Abstract
Demyelination has been recognized as the principal lesion in many encephalopathies of man and animals. Multiple sclerosis (MS) is perhaps the best known of these demyelinating diseases. Demyelination has also been described, however, as the most prominent lesion in copper deficiency and visna in sheep, as well as in several so-called degenerative diseases of the central nervous system (CNS) in man, such as subacute sclerosing panencephalitis (SSPE), Schilder’s disease, neuromyelitis optica, and the various leukodystrophies. Whereas the leukodystrophies are recognized as inherited degenerative disorders, there is no evidence of a genetic basis for other primary demyelinating diseases in man. A turning point in our understanding of the mechanisms of demyelination came when the occasional neurologic complications after rabies vaccination (Pasteur treatment) were recognized as demyelinating encephalopathies and correctly linked to the injection of rabbit spinal cord material contained within the vaccine. The postvaccinal disease was reproduced experimentally in animals by injection of heterologous or autologous spinal cord alone or in combination with Freund’s complete adjuvant. This induced disease has been thoroughly explored and is well known as experimental allergic encephalomyelitis (EAE). The basic mechanism underlying EAE is a cell-mediated immune response of the host to myelin basic protein.
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Koestner, A., Krakowka, S. (1977). A Concept of Virus-Induced Demyelinating Encephalomyelitis Relative to an Animal Model. In: ter Meulen, V., Katz, M. (eds) Slow Virus Infections of the Central Nervous System. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-9883-0_17
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DOI: https://doi.org/10.1007/978-1-4612-9883-0_17
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