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Immunology of Neuromuscular Disease pp 7–31Cite as

Neuropathies associated with antimyelin antibodies

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Part of the book series: Immunology and Medicine Series ((IMME,volume 24))

Abstract

A number of peripheral neuropathies present with primary demyelination, in which myelin is preferentially damaged or lost and axons remain largely intact. As is the case for other major neurological disorders such as multiple sclerosis and myasthenia gravis, demyelinating neuropathies are likely to be associated with an autoimmune response to structures of the nervous system. Indeed, in these diseases, the pattern of injury to the nervous system is extremely selective, and antibodies and/or pathogenic T cells directed to components of the tissue involved in the disease process can be detected in most patients. Autoimmune diseases result from T or B lymphocytes entering an abnormal state of development in which they escape existing mechanisms that regulate their immunoreactivities and/or other functional activities. However, the mechanisms by which the autoantibodies (produced by pathological B cells) and/or pathogenic T cells cause demyelination remain unknown. In demyelinating lesions of peripheral nerves the final common pathway is invasion of Schwann cell basal lamina by macrophages, penetration of myelin lamellae, phagocytosis of myelin and debris, and stripping of axons. The physiological consequence of this process is the production of conduction blocks. The steps preceding this final damage in autoimmune demyelinating neuropathy are likely to be T cell mediated and/or antibody mediated.

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Authors
  1. D. Burger
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  2. A. J. Steck
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Editors and Affiliations

  1. Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians University, Munich, Germany

    R. Hohlfeld

  2. Department of Neuroimmunology, Max-Planck Institute, Martinsried, Germany

    R. Hohlfeld

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Burger, D., Steck, A.J. (1994). Neuropathies associated with antimyelin antibodies. In: Hohlfeld, R. (eds) Immunology of Neuromuscular Disease. Immunology and Medicine Series, vol 24. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1422-6_2

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  • DOI: https://doi.org/10.1007/978-94-011-1422-6_2

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