Overwhelming evidence now supports Simpson's concept, originally proposed in 1960, that acquired myasthenia gravis (MG) is an autoimmune disease in which antibodies are directed against the nicotine postsynaptic acetylcholine receptor (AChR).1 An autoimmune pathogenesis of acquired MG implies that those myasthenic syndromes which occur in a congenital and familial setting may have a different, non-autoimmune basis. This paper focuses on ultrastructural, immunoelectron microscopic and cytochemical aspects of acquired autoimmune MG and some recently recognised congenital myasthenic syndromes.
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