Myasthenia gravis (MG) is the prototypic autoimmune neurological disorder. Weakness and muscle fatigue in MG result from an autoimmune attack on the neuromuscular junction, which causes a failure of neuromuscular transmission.1 The autoimmune nature of the disease was initially proposed in 1960, and in the 1970s, serum antibodies against the acetylcholine receptor (AChR) were identified in patients with MG.2 Subsequently, many convincing experiments demonstrated that these AChR antibodies produce direct effects on the neuromuscular junction.
Vernino S. Unraveling the Enigma of Seronegative Myasthenia Gravis. JAMA Neurol. 2015;72(6):630-631. doi:10.1001/jamaneurol.2015.0205