We studied seven children with congenital myotonic dystrophy, aged 2.1-8.3 years, and the results of computed tomography and magnetic resonance imaging of the brain were analyzed and neurological development was assessed from the neonatal period. We found that ventricular dilatation that had been seen on the first day of life in two of three infants had not progressed in sequential follow-up computed tomography scans taken at intervals of one to six years. Also, in T2-weighted magnetic resonance imagings, areas of periventricular hyperintensity were identified in all children, as well as areas of subcortical hyperintensity in one child. Further, an asphyxial episode had occurred at birth in five patients and the extent of the periventricular hyperintensity was found to correlate significantly with Apgar scores, indicating that the degree of perinatal asphyxia that had occurred was responsible for the abnormalities uncovered by the magnetic resonance imagings. However, there was no correlation between the neurodevelopment outcome and the extent of the periventricular hyperintensity or ventriculomegaly. Therefore, in patients with congenital myotonic dystrophy, a neonatal episode of asphyxia can be responsible for a finding of periventricular hyperintensity, but it is unlikely that an integral part of the mental retardation is attributable to brain damage due to perinatal asphyxia.

Mycoplasma pneumoniae was isolated from pleural exudates of 2 children with pleuropneumonia. The organism was also isolated from cerebrospinal fluid of a child with meningeal manifestations and from the cerebrospinal fluid as well as pleural exudate of another child who died 21 days after onset of disease. More extensive attempts to cultivate M. pneumoniae from nonpulmonary sites are recommended.

No abstract

No abstract

Several types of transient thyroid dysfunction in infants born to mothers with Graves' disease have been described, ranging from completely unaffected infants to those with hyperthyroidism or hypothyroidism, depending on maternal thyroid function, activity of maternal TSH receptor antibody (TRAb) and maternal antithyroid agents due to transplacental passage. We observed a premature neonate born to a mother with three-year-untreated Graves' disease, who developed transient central hypothyroidism in the immediate postnatal period. Placental transfer of thyroxine and TRAb from the thyrotoxic mother may cause fetal peripheral thyrotoxicosis resulting in suppression of the fetal pituitarythyroid axis.