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Ludwig Gutmann, MD
Department of Neurology West Virginia University Medical Center Morgantown, WV 26506

Marjorie E. Seybold, MD
University of California, San Diego San Diego, CA 92037

Arch Neurol. 1980;37(11):738.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Antibodies of acetylcholine receptors (AchRs), present in most cases of myasthenia gravis (MG), play an etiologic role in this disease.¹ Although they accelerate the degradation of AchRs,² their titer level does not predict the magnitude of generalized symptoms.¹

Antibodies to AchRs cross the placental barrier and their presence has been documented in infants with transient neonatal MG.^3-5 We recently documented high AchR-antibody titers in two myasthenic mothers (one with moderate generalized weakness who received prednisone, and the other with only mild facial weakness who received no medication) and their three asymptomatic infants (Table). Despite the high titers of antibodies to AchRs, all infants (including one with respiratory distress due to hyaline membrane disease and pneumonia that was treated with ampicillin sodium and gentamycin sulfate) showed no weakness or decremental responses on two per second nerve stimulation during the neonatal period. A few asymptomatic . . . [Full Text PDF of this Article]

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