Their prevalence of 2–2.5 per 1000 births has changed little since cerebral palsy registers began 57 years ago, despite a sixfold increase in caesarean birth. They are heterogeneous in clinical type, in brain imaging pathology, in their association with other neurological disability and in their genetic and epidemiological associations.
In a recent paper published in Obstetrics and Gynecology researchers describe a case–control study of 494 singleton infants with cerebral palsy born after 35 weeks gestation, included on theWA Register of Developmental Anomalies, and 508 matched controls. They found that birth defects (42.3%) and fetal growth restriction (16.5%) contributed more to cerebral palsy than potentially asphyxial birth events (8.5%) and inflammation (4.8%).
These data confirm and extend the findings of other epidemiological studies and particularly underline the antenatal origins of most of the cerebral palsies.
The strong association of cerebral palsy with birth defects suggests genetic and epigenetic pathways to many of these cases. Very preterm delivery can initiate another common pathway via intraventricular haemorrhage, ventriculomegaly and white matter damage.