Causalgia and Reflex Sympathetic Dystrophy Syndrome (RSDS) are significant public health problems affecting mostly patients with peripheral nerve injuries. Although causalgia-RSDS was orginally described over a century ago and research efforts have multiplied since that time; its pathophysiological mechanisms are incompletely understood. The proposed research will investigate aspects of neural mechanisms involved in causalgia-RSDS. Based upon the most scientifically sound hypothesis emerging from animal experiments, we will explore, both for spontaneous and stimulus-induced pains, the roles of a) sympathetic efferent neural signals (and/or neurotransmitters) and b) afferent neural signals, as determinants of such pains in patients. This has become possible since the advent of single fiber recordings in awake human subjects through the microneurographic technique currently available to us. Specific questions will be: a. Do sympathetic efferent neural signals activate i. Mechanoreceptors or ii. Nociceptors in nerve fascicles supplying the symptomatic region of causalgia-RSDS patients? b. Do low threshold mechanoreceptors supplying the symptomatic region evoke pain when selectively activated by intraneural microstimulation? Given the scientific strength of the hypothesis, the power of the techniques to be applied and the straightforwardness of the experimental plan, the proposal is bound to generate significant data with well-defined health related repercussions.
| Dotson, R; Ochoa, J; Marchettini, P et al. (1990) Sympathetic neural outflow directly recorded in patients with primary autonomic failure: clinical observations, microneurography, and histopathology. Neurology 40:1079-85 |
