Acquired myasthenia gravis is an autoimmune disorder. The myasthenic patient has fewer available skeletal muscle acetyl-choline receptors because of antibodies produced against these receptors130 and also because of complement activation.16 Neu-romuscular transmission is thereby poised to fail. Normally, with repetitive stimulation of a motor nerve, the amount of acetylcholine released from that nerve diminishes. In the delicately balanced myasthenic, this decrease in neurotransmitter may well lead to a failure of muscular response. In this context, it is easy to understand why muscle fatigue is the clinical hallmark of myasthenia gravis and why the constant activity of the extraocular muscles, among other activities,243,354 particularly predisposes them to demonstrate fatigue. The exact reasons for predilection for the extraocular muscles are under study, one explanation potentially lying in the differential expression of acetylcholine receptor subunits in extraocular versus skeletal muscle.47,244,301
A number of medications are known to produce myasthe-nia gravis in normal individuals or to exacerbate already existing disease. The list includes D-penicillamine, antibiotics, anticonvulsants, intravenous contrast dye, anticholinesterase agents, neuromuscular blocking agents, antiarrhythmic drugs, phenothiazines, beta-blockers, and quinine. For example, myas-thenia produced by D-penicillamine is indistinguishable from primary acquired myasthenia clinically, immunologically, and electrophysiologically.519
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