Myasthenia Gravis

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Abstract
Introduction IN RECENT years there has been increasing interest in autoimmune phenomena in myasthenia gravis. The accumulation of evidence along these lines began with the observation of Nastuk, Strauss, and Osserman in 1959 that there are fluctuations in serum complement levels in myasthenia gravis, with a tendency for complement levels to fall during exacerbations.1 Simpson, in 1960, theorized that many of the puzzling features of myasthenia gravis (MG) could be explained by the presence of antibodies to the motor endplates of skeletal muscle fibers.2 That same year Strauss and associates reported that pooled crude globulin from MG patients, when tagged with fluoresceinisothiocyanate, would react in antibody antigen-like fashion with normal, myasthenic, or cardiac muscle, and that complement was fixed in the reaction.3 They subsequently demonstrated that the antimuscle globulin was in the 7 S fraction and that it bound rather specifically to the "A" band of skeletal

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