The Pathophysiology of Myasthenia Gravis

Myasthenia gravis (MG) is an autoimmune disease directed against the nicotinic acetylcholine receptor (AChR) of skeletal muscle. Unlike many presumed autoimmune diseases, both the antigen (theAChR) and the antibody (AChR-ab) for MG have been identified. A naturally occurring form of the disease exists in dogs and similar disease is induced in some rats and other animals following injection of AChR with adjuvant. From the study of these resources, MG has become among the best understood of the organ?specific autoimmune disorders. Nevertheless, much remains to be discovered regarding the disease. No one has yet identified the events leading to the induction of the disease, the mechanisms of remissions and exacerbations, the exact role of the thymus in the perpetuation of the disease, nor explained the role of heredity in the development of MG. To discuss the pathophysiology ofMG, it is important to frrst review the structure and function of neuromuscular transmission. The deleterious effects of the AChR-ab on t post synaptic junction can then be examined. From this background, defective neuromuscular transmission and resulting clinical fatigue and weakness, can then be appreciated.