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.

A radioimmunoprecipitation assay (RIA) using solubilized human AChR complexed to ¹²⁵I-labeled α-bungarotoxin has been considered the most sensitive method for detection of AChR antibodies in human serum and has remained largely unchanged for the past 40 years. Using this assay, AChR antibodies are found in about 80% of patients with MG.¹ A small number of these patients may eventually be diagnosed as having a disorder other than autoimmune myasthenia (including Lambert-Eaton syndrome or congenital myasthenic syndromes). However, ever since the development of the antibody assay, seronegative patients have been a cause of clinical consternation.