Complex Regional Pain Syndrome and Spontaneous Pain Following Simple Incision With Immobilization: A Case Report

Abstract

Complex regional pain syndrome (CRPS) is characterized by vasomotor and sudomotor changes. Its etiology generally includes trauma, fracture, stroke, and coronary disease. It is evaluated in two subtypes: CRPS type I (reflex sympathetic dystrophy), presenting with complex regional pain syndromes accompanied by spontaneous pain, hyperalgesia, allodynia, edema, autonomic anomalies, and trophic changes; regional pain occurring after minor injuries and fractures in the extremities; and coexisting vasomotor, sudomotor changes, and sensorial changes, and CRPS type II (coxalgia), including major peripheral nerve injuries, in addition to all of these symptoms (1, 2). Although the pathogenesis of CRPS is not exactly known, peripheral and central sensitization, which causes neurogenic inflammation, is held responsible. The most possible mechanism is considered to be increased sensitivity against catecholamine, depending on sympathetic denervation, in addition to increased numbers or sensitivity of peripheral axonal adrenoreceptors. Moreover, some mechanisms, such as the release of neuropeptides from primary nociceptive afferents and sympathetic efferents [substance P, calcitonin gene-related peptide (CGRP) and neuropeptide Y] and the development of neurogenic inflammation, are suggested. This results clinically in hyper algesia and central sensitization, in which allodynia develops (3, 4). CASE REPORT