Continuously recorded amplitude-integrated EEG (aEEG) traces of 77 preterm babies were analysed retrospectively, to study the effect of different sedative drugs over a 24-h period. Thirty-seven babies were treated with phenobarbitone, 18 received morphine and 22 babies received no regular sedation. A "burst" was defined as a discharge of integrated amplitude greater than 10 microV and maximum interburst intervals in 10-min epochs over a 2-h period were measured. Maximum interburst was prolonged in babies given either morphine or phenobarbitone for sedation. Administration of a single dose of diazepam for intubation had a marked additive effect on the EEG depression caused by the base sedative and prolonged the effect for 11 to 12 h after drug administration. We conclude that the effect of sedative drugs must therefore be accounted for when interpreting records of quantified EEG for 12 to 24 h after drug administration.
Spectral edge frequency (SEF) of the EEG was studied in 51 healthy neonates to assess its value as a measure of cerebral maturation. SEF was calculated as the frequency below which 95% of the power in the power spectrum resides. Summated SEF (sSEF) of 4 EEG channels correlated significantly with gestational age (r = 0.83).sSEF varied with behavioural state and with EEG derivation. Intra- and interindividual variability were both greater in preterm compared to term babies. We conclude that SEF is a useful measure of cerebral maturation in the newborn and may have a role in studying stressed newborns.
During surfactant treatment of respiratory distress syndrome, 23 premature newborns were investigated with continuous amplitude-integrated electroencephalography (cerebral function monitors). Simultaneously, arterial blood pressure and transcutaneous blood gas values were recorded. A short(<10 minutes) but significant decrease in cerebral activity was seen in almost all neonates immediately after the surfactant instillation, in spite of an improved pulmonary function. In 21 of 23 neonates, a transient fall in mean arterial blood pressure of 9.3 mm Hg (mean) occurred coincidently with the cerebral reaction. Neonates in whom intraventricular hemorrhage developed tended to have lower presurfactant mean arterial blood pressure (P> .05), but they had a significantly lower mean arterial blood pressure after surfactant instillation (P < .05). No other differences were found between neonates in whom intraventricular hemorrhage developed and those without intraventricular hemorrhage. The present findings demonstrate that an acute cerebral dysfunction may occur after surfactant instillation. In some vulnerable neonates with arterial hypotension and severe pulmonary immaturity,the fall in mean arterial blood pressure may increase the risk of cerebral complications and could be related to an unchanged rate of intraventricular hemorrhage after surfactant treatment.
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