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NEUROLOGY 1981;31:476-480
© 1981 American Academy of Neurology

Myasthenia gravis in infancy

Marjorie E. Seybold, M.D. and Jon M. Lindstrom, Ph.D.

From the San Diego VA Medical Center, San Diego, CA, and the Departments of Neurosciences and Surgery, University of California, San Diego (Dr. Seybold) and the Salk Institute for Biological Studies (Dr. Lindstrom), San Diego, CA.

Address correspondence and reprint requests to Dr. Seybold, (V-1271, San Diego VA Medical Center, 3350 La Jolla Village Drive, San Diego, CA 92161.

Symptoms of myasthenia gravis in infancy may occur from passive transfer of maternal disease, acquired autoimmune disease, or nonautoimmune hereditary disease. Of nine patients with infantile-onset myasthenia who were not born to mothers with the disease, two had detectable antibody to acetylcholine receptor. Patients with or without antibodies were clinically indistinguishable, except for the occurrence of similar disease in siblings of patients without antibody. Differentiation of autoimmune and hereditary myasthenia in infancy is necessary for appropriate therapeutic measures and genetic counseling. Antibody determinations provide a useful aid in this differentiation.

This investigation was supported in part by the Veterans Administration.

Acknowledgment Drs. M. Bauman, S. Clay, Z. Hart, K. Ivanoff, C. Jablecki, C. Sanchez, P. Schultz, R. Skoglund, E. Streib, and A. Wilbourn contributed patient information for this study.

Accepted for publication July 22, 1980






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