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Neonatal seizures are a frequent problem encountered in neonatal nurseries, but their significance is controversial. Some investigators regard newborn seizures as simply epiphenomena and reflective of brain injury, whereas others note associated metabolic and physiologic aberrations suggesting that seizures per se are injurious to the central nervous system. The proper approach to the treatment of neonatal seizures depends on the etiology because treatment differs if seizures are of metabolic, toxic, or structural origin. Most studies reporting the efficacy of anticonvulsant agents neither define the seizure characteristics being treated nor use electroencephalographic documentation of seizure activity. The choice of anticonvulsants has been based on tradition rather than on the proven superiority of one agent over another. Although several anticonvulsants are available, phenobarbital remains the drug most frequently chosen as the initial agent in treatment. The important pharmacologic considerations of anticonvulsants include route of administration, ability to achieve therapeutically efficacious and predictable plasma levels rapidly, drug distribution, the availability and affinity of receptor sites, protein-binding characteristics, effects on brain growth, and cardiovascular toxicities. At the present time, critical questions remain regarding the effects of both seizures and anticonvulsants on the developing central nervous system.

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The development of 50 children relative to the fetal heart rate patterns they demonstrated during labor and delivery was prospectively studied. Normal deceleration patterns were recorded for 12 of the children, while 16 were recorded as moderately severe and 22 as severe variable or late deceleration patterns. The parity and socioeconomic status of the mothers and the sexes of the infants were similar among the groups. A statistically significant developmental difference in favor of children with normal fetal heart rate patterns was seen in the first year of life. However, at 6 to 9 years of age the difference in neurologic and cognitive development was no longer evident. These data do not support the hypothesis that brief abnormal fetal heart rate patterns recorded during labor are indicative of irreversible central nervous system injury.

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The neurologic, psychologic, language, and academic skills were evaluated and compared in children who had had enteroviral meningitis in infancy and their siblings. The study population consisted of 45 children in whom enteroviral meningitis developed between the ages of 4 days and 12 months. Three died of heart failure caused by viral myocarditis. Thirty-three survivors and 31 siblings were comprehensively evaluated with physical and neurologic examinations; hearing, vision, and achievement tests; and tests of cognitive, perceptual-motor, language, memory, and emotional-behavioral functions. The remaining nine survivors of meningitis and eight of their siblings were assessed by telephone interviews and analysis of school and medical records. None of the survivors had major adverse neurologic sequelae. In addition, they performed as well as their siblings on all tests administered. Our study did not demonstrate either overt or covert impairments of neurologic function or development in survivors of infantile enteroviral meningitis.

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Bilateral hearing loss occurred in 9.7% of infants who survived despite very low birth weight (less than or equal to 1500 gm), 16.7% of infants who survived neonatal seizures, and 28.6% of infants who survived both low birth weight and neonatal seizures. All neonates received treatment in a single neonatal intensive care unit between 1976 and 1980. Twenty-two of 36 hearing-impaired children were normal physically and mentally, with IQ scores of greater than or equal to 85. Significant neonatal predictors of hearing loss in high-risk premature infants (less than or equal to 36 weeks gestation), as determined by multivariable testing, were prolonged respirator care, high serum bilirubin concentration, and hyponatremia. Exchange transfusions were associated with a decreased risk of hearing loss.

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Neonatal asphyxia, defined in this study as delay of greater than 1 minute in onset of spontaneous respiration at birth, occurred in 1% of 13,221 live-born infants of birth weight greater than 500 gm between 1970 and 1971. Seventy-five (56%) of 133 asphyxiated infants survived the neonatal period. Survival was directly related to gestational age. The 65 survivors of asphyxia available for study were seen at a mean age of 4.8 years to determine the incidence and extent of neurologic and developmental abnormalities. Twelve children (18.5%) had severe impairment: nine had both neurologic and intellectual handicaps, two had neurologic impairment alone, and one had intellectual impairment alone. The incidence and severity of impairment were not related to gestational age. Postasphyctic seizures were associated with poor outcome.

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Little information is available regarding appropriate plasma levels of anticonvulsant drugs in neonates. We determined the plasma levels of phenobarbital and diphenylhydantoin following initial administration and during maintenance therapy in 59 neonates with seizures. Following intravenous administration of 15 to 20 mg/kg, levels of 20.7 +/- 4.4 microgram/ml were achieved for phenobarbital and levels of 14.5 +/- 3 microgram/ml for DPH. Maintenance doses of 5 mg/kg of phenobarbital resulted in initial drug accumulation followed by more rapid elimination of the drug with increasing duration of exposure. Therapeutic plasma levels of DPH could not be achieved by oral administration in the neonate.

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