Conventional treatments for myasthenia gravis include (Drachman 1994):
Acetylcholinesterase inhibitors. These drugs work by blocking the enzyme that normally destroys acetylcholine in the synapse, which allows existing acetylcholine more time to interact with available receptors. The result is stronger and more complete muscle contractions. Excessive use of antiacetylcholinesterase drugs can have fatal side effects. The most commonly used acetylcholinesterase inhibitors in myasthenia gravis are pyridostigmine and neostigmine.
Thymectomy. Dozens of studies support the use of thymectomy (surgical removal of the thymus gland) to treat myasthenia gravis patients (Roberts 2001). There is some debate, however, over how effective the procedure is among patients without a thymoma: one review suggested no benefit from thymectomy in myasthenia gravis patients who lacked a thymoma (Gronseth 2000). Other reports suggest that the procedure is especially valuable in early-onset myasthenia gravis (Onodera 2005). Following a thymectomy, patients often report that symptoms lessen and, in some cases, disappear completely.
Immunosuppressants. Immunosuppressants are often used in myasthenia gravis to blunt the overactive immune response. These drugs might include glucocorticoids such as prednisone, azathioprine, cyclosporine, and others. Although they are effective in many patients, careful management of patients on long-term glucocorticoid therapy is crucial because of the significant side effects associated with these drugs. Glucocorticoid use over the long term is associated with significant metabolic side effects, including central obesity, impairment of insulin sensitivity, and bone loss.
Plasmapheresis. Plasmapheresis separates plasma, which contains the autoantibodies, from red blood cells, which then return to the body. This treatment temporarily improves symptoms and is especially valuable in preparation for surgical removal of the thymus. Several studies have reported that plasmapheresis is tolerated well in patients. The most common side effects are reversible hypotension (low blood pressure) and mild tremor. Several studies indicated that infection and mortality rates due to plasmapheresis were negligible, and all patients had immediate benefit from the procedure (Carandina-Maffeis 2004; Chiu 2000).
Intravenous immunoglobulin. High-dose intravenous human immunoglobulin (IVIg) has emerged as a therapy for various neurologic diseases, including myasthenia gravis. Rather than expunging abnormal antibodies from the blood, the procedure floods the body with gamma globulin antibodies from several donors. In controlled clinical trials, IVIg was effective in treating chronic inflammatory demyelinating polyneuropathy (Van Doorn 1990). IVIg has also produced improvement in some patients with myasthenia gravis (Ronager 2001; Wegner 2002). IVIg therapy generates temporary relief lasting weeks to months. Studies comparing plasmapheresis and IVIg found that although both treatments demonstrated a clinically significant effect in patients with chronic myasthenia gravis, the improvement had a more rapid onset after plasmapheresis than after IVIg (Ronager 2001).