What is myasthenia gravis?

Myasthenia gravis is an autoimmune condition that causes muscle weakness. The immune system makes antibodies that attack the connection between nerves and muscles, so signals from nerves do not reach muscles properly. The classic features are weakness that worsens with use and improves with rest, drooping eyelids, double vision, weakness in face and throat muscles, and limb weakness.

The two main forms. Ocular myasthenia gravis affects only the eye muscles. Generalised myasthenia gravis affects muscles throughout the body and is the form that requires more intensive therapy. A small proportion of patients with generalised disease have severe weakness affecting breathing or swallowing (myasthenic crisis), which is a medical emergency.

The immune biology. Most patients have antibodies against the acetylcholine receptor on muscle cells. A smaller group has antibodies against MuSK, a protein that helps maintain the nerve-muscle connection. A few patients have neither identifiable antibody (so-called seronegative myasthenia).

The therapy options.

Symptom relief: pyridostigmine (an acetylcholinesterase inhibitor) increases the amount of the nerve-signalling chemical that survives long enough to reach muscle, partially compensating for the autoantibody attack.

General immune suppression: corticosteroids and other immunosuppressants reduce overall immune activity. They work but carry side effects with long-term use.

Modern biologic options: FcRn antagonists reduce circulating antibodies including the pathogenic ones causing the disease. Complement inhibitors block downstream damage caused by the antibodies binding their target. B-cell-depleting therapies remove the cells that produce the autoantibodies.

Living with myasthenia gravis. The condition is lifelong but is increasingly well-managed with the modern therapy options. Most patients can lead a normal life with appropriate therapy, though severity varies.