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Articles

Vol. 1 No. 1 (2010): January-March 2010

Pathophysiological Mechanisms and Therapeutic Drug Targets for Complex Regional Pain Syndrome – Type I

DOI
https://doi.org/10.37285/ijddd.1.1.1
Submitted
October 28, 2024
Published
2010-10-15

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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