ABSTRACT
STUDY DESIGN: Investigation of intraneural inflammation induced by mechanical compression. OBJECTIVES: In order to investigate the mechanism of neuropathy, this study used a median nerve compression model in dogs. Immunohistochemistry was used to examine the localization and changes of inflammatory cytokines and nitric oxide (NO). SUMMARY OF BACKGROUND DATA: The manifestation of pain at sites of inflammation has a close relationship with the release of mediators from macrophages such as interleulin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), as well as with NO. However, the mediators involved in inflammation of nerve due to mechanical compression remain almost unknown. METHODS: In this study, the median nerve of dogs was compressed with a clip for three weeks to observe the changes caused by compression. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against IL-1beta, TNF-alpha, and inducible nitric oxide synthesis (i-NOS) were used to examine the localization and changes of these mediators caused by nerve compression. RESULTS: In control animals, resident T cells were detected, but there were no macrophages. IL-1beta was positive in the Schwann cells and vascular endothelial cells. However, no cells showed TNF-alpha or i-NOS positively. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for IL-1beta, TNF-alpha and i-NOS. CONCLUSION: Inflammatory cytokines and NO may be involved in intraneural inflammatory changes arising from mechanical compression. Such mediators may be of importance in the manifestation of neuropathy.
Subject(s)
Interleukin-1/metabolism , Median Neuropathy/immunology , Nerve Compression Syndromes/immunology , Nitric Oxide Synthase/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Dogs , Immunohistochemistry , Macrophages/immunology , Macrophages/metabolism , Median Nerve/immunology , Median Nerve/metabolism , Median Nerve/ultrastructure , Median Neuropathy/metabolism , Median Neuropathy/physiopathology , Microscopy, Electron, Transmission , Myelin Sheath/immunology , Myelin Sheath/metabolism , Myelin Sheath/ultrastructure , Nerve Compression Syndromes/metabolism , Nerve Compression Syndromes/physiopathology , Nitric Oxide/metabolism , Nitric Oxide Synthase Type II , T-Lymphocytes/immunology , T-Lymphocytes/metabolism , Wallerian Degeneration/immunology , Wallerian Degeneration/metabolism , Wallerian Degeneration/physiopathologyABSTRACT
We report the case of a 47-year-old woman with a left anterior interosseous nerve palsy. Surgical release of the anterior interosseous nerve was initially proposed, but electrodiagnostic evaluation demonstrated that the neuropathy was due not to compression or to neuralgic amyotrophy but to a proximal conduction block. At that time, the conduction block could be defined only by indirect electrodiagnostic criteria. A multifocal motor neuropathy with persistent conduction block was subsequently diagnosed, and the patient was treated with intravenous immunoglobulins. The efficacy of this treatment and the subsequent disclosure of conduction block in the right posterior interosseous and peroneal nerves definitively confirmed the multifocal motor neuropathy.
