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THERE is a group of neuromotor disorders of early life in which the disease process becomes evident clinically before birth. The prenatal manifestations of the disorder are a delay of quickening and a reduction in the amount of fetal activity. This symptom of impaired fetal movement has been previously reported in a number of cases of amyotonia congenita (Oppenheim), apparently having first been noted by Foot1 in 1913. Fetal inactivity does not refer to a specific clinicopathologic disease process, but merely indicates prenatal suppression of neuromuscular mechanisms controlling motor behavior. Thus, in the following cases a myasthenic syndrome was present from birth, and one may surmise from the prenatal history that muscular function (or neuromuscular transmission) of the fetus was similarly defective. REPORT OF CASESCase 1.\p=m-\Inthe case of J. E. B., a male infant, quickening began during the seventh month of the mother's pregnancy and was always infrequent and weak. The birth was uneventful, the infant weighing 9 pounds (4,082 Gm.). Immediately after delivery he was pink but within thirty minutes he became cyanotic ("black"), an episode which was attributed to his swallowing the tongue. He had great difficulty in sucking and swallowing, so that he had to be fed with a spoon until he was 3 years old. Thick mucus collected in his throat, and his mother would turn him over to let it run out of his mouth. He cried frequently from hunger, as on some days he could take only 2 or 3 ounces (60 or 90 cc.) of milk. His general activity as an infant seemed normal, and he did not appear to have any definite atonia. He sat alone at 10 months and walked at 17 months of age. He fell frequently, was unable to run and had to crawl upstairs. He began to talk at about the age of 1 year but his speech was always indistinct, and he was 4 years old before his mother could understand him..

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