Algodystrophy (reflex sympathetic dystrophy syndrome) and causalgia: novel concepts regarding the nosology, pathophysiology, and pathogenesis of complex regional pain syndromes. Is the sympathetic hyperactivity hypothesis wrong?

Concepts regarding the nosology, pathophysiology and pathogenesis of reflex sympathetic dystrophy syndrome are currently in a state of flux. Causalgia and reflex sympathetic dystrophy syndrome are now generally felt to be on the same continuum and as a result interest for defining criteria for the latter condition has waned. The pathogenic role of adrenergic sympathetic activity has been so successfully challenged that the last international consensus conference judged inappropriate any reference to the sympathetic system in the terms used to designate these conditions, thus confirming the position long defended by most French authors. The vasomotor abnormalities may be due to antidromic release of neuromediators by the endings of polymodal C fibers. These fibers do not belong to the sympathetic system but often travel with sympathetic nerves, a characteristic that may explain the efficacy of sympathetic nerve blocks, although other possibilities exist including a placebo effect. Also, efferent sympathetic fibers may undergo activation by nonadrenergic mediators. The mechanisms capable of initiating and perseverating activation of polymodal C afferents are being actively investigated and have been found to exhibit similarities with the mechanisms underlying peripheral and central sensitization of pain-producing afferents. Growth factors, such as nerve growth factor, may play an important role in causalgia. In "reflex sympathetic dystrophy syndrome", microcirculatory stasis may contribute to the initiation or perpetuatation of the disorders. Further work on the nerve supply to the venular network and on the venoarterial reflex is needed.