An elegant chapter of recent medical history is the clarification of the pathogenesis of acquired myasthenia gravis.1 It is now recognized as an immunologic disorder, a principal aspect of which is antibody attack on the acetylcholine receptor protein. The muscle cell receptor apparatus is perturbed, and many remaining binding sites for the neuromuscular excitatory transmitter, acetylcholine, may be disrupted by antibody, giving rise to the fatigability and weakness that are the clinical hallmarks of the disease.
Transient neonatal myasthenia gravis,2 which occurs in about 10% to 15% of offspring of affected mothers, for many years has provided a provocative clue that humoral factors are important in this disease. The report in this issue of the Journal by Donaldson and five collaborators from three medical centers, "Antiacetylcholine Receptor Antibody in Neonatal Myasthenia Gravis" (p 222), provides confirmation that maternal antibody crosses the placenta to the infant. The elevated antibody