Neonatal EEG-sleep disruption mimicking hypoxic-ischemic encephalopathy after intrapartum asphyxia.

OBJECTIVES: EEG-sleep organization of asphyxiated and non-asphyxiated full-term neonates was compared during the first 3 days after birth.
BACKGROUND: Aggressive fetal and neonatal resuscitative efforts have reduced the severe expression of the neonatal brain disorder termed hypoxic-ischemic encephalopathy. Neonates may alternatively express altered EEG-sleep organization over the first days of life after asphyxia which may mimic mild or moderate hypoxic-ischemic encephalopathy. None of ten asphyxiated infants had EEG-confirmed seizures or pharmacologically-induced encephalopathies. All asphyxiated infants expressed fetal distress on fetal heart monitoring prior to delivery, and required neonatal resuscitation, as reflected in depressed 1, 5, and 10 min Apgar scores. Moderate to severe metabolic acidosis was also documented at birth in the asphyxiated group. All ten asphyxiated infants displayed either hyperalertness/irritability or somnolence/lethargy during the first 24 h after birth, suggesting mild to moderate post-asphyxial encephalopathy. Twenty-two 1 h 21-channel EEG polygraphic studies were obtained from the first through third days of life on nine asphyxiated infants and scored for EEG-sleep states. Studies on 23 non-asphyxiated newborns were also obtained between 1 and 3 days of life and scored for EEG-sleep state. EEG-sleep states were assigned to every minute of each record by visual analyses, without knowledge of the presence or absence of asphyxia. Comparisons of active, quiet, and indeterminate sleep percentages between neonatal groups were performed. Nested MANOVA was used which took into account multiple observations per child in the asphyxiated group.
RESULTS: The percent of active sleep was 44.7% (+/-14.7), the percent of quiet sleep was 38.7% (+/-14.3), and the percent of indeterminate sleep was 13.3% (+/-11.4) in the non-asphyxiated group. The percent of active sleep was 18.9% (+/-18.5), the percent of quiet sleep was 46.5% (+/-21.1), and the percent of indeterminate sleep was 33.4% (+/-19.7) in the asphyxiated group. A significant decrease in active sleep (F=39.5, P<0.0001), and significant increases in quiet sleep (F=4.6, P<0.05) and indeterminate sleep (F=21.5, P<0.0005) were noted in the asphyxiated group. Shorter active sleep bout lengths were noted (F=21.8, P<0.001), while the quiet sleep bout lengths remained unchanged for the asphyxiated group.
CONCLUSIONS: An increased percentage of quiet sleep and indeterminate sleep at the expense of decreased active sleep reflects postnatal brain adaptation to asphyxia in infants despite the absence of overt clinical or electrographic evidence of hypoxic-ischemic encephalopathy. Brain adaptation in newborns after acute asphyxial stress may be expressed as altered sleep organization, despite clinical signs which may masquerade as mild to moderate post-asphyxial encephalopathy. EEG-sleep studies can assist in a more accurate classification of newborn encephalopathy that does not satisfy the criteria for hypoxic-ischemic encephalopathy.