A-fibers mediate mechanical hyperesthesia and allodynia and C-fibers mediate thermal hyperalgesia in a new model of causalgiform pain disorders in rats.

Unilateral tight ligation of about half of the sciatic nerve in rats rapidly produces sympathetically dependent neuropathic pain which lasts many months and resembles causalgia in humans. The sensory abnormalities detected at the plantar side of the hindpaws include: (1) nocifensive responses to repetitive light touch (allodynia); (2) bilateral reduction in withdrawal thresholds to repetitive von-Frey hair stimulation (mechanical hyperesthesia); (3) bilateral reduction in withdrawal thresholds to CO2 laser heat pulses; and (4) unilateral increase in response duration to an intense laser heat pulse (thermal hyperalgesia). Using neonatal capsaicin treatment, we determined the type of afferent fiber remaining in the partially injured nerve, which mediates these disorders. Capsaicin, which destroys most C- and some A delta-fibers in peripheral nerves, had no effect on the touch-evoked allodynia and mechanical hyperesthesia that are produced by partial sciatic nerve injury. These disorders were, therefore, mediated by myelinated fibers. In contrast, thermal hyperalgesia failed to develop in capsaicin-treated rats following partial nerve injury. Thus, thermal hyperalgesia produced by partial nerve injury appears to be mediated by heat-nociceptive C-fibers.