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Books, Journals, New Media
February 12, 2003

Myasthenia Gravis

Author Affiliations

Books, Journals, New Media Section Editor: Harriet S. Meyer, MD, Contributing Editor, JAMA; David H. Morse, MS, University of Southern California, Norris Medical Library, Journal Review Editor; adviser for new media, Robert Hogan, MD, San Diego.

JAMA. 2003;289(6):758-759. doi:10.1001/jama.289.6.758

Myasthenia gravis (MG) is the most thoroughly understood autoimmune disease. The target antigen is the skeletal muscle nicotinic acetylcholine receptor. The disease is clearly caused by antibodies directed at the acetylcholine receptor. The autoimmune attack directed at the acetylcholine receptors damages the endplate membrane where the acetylcholine receptors are concentrated. Acetylcholine receptors and other critical membrane proteins, such as voltage-gated sodium channels, are lost from the endplate membrane, which compromises neuromuscular transmission. The endplate membrane becomes less sensitive to acetylcholine released by the motor nerve terminal, and the excitability of the endplate membrane is reduced. Weakness develops when activation of the nerve terminal no longer stimulates action potentials in the muscle fiber. The autoimmune nature of MG is reinforced by several observations. Inducing an allergic reaction to the acetylcholine receptor is the basis for one animal model of MG. Serum from patients with myasthenia can produce MG when injected into appropriate animals. The disease is treated by interventions that attenuate the immune response or enhance neuromuscular transmission.