Infection in the Premature Infant as a Cause of Cerebral Palsy 1/2006 

SUMMARY:
Two recent studies present evidence suggesting that inflammation of the placenta alone is insufficient to produce cerebral palsy in the premature infant. Neither addresses potential effects of inflammation elsewhere in the mother nor in the postpartum infant. Kaukola and her colleagues observed that the combination of inflammation and placental defects were predictive of cerebral palsy.

In December 2004 the Research Fact Sheet reported on a very large study performed by the National Institute of Child Health and Human Development implicating “either maternal or fetal infection as a major element in the cause of Cerebral Palsy.” Among other findings, that Fact Sheet¹ reported that “For cerebral palsy alone, 16% of children who acquired any kind of infection in the post natal period developed cerebral palsy while only 8% of those without infection developed cerebral palsy.”

Two recent papers recently published have addressed the specific question as to whether infection of the placenta (chorioamnionitis) may be a causal factor in the development of cerebral palsy in the premature infant. Our readers are reminded that the placenta is actually part of the child and not of the mother.

Polam and his associates² at the University of New Jersey studied the outcome of surviving infants born after 22-29 weeks of gestation whose placentas had been examined pathologically for evidence of inflammation. Evidence of inflammation was found in 186 placentas (including 37 placentas from infants who died) while 251 placentas had no evidence of inflammation. Children were physically examined at several ages with an average follow up of 19 months corrected age. Some children were lost to follow up. Children whose placentas were inflamed (102) were compared with a selected control group of children (75) whose placentas were not. Those with inflammation had higher rates of bleeding into their cerebral ventricles and a higher incidence of visual impairment but the rates of cerebral palsy were approximately the same (8.6% vs. 8%).

Kaukola and her associates³ at the University of Oulu in Finland performed a similar study. They followed 61 extremely low birth weight infants not only examining the placenta for evidence of inflammation but also collecting placental blood for evidence of inflammation. Both were predictors of premature birth and bleeding into the cerebral ventricles. Although neither placental inflammation nor evidence of inflammation in the cord blood predicted the development of cerebral palsy, the combination did.

Comment:
There is a great deal of interest in the relative contributions of inflammation and hypoxia/ischemia as causative agents producing cerebral palsy in the premature infant. In parallel with these investigations, other research is targeting the resulting biochemical reactions in order to develop interventions that may reduce the incidence of cerebral diplegia. Although inflammation placenta alone may not be enough to produce cerebral palsy, these studies do not address the possible effect of inflammation elsewhere in the mother or the infant, especially in the infant in the immediate neonatal period. The second study presents some intriguing data to support the idea that inflammation and hypoxia/ischemia work together as causes of cerebral diplegia.