• G J Bennett.
• Department of Neurology, MCP Hahnemann University, Philadelphia, Pennsylvania 19102-1192, USA. Gary.Bennett@drexel.edu
• Clin J Pain. 2000 Sep 1; 16 (3 Suppl): S139-43.

BackgroundIn almost every neuropathic pain state caused by peripheral nerve damage, whether due to trauma or disease, both structural damage and an inflammatory response exist.ObjectiveThe goal of this study was to determine the contribution, separate from the effects of the structural lesion, of the inflammatory response to neuropathic pain.MethodsTwo sets of experiments were performed. In the first, an experimental inflammation of the nerve (a neuritis) and an experimental inflammation of the muscle (a myositis control group) were produced in two groups of rats. The pain responses to stimuli applied to the sciatic nerve territory on the plantar hind paw were evaluated through tests of (1) heat hyperalgesia; (2) mechanical allodynia; (3) mechanical hyperalgesia; and (4) cold allodynia. In the second set of experiments, thalidomide or cyclosporin-A was used to block the production of immune modulators in the neuritis model and in a chronic constriction injury model (which involves structural damage and an inflammatory response in the sciatic nerve) to determine the contribution of the immune response to the pain observed in the first set of experiments.ResultsIn experiment 1, rats with the neuritis but not those with the myositis developed neuropathic pain symptoms. In experiment 2, thalidomide produced a partial but significant reduction in pain in the chronic constriction injury model across all four tests, but there was no effect in the neuritis model in any of the tests. Cyclosporin-A resulted in a dose-related reduction in pain in both models across all four tests.ConclusionsThese data suggest the possibility of an important interaction between the immune system and the nervous system in neuropathic pain and suggest that drugs modulating the immune system may be useful therapies in at least some neuropathic pain states.

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