Pathophysiology

Myasthenia gravis results from an autoimmune process in which autoantibodies, mainly IgG, target and attack the acetylcholine receptors (AChR) at the neuromuscular junction. This immune response leads to decreased receptor density, impaired neuromuscular transmission, and muscle weakness. The thymus gland, which plays a crucial role in T-cell maturation, is often implicated in MG cases. In some patients, it is associated with thymic abnormalities such as thymoma or thymic hyperplasia, reinforcing the connection between the disease and the immune system. Additionally, there is a subset of MG patients who present with autoantibodies against muscle-specific kinase (MuSK), indicating heterogeneity in the pathophysiology of the disease.