SERUM ACETYLCHOLINE‐RECEPTOR ANTIBODIES IN MYASTHENIA GRAVIS *

The etiology as well as the pathogenesis of myasthenia gravis remain unknown. The clinical symptomatology has been attributed to a defect in transmission at the neuromuscular junction, which is physiologically manifest as a diminution in the amplitude of miniature end-plate potentials. Recent evidence supports a postsynaptic localization of the functional defect, although it is unclear to what extent alterations at the nerve terminal also contribute to the pathogenesis. The morphology of both sites is altered; and the gap between nerve terminal and muscle end plate is considerably widened. Drugs that function primarily at the nerve terminal (hemicholinium) simulate certain myasthenic features, but compounds that function at the postsynaptic membrane (e.g., cobra a-toxin) appear to simulate a larger number of such features. The normal depolarization of end-plate regions by decamethonium and carbachol applied in a bath as well as the normal response to the iontophoretic microapplication of acetylcholine have suggested a presynaptic origin of the On the other hand, the increased dose of intra-arterial acetylcholine required to alter the spontaneous end-plate potentials of opponens pollicis muscle of myasthenic patients has suggested that the primary defect is of postsynaptic origin.? A postsynaptic defect is also supported by a decrease in the binding of abungarotoxin to biopsies of myasthenic muscle.8 A complete explanation of the pathogenesis of myasthenia gravis must also encompass the immunological features of the condition. Thymic hyperplasia is present in a high percentage of patients,Q circulating antibodies which react with muscle proteins are present in some patients; lo lymphocytes toxic to muscle in vitro are noted in this disorder; l1 lymphatic drainage has been reported to be beneficial in the treatment of myasthenia gravis; l2 and a myasthenic-like syndrome has been produced experimentally in rabbits by the inoculation of electric eel acetylcholine receptor.13

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