It is well known that preterm birth increases the risk of cerebral palsy (CP), but more than half of affected children are born at term and the prevalence of CP in term infants has not declined in recent years. Because there is evidence that chorioamnionitis could substantially raise the risk of CP in term infants, a case–control study was done to clarify this relationship. The study population consisted of 231,582 singleton infants born alive at 36 or more weeks gestation in the years 1991–1998. The case group included 109 children having moderate to severe spastic or dyskinetic CP that could not be ascribed to postnatal brain injury or developmental abnormalities. Control subjects were 218 randomly selected women from the study population. CP was taken to mean a congenital nonprogressive motor dysfunction with spasticity, rigidity, or choreoathetosis. The prevalence of CP in this population was 0.9 per 1000 live births. More than 90% of children were followed up for 2 years or longer. Chorioamnionitis was diagnosed in 14% of the case group and 4% of control children, for an odds ratio (OR) of 3.8. On univariate analysis, CP also was associated with maternal fever, prolonged membrane rupture, nulliparity, and intrauterine growth retardation (IUGR). Intrapartum antibiotic treatment did not appear to have altered the OR of chorioamnionitis and CP. Chorioamnionitis was an independent risk factor for CP on multivariable analysis (OR, 4.1; 95% confidence interval, 1.6–10.1). Other risk factors were IUGR (OR, 4.0), a maternal age more than 25 years (OR, 2.6), being black (OR, 3.6), and nulliparity (OR, 1.8). These findings suggest that clinical chorioamnionitis is an independent risk factor for CP in term and near-term infants. Possible explanations include direct injury of the fetal brain by cytokines in the presence of maternal infection; inflammation of the placental membranes that interrupts gas exchange and blood flow, causing hypoxic–ischemic injury of the fetal brain; elevated core temperature in the fetus; and direct infection of the fetal brain or meninges secondary to maternal intrauterine infection.
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Wu et al. (2004) studied this question.
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