Pathophysiology of Myasthenia Gravis

Overview of Myasthenia Gravis

Myasthenia Gravis (MG) is a chronic autoimmune neuromuscular disorder characterized by weakness in the skeletal muscles. It occurs due to a breakdown in communication between nerves and muscles.

Pathophysiology

Neuromuscular Transmission

The disorder is primarily caused by autoantibodies targeting acetylcholine receptors (AChRs) at the neuromuscular junction, leading to impaired signal transmission.

Immunological Mechanisms

• Presence of anti-AChR antibodies that block or degrade receptors.
• Thymic abnormalities contributing to immune dysregulation.
• Reduction in available acetylcholine binding sites.

Clinical Manifestations

Patients experience fluctuating muscle weakness, typically affecting ocular, bulbar, and limb muscles.

Diagnosis and Treatment

Diagnostic Tests

• Edrophonium test for temporary symptom relief.
• Electromyography (EMG) to assess neuromuscular transmission.
• Serological tests for autoantibodies.

Treatment Approaches

• Acetylcholinesterase inhibitors to enhance neuromuscular function.
• Immunosuppressive therapies, including corticosteroids.
• Plasmapheresis and intravenous immunoglobulin (IVIG) for severe cases.

Conclusion

Myasthenia Gravis is a complex neuromuscular disease requiring targeted medical interventions. Early diagnosis and appropriate treatment can significantly improve patient quality of life.