Patients with reflex sympathetic dystrophy or causalgia often experience mechanical allodynia; lightly touching or brushing the skin produces a painful sensation. We showed previously that allodynia in these patients was mediated by Abeta low-threshold mechanoreceptor afferents which under normal conditions mediate only non-painful touch sensation. Based on further tests we concluded that Abeta-LTM pain resulted from a central process maintained dynamically by ongoing input from a site of peripheral injury. In a subset of patients, limb ischemia abolishes the allodynia after 2-6 minutes, too soon to result from neural blockade. We studies this effect in two cases with lower leg allodynia following a knee or ankle injury. Limb elevation abolished allodynia in these patients. Allodynia returned if the limb was lowered but this return was blocked if circulation was occluded before lowering. This indicated that the allodynia was sensitive to minor changes in circulation or flood pressure, and a further study implicated the injury area as the locus of this effect. Allodynia disappeared if the injury site but not the allodynic area was rendered ischemic, but remained if only the allogynic area was rendered ischemic. In a separate set of experiments, capsaicin, the active ingredient in chili pepper was injected into the volar forearm or dorsum of the foot in normal volunteer subjects. Injection of 100 ug produced both spontaneous pain and in some cases an area of mechanical allodynia which also appeared to be Abeta-LTM mediated. At stimulus intensities corresponding to detection threshold, both mechanical von Frey stimulation and cutaneous electrical stimuli produced innocuous tactile sensations before the injection but evoked a painful, stinging sensation once the allodynia had developed after the injection. In addition, reaction time latencies for painful sensations evoked by threshold-strength electrical stimuli were too fast to include a contribution from unmyelinated C-fiber nociceptive afferents. Capsaicin produces effects which duplicate many of the features of reflex sympathetic dystrophy and may serve as an experimental model of pain mechanisms.
