Asphyxial Birth Events Not Main Cause of Cerebral Palsy


Birth defects and poor fetal growth are more substantial contributors to cerebral palsy than asphyxial birth events or inflammation, a new study finds.

The most common risk factors for cerebral palsy and infant death are birth defects and poor fetal growth, concluded a new study.1

Previous research has focused on asphyxial birth events as being the primary cause of cerebral palsy and infant death. However, a group of researchers, led by Karin B. Nelson, MD, scientist emeritus at the National Institutes of Health, have found that this is not the case. Nelson and colleagues investigated the degree to which 4 risk factors-asphyxial birth events, inflammation, birth defects, and poor fetal growth-contributed to cerebral palsy and young infant death.

The researchers evaluated the medical records of singletons born at or after 35 weeks’ gestation. The neonates were categorized as follows: 494 had cerebral palsy, 508 were matched controls, 100 died within the first month of life, and 73 were intrapartum stillbirths. By comparing the medical records of children with cerebral palsy and infants who were stillborn or who died within the first month of life with those of healthy children, the researchers were able to identify the frequency with which the 4 prespecified risk factors occurred.

In almost half of the cases of cerebral palsy, birth defects (recognized by age 6 years) and/or poor fetal growth were reported. Of the 4 risk factors studied, only birth defects and poor fetal growth were able to predict the occurrence of quadriplegia or dyskinesia, symptoms characteristic of the 2 most common types of cerebral palsy (spastic and dyskinetic, respectively).

Among children with cerebral palsy, 12.6% experienced a potentially asphyxial birth event, inflammation, or both, whereas 48.6% experienced growth restriction, a birth defect, or both (P<0.001). To compare, a potentially asphyxial birth event occurred in 34% of stillborns and 21.6% of neonates with cerebral palsy after hypoxic ischemic encephalopathy (HIE). Inflammatory markers occurred in 13.9% of stillborns and 11.9% of neonates with cerebral palsy after HIE. Growth restriction was a significant contributor to all poor outcome groups. Birth defects were present in 5.5% of neonates in the control group, 60% of neonates who died within the first month of life, and more than 50% of neonates with cerebral palsy without HIE.

These findings suggest that, going forward, research should focus on the role that birth defects and poor fetal growth play in cerebral palsy. Although the overarching cause of cerebral palsy is known to be an abnormality or disruption in brain development, the specific triggers behind the abnormality or disruption are largely unknown.

Pertinent Points:
- Fetal growth restriction and birth defects are more substantial contributors to cerebral palsy and neonatal death than potentially asphyxial birth events and inflammation.
- Birth defects and/or poor fetal growth are the only risk factors that predicted dyskinesia or quadriplegia in children with cerebral palsy.


1. McIntyre S, Blair E, Badawi N, et al. Antecedents of cerebral palsy and perinatal death in term and late preterm singletons. Obstet Gynecol. 2013. DOI: 10.1097/AOG.0b013e3182a265ab.

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