Myasthenia gravis (MG) is an autoimmune disease, characterized by disturbances of neuromuscular transmission. In this paper immunological aspects of the disease are discussed. Antigenic characteristics of acetylcholine receptors (AchR), ethiology, pathogenesis and immunodiagnostics of MG are described.
This paper describes two condition caused by disfunction of neuromuscular transport: experimental autoimmune myasthenia gravis (EAMG) and Lambert-Eaton myasthenic syndrome (LEMS). EAMG can be caused by immunization with acetylcholine receptors (AChR). As in myasthenia gravis, anti-AChR antibodies reduce the number of these receptors, which impedes normal neuromuscular transmission. LEMS patients have normal AChR function: however there is a disfunction of acetylcholine release from the presynaptic terminals. This is due to the formation of antibodies against the voltage gated calcium channels on the presynaptic nerve terminals.