Abstract
Acquired myasthenia gravis (MG) is a chronic autoimmune disorder of the neuromuscular junction, characterized by muscle weakness and fatigability on exertion. MG is caused by autoantibodies against acetylcholine receptors in the postsynaptic membrane. [1] Gilhus N.E. Myasthenia and the neuromuscular junction. Curr Opin Neurol. 2012; 25: 523-529 Crossref PubMed Scopus (51) Google Scholar The pathogenesis involved in acetylcholine receptor impairment includes: accelerated endocytosis and degradation of acetylcholine receptors, functional blockade of the acetylcholine binding site, and complement-mediated damage of the postsynaptic membrane. [1] Gilhus N.E. Myasthenia and the neuromuscular junction. Curr Opin Neurol. 2012; 25: 523-529 Crossref PubMed Scopus (51) Google Scholar The initiating event of MG is unknown, but speculations have been made about viral infections as a possible trigger. [1] Gilhus N.E. Myasthenia and the neuromuscular junction. Curr Opin Neurol. 2012; 25: 523-529 Crossref PubMed Scopus (51) Google Scholar
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