PERINATAL CORRELATES OF CEREBRAL-PALSY AND OTHER NEUROLOGIC IMPAIRMENT AMONG VERY-LOW-BIRTH-WEIGHT CHILDREN

Background and Objective. The etiology of neurologic impairments among very low birth weight (VLBW, <1.5 kg) children is poorly understood. We sought to investigate the perinatal predictors of major neurologic impairment, including cerebral palsy, among VLBW children. Methods. An tenatal, intrapartum, and neonatal events and therapies were compared between 72 singleton inborn VLBW children born between 1983 to 1991 wh o had neurologic impairment at 20 months corrected age (including 50 w ith cerebral palsy and 22 with other neurologic impairments) and 72 ne urologically normal VLBW children matched by birth weight, gestational age, race, and sex via a retrospective case-control method. Multiple logistic regression was conducted, entering only those variables found to be significant at the bivariate level. Results. There were no sign ificant differences in the rates of pregnancy-induced hypertension, ma ternal tocolytic use including magnesium, or antenatal steroid therapy . Higher rates of clinical chorioamnionitis were found among the mothe rs of the neurologically impaired children as compared with controls ( 31% vs 11%), but not among the subgroup of mothers of children with ce rebral palsy (22% vs 12%). Significant differences in neonatal factors among the total neurologically-impaired group (n = 72) versus control s included oxygen dependence at 36 weeks (31% vs 15%), septicemia (53% vs 31%), severe cranial ultrasound abnormality (50% vs 17%), and hypo thyroxinemia (43% vs 25%). In the subgroup with cerebral palsy (n = 50 ), significant differences included days on the ventilator (23 vs 14 d ays), septicemia (54% vs 33%), and severe cranial ultrasound abnormali ty (52% vs 12%). Multivariate analysis controlling for birth weight, g estational age, race, sex, and the birth period (before 1990 versus 19 90 and after) revealed direct and independent effects of clinical chor ioamnionitis [odds ratio (OR), 3.79; confidence interval (CI), 1.34-10 .78], severe cranial ultrasound abnormality (OR, 9.97; CI, 3.84-25.87) , and septicemia (OR, 2.46; CI, 1.10-5.52) on total neurologic impairm ent. Consideration of the 50 cases with cerebral palsy revealed direct and independent effects of severe cranial ultrasound abnormality only (OR, 15.01; CI, 4.34-51.93). Conclusions. Both antenatal and neonatal risk factors contribute to the development of severe neurologic impai rment, including cerebral palsy among VLBW children. Because preventio n of chorioamnionitis may not be feasible in the near future, attempts to decrease neonatal risk factors such as severe cranial ultrasound a bnormalities and sepsis may be most feasible at this time.