting regional inflammation, ion channels, spinal pain pathways, sympathetic nervous system and the NMDA receptor. Hence, the aim of the present article is to comprehensively review the multifarious pathophysiological mechanisms underlying pain in CRPS-I and the molecular drug targets that are studied to develop newer drug molecules for the effective treatment of this pain condition.
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