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Myasthenia gravis: Current State of Knowledge

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Therapeutic Plasma Exchange

Abstract

Myasthenia gravis (MG) is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscle. When the beneficial effects of neostigmine were first observed in 1934 [106] the neuromuscular junction was thought to be the site of the disorder. The nature of the specific defect in neuromuscular transmission was elucidated about 40 years later through the important finding of Fambrough et al at John Hopkins [38] showing a marked reduction in postsynaptic acetylcholine receptors (ACh-R) in patients with MG. In 1973 Patrick and Lindstrom [79] and Sugiyama et al [95] also induced an experimental counterpart of the disease, experimental autoimmune myasthenia gravis (EAMG), by immunization with purified ACh-R. In the past seven years a large body of evidence has accumulated regarding the pathogenesis of MG which has had an immediate impact on the management of these patients. It is the aim of this paper to summarize some of the physiological and immunological aspects pertinent to our present understanding of the autoimmune process involved and focus on the role of circulating antibodies to ACh-R in the diagnosis and treatment of MG. For more detailed reviews of the subject the reader is referred to the recent reviews by Drachman [29], Lennon [62], and Heilbronn and Stalberg [46].

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Toyka, K.V., Besinger, U.A., Fateh-Moghadam, A. (1981). Myasthenia gravis: Current State of Knowledge. In: Gurland, H.J., Heinze, V., Lee, H.A. (eds) Therapeutic Plasma Exchange. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67956-8_4

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  • DOI: https://doi.org/10.1007/978-3-642-67956-8_4

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