Maternal Infection and Cerebral Palsy
October 1, 1997 2 minutes read
Maternal Infection and Cerebral Palsy
Abstract & Commentary
Synopsis: Intrauterine exposure to maternal infection is associated with a significant increase in the risk of cerebral palsy in infants of normal birth weight.
Source: Grether JK, Nelson KB. JAMA 1997; 278: 207-211.
To determine the role of maternal infection recognized at the time of delivery as a cause of cerebral palsy (CP) in infants weighing 2500 g or more, Grether and Nelson performed a population-based case control study between 1983 and 1985 in four northern California counties. Maternal labor and delivery and newborn records were reviewed to identify maternal infection, recognized as the clinical diagnosis of chorioamnionitis, histological diagnosis of inflammation of the placental membranes, gross or microscopic diagnosis of cord inflammation, or a maternal temperature greater than 38°C. Data were available on 46 of 48 children with unexplained spastic CP who survived to age 3 years. These children were compared to 391 controls. Both groups were delivered at about 39 weeks. Maternal fever, clinical chorioamnionitis, and histological evidence of inflamed amniotic membranes or cord were associated with a nine-fold or greater increased risk for CP. When confounding variables that might explain the association between maternal infection and CP were examined, an increased risk of almost nine-fold for CP remained. Children with CP whose mothers were infected at the time of delivery were much more likely to have low APGAR scores, require intubation, demonstrate hypotension and neonatal seizures, and have meconium aspiration syndrome.
Grether and Nelson conclude that intrauterine exposure to maternal infection is associated with a significant increase in the risk of CP in infants of normal birth weight.
COMMENT BY STEVEN G. GABBE, MD
Of all cases of CP, approximately 25% occur in term infants. Grether and Nelson have played an important role in identifying the causes of CP, demonstrating that only about 10% of cases of CP can be attributed to birth asphyxia. Now, Grether and Nelson report that maternal infection identified at the admission for delivery significantly increases the risk for CP in infants weighing 2500 g or more. Why? As emphasized by David Eschenbach, MD, in an accompanying editorial, CP in this setting may result from the effects of inflammatory cytokines on the fetal brain.1
The effect of infection on the brain of the preterm, low birth weight infant might be even more devastating. Can we use this new information to reduce the rate of CP through broader use of antibiotics or corticosteroids? The answers to those questions will depend on further investigation.
Reference
1. Eschenbach D. JAMA 1997;278:247.
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