Causes of Myasthenia Gravis

Myasthenia gravis is a chronic autoimmune disorder that affects the neuromuscular junction. Research since the 1960s has revealed that the condition is primarily caused by the body's immune system mistakenly attacking its own acetylcholine receptors located on the postsynaptic membrane of the neuromuscular junction. This leads to impaired nerve-to-muscle communication and results in muscle weakness and fatigue. Several lines of evidence support this autoimmune theory.

Presence of Acetylcholine Receptor Antibodies

One of the most compelling pieces of evidence is that approximately 90% of patients with myasthenia gravis test positive for acetylcholine receptor antibodies in their blood serum. These antibodies interfere with the normal function of the receptors, which are crucial for muscle contraction. Notably, symptoms often improve significantly after plasma exchange, a procedure that removes harmful antibodies from the bloodstream.

Transfer of Symptoms Through Antibodies

Another key finding is that when serum from a patient with myasthenia gravis is injected into mice, the animals develop symptoms similar to those seen in humans, including muscle weakness and abnormal neuromuscular transmission. Similarly, newborns of mothers with the disease may also exhibit temporary symptoms due to the passive transfer of maternal antibodies across the placenta.

Role of the Thymus Gland

The thymus gland plays a significant role in the development of myasthenia gravis. Around 80% of patients show signs of thymic hyperplasia or lymphoid follicle formation, while approximately 20% develop thymomas, which are tumors of the thymus. Surgical removal of the thymus (thymectomy) has been shown to improve symptoms in about 70% of patients, and in some cases, it may even lead to long-term remission or complete recovery.

Association with Other Autoimmune Diseases

It is also common for individuals with myasthenia gravis to suffer from other autoimmune conditions. These may include Graves' disease (an overactive thyroid), systemic lupus erythematosus, and rheumatoid arthritis. This suggests a broader underlying immune dysregulation, which may contribute to the development of multiple autoimmune disorders in the same individual.