Transient neonatal myasthenia gravis is a rare disease; it affects an estimated 15% of all babies born to myasthenic mothers. Since the condition was first described by Strickroot, Schaeffer, and Bergo (1942), reports have appeared in English of 42 patients, 4 of whom died in the neonatal period.Intestinal smooth muscle hypertrophy is extremely rare in infancy and childhood; to our knowledge only 2 cases have been recorded (Pritchard and Hillier, 1920;Guthrie, 1945). We present a further case of intestinal smooth muscle hypertrophy in an infant dying soon after delivery from a myasthenic mother who had been treated with large doses of neostigmine throughout pregnancy. A possible relationship between the two is considered.Case Report A woman of 37 who had been myasthenic since the age of 20 had a thymectomy when she was 22. Her first two pregnancies were terminated because of deterioration in her disease. The first and second trimesters of her third pregnancy were uneventful. She was admitted to St. Mary's Hospital at 36 weeks with ruptured membranes and draining slightly meconium-stained liquor, but not in labour. Her treatment was 45 mg. neostigmine hourly throughout pregnancy, pyridostigmine 60 mg. every 3-4 hours as required after admission, atropine 0 6 mg. orally with the first daily dose of neostigmine and once during the evening. A myasthenic crisis occurred, during which she stopped breathing, became cyanotic, and comatose. A period of anoxia ensued before a tracheostomy was performed, because of difficulty in maintaining an airway. She never regained consciousness and died 35 hours later. Necropsy showed multiple recent infarcts of the brain and thrombi in both arteries and veins supplying the infarcted areas.A limp cyanosed infant with a heart rate of 60 beats a minute was delivered by caesarean section 4 hours after the initial episode. Mucus and liquor were sucked out of the mouth and oxygen was given by face mask. Only 3 gasps occurred in the first 5 minutes, but despite an improvement in colour the heart rate remained the same; so the infant was intubated and oxygen was given by Received October 12, 1965. * Present address: Department of Pathology, Derbyshire Royal Infirmary, Derby. intermittent positive pressure. No further spontaneous respiration occurred. Neostigmine 0 -1 mg. and lobeline gr. 1/40 were given intravenously at 9 minutes with no response, the heart stopped at 15 minutes.Necropsy. The infant, weight 3 * 02 kg., crown heel length 49 cm., had no external evidence of disease. The cerebral white matter and meningeal vessels were moderately congested. The heart (42 g.) was enlarged to twice its normal weight because of gross hypertrophy and dilatation of the right ventricle and moderate hypertrophy of the left ventricle. The valves, septa, and great vessels were normal. The lungs were small (weight 27 g., expected weight 55 g.) and very congested. The left lung had interstitial emphysema on its cardiac surface.The peritoneal cavity contained amber fluid, and there was considerable retrop...

SUMMARY Two cases of cerebral infarction due to obstructive lesions of the middle cerebral artery are described and their causation is discussed. It is concluded that the arterial lesions occurred at or near birth and were of embolic origin, probably arising from the foetal veins of the placenta. In view of the apparent insignificance of the arterial lesions in these cases, the vessels supplying an infarct should be examined by serial sections at intervals short enough to ensure the discovery of even the smallest lesions. RÉSUMÉ Occlusion périnatale de l'artère cérébrate moyenne Deux cas d'infarctus cérébral dûà des lésions obstructives de l'artère cérébrale moyenne sont décrits et leurs causes sont discutées. La conclusion est que les lésions artérielles sont survenues à la naissance ou aux environs de la naissance, elles étaient d'origine embolique provenant probablement des veines foetales du placenta. Vu l'insignifiance apparente des lésions artérielles dans les cas décrits, les vaisseaux irrigant l'infarctus doivent être examinés par des séries de sections pratiquées à intervalles assez courts pour assurer la découverte des lésions même les plus petites. ZUSAMMENFASSUNG Perinatale Okklusion der mittleren Gehirn‐Arterie Zwei Fälle werden beschrieben bei denen ein Gehirn‐Infarkt von obstruktiven Verlet‐zungen der mittleren Gehirn‐Arterie verursacht wurde, und ihre Kausation wird erörtert. Es wird gefolgert dass die Arterienverletzungen bei der Geburt oder kurz vor‐ oder nachher entstanden und embolischen Ursprungs waren, wahrscheinlich von den foetalen Adern der Plazenta herrührend. Im Hinblick auf die scheinbare Geringfügigkeit der Arterienverletzungen in diesen Fällen sollten die Blutgefässe, die einen Infarkt beliefern, in seriellen Abschnitten untersucht werden und in genügend kurzen Zeitabständen, so dass selbst die kleinsten Verletzungen festgestellt werden können. RESUMEN La oclusión perinatal de la arteria cerebral media Se describen dos casos de infarto cerebral resultando de lesiones obstructivas de la arteria cerebral media, y se discute la causa. Se concluye que las lesiones arteriales ocurrieron durante o cerca del nacimiento, que eran de origen embólico, y que provinieron probablemente de las venas fetales de la placenta. Puesto que las lesiones arteriales en estos casos parecian insignificantes, los vasos que proveen un infarto deberian examinarse por medio de secciones en serie, con intervalos bastante cortos para asegurar el descubrimiento de toda lesión, por muy pequena que sea.

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