ABSTRACT
Myasthenia gravis (MG), also called "Erb–Goldflam syndrome", is a chronic autoimmune neurological disorder. It is caused by formation of autoantibodies against postsynaptic cholinergic receptors at the motor end plate. The disease is caused by destruction of postsynaptic acetylcholine receptors (AChRs) by autoantibodies at the neuromuscular junction (NMJ). Patients with MG classically present with fatigability of voluntary muscles that worsens with repetitive activities and improves with rest. Extraocular muscle involvement with pupillary sparing is one of the most important clinical features. Common precipitating factors for myasthenic crisis include respiratory infections, aspiration, sepsis, surgical procedures, rapid tapering of immune modulation, beginning treatment with corticosteroids, exposure to drugs that may increase myasthenic weakness, and pregnancy. Acetylcholinesterase inhibitors are used as the first-line symptomatic treatment for MG. Corticosteroids are the most commonly used immune-modulating therapy in MG. Intravenous immunoglobulin (IVIg) may provide a short-term improvement in patients with MG.
