The mechanisms underlying neuropathic pain remain incompletely understood. Using a modification of the spinal nerve ligation model of Chung, have observed: 1) hyperalgesia is not reversed by dorsal rhizotomy, 2) spontaneous activity develops among C fibers of adjacent, uninjured roots, 3) prominent remodeling of Remak bundles containing surviving C fibers in distal branches. We hypothesize that selective lesion of L5 nerve leads to Wallerian degeneration distally and partial Remak bundle denervation. Remak, bundles react as if completely denervated and release excessive growth factors and cytokines. Intact L4 fibers transport these agents to nerve cell bodies they induce changes in excitability and hyperalgesia. In the proposed study, capsacin will be applied to the L5 mixed spinal root. This technique will provide a selective lesion of nociceptive afferents and elaborate the role of this lesion in hyperalgesia, Remak bundle remodeling, and spontaneous activity in the uninjured fibers. This will clarify neuropathic pain phenomena.
