Myasthenia gravis is an acquired auto immune disorder of the myoneural junction resulting from attack of antibodies to acetylcholine receptors.
The antibodies originate in thymus, reaching skeletal neuro muscular junctions via blood stream. The antibodies cause complement mediated damage at the neuro muscular junction producing functional blockage at the antibody binding sites.
Autoimmune myasthenia gravis cases are sporadic and familial involvement is also less. Up to 30% of patients of myasthenia gravis have a family history of the disease as well as of other immunological disorders.
Genetic predisposition to this disorder is known and concordance has been shown in monozygotic twins. There is strong association of HLAA1, B8 and DRW3 antigens in females and HLA A3, BW21, BW35 and DR2 antigens in male patients of myasthenia gravis.
The disease occurs at all ages and the onset may be either insidious or sudden. Thymus is unequivocally involved in the pathogenesis of the disease.
Treatment is aimed at immune suppression and surgical removal of thymus is often associated with improvement in the severity of disease.