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.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32NS047002-02
Application #
6943432
Study Section
Special Emphasis Panel (ZRG1-F01 (20))
Program Officer
Porter, Linda L
Project Start
2003-07-01
Project End
2005-06-30
Budget Start
2004-07-01
Budget End
2005-06-30
Support Year
2
Fiscal Year
2004
Total Cost
$52,492
Indirect Cost
Name
Johns Hopkins University
Department
Neurology
Type
Schools of Medicine
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21218