RESUMEN
Nerve granulomas occur at all points across the leprosy spectrum. Studies have been made using experimental models in which mycobacteria were injected directly in the sciatic or posterior tibial nerve of the guinea pig. Clinical and electrophysiological studies demonstrated axonal damage which was confirmed by morphometric studies showing disrupted myelin sheaths and in places complete demyelination. Further immunohistological studies showed a complete disappearance of staining for certain neuropeptides. The role of Schwann cells has also been investigated. Schwann cells in nerves affected by mycobacterial granulomas, both experimental and in leprosy patients were not demonstrated to be MHC class II positive suggesting that they did not play a role in antigen presentation. Macrophages in leprosy granulomas were shown to contain TNF alpha, suggesting that this cytokine played a role in axonal damage. The role of mycobacterial heat-shock protein in nerve granulomas has not as yet been determined. The localized nature of granulomas in leprosy nerves and nerves with experimental mycobacterial granulomas has been studied by a process of excision and repair with muscle grafts. Marked recovery has been demonstrated by clinical, electrophysiological, morphometric and immuno-histochemical techniques, the latter demonstrating a return of neuropeptide production.