Sympathetically-maintained causalgiform disorders in a model for neuropathic pain: a review

Partial nerve injury is the main cause of sympathetically maintained causalgiform pain disorders in humans. We present here an animal model of this condition, produced in rats by a unilateral ligation of about half of the sciatic nerve. Starting hours after the operation and for several months thereafter, the rats developed signs of spontaneous pain, touch-evoked allodynia and hyperesthesia, and mechanical and thermal hyperalgesia in the partially denervated as well as the intact contralateral foot. These disorders were maintained by the sympathetic outflow and disappeared following postoperative sympathectomy. In neonatally capsaicinated rats we found that touch-evoked allodynia and hyperesthesia were mediated by A-fibers whereas thermal hyperalgesia was mediated by C-fibers. These disorders were not due to receptor sensitization of remaining afferent fibers by prostaglandins. We found strain differences and genetic inheritance of these causalgiform disorders which were correlated with the expression of autotomy to hind-paw denervation.