Myasthenia Gravis (MG) is an autoimmune disorder characterized by the production of antibodies against the acetylcholine receptors (AChRs) at the neuromuscular junction of skeletal muscles. This autoimmune attack leads to a decrease in the number of available AChRs, resulting in impaired synaptic transmission. The hallmark of MG is muscle weakness and fatigue, which worsens with continued activity and improves with rest.
The pathophysiological process in MG primarily involves the binding of autoantibodies to AChRs, which can lead to three main outcomes:
- Accelerated Degradation: The cross-linking of receptors by antibodies leads to their accelerated internalization and degradation.
- Functional Block: Antibodies may directly block the acetylcholine binding sites on the AChRs, preventing normal neuromuscular transmission.
- Complement Activation: The binding of antibodies can activate the complement system, leading to the formation of membrane attack complexes that disrupt the post-synaptic muscle membrane and further reduce the density of AChRs.
These processes result in a diminished ability to propagate muscle action potentials, leading to the variable degrees of muscle weakness that are symptomatic of the disease.
