Cerebral palsy and intrauterine growth in single births: European collaborative study

In developed countries, cerebral palsy (CP) remains the most common form of severe physical disability in children. Approximately 25 years ago, the rate of CP was found to be substantially increased in low-birth-weight children, but the cause of CP still is poorly understood. The authors report a survey of 10 European registers totaling 4503 singleton children with CP who were born in the years 1976 through 1990. The goal was to learn whether altered intrauterine growth is a pathologic factor in the origin of CP. CP was defined as a group of disorders that involve disordered movement, posture, or both as well as motor dysfunction. It is a permanent condition that can change but is not progressive. Using conventional fetal growth standards, infants born at 32 to 42 weeks gestation whose birth weight for gestational age was below the 10th percentile were 4 to 6 times more likely to have CP than were reference children with birth weights between the 25th and 75th percentiles. The increase in risk was considerably less (1.6- to 3.1-fold)-but still significant-in children whose birth weights were above the 97th percentile. The risk of CP was lowest in children whose birth weights were approximately 1 standard deviation above average. Similar findings were obtained for infants having unilateral or bilateral spasticity, and also for those who were dyskinetic or ataxic. The relationship between birth weight and risk of CP, if any, was less clear in children who were born before 32 weeks gestation. As is the case for perinatal death, the risk of CP is lowest in infants who at birth are above average weight for gestational age. However, the risk of CP increases not only when birth weight is well below normal, but also when it is well above normal. Possibly an abnormal growth pattern causes CP, or vice versa, or there could be some factor that is linked independently to both growth and the risk of CP. Conceivably, brain damage or impaired development in utero triggers an abnormal growth pattern through an endocrine pathway or some other mechanism. An alternative explanation is that abnormal growth renders the fetus more vulnerable physiologically, and that the brain is exposed to irreparable darnage during or after delivery.