Sensitized nociceptors in reflex sympathetic dystrophies

Abstract

Painful neurogenic syndromes commonly diagnosed as reflex sympathetic dystrophy (RSD) may not be the consequence of sympathetic dysfunction. Recent experimental data on the mechanism of hyperalgesia indicate that the primary pathophysiological mechanism of RSD may be sensitization of either peripheral nociceptors, or central neurons, or both. The sympathetic system might be involved in maintaining this condition, but this is not always the case. This presentation is an attempt to interpret clinical neuropathic syndromes on the basis of new scientific knowledge.