Cerebral palsy and the placenta: A review of the maternal-placental-fetal origins of cerebral palsy

Accumulating evidence from clinical and neuropathological study has identified a number of seemingly disparate associations carrying a predisposition for cerebral palsy (CP). We narratively reviewed clinical studies reporting associations between prenatal and perinatal environmental factors and the risk of developing CP. As expected, some processes with direct central nervous system involvement (e.g. perinatal hypoxic-ischemic encephalopathy or infectious encephalomalacia) carry >10% absolute risk of CP. Other acute perinatal processes including placental abruption, uterine rupture, and neonatal sepsis are also associated with increased risk of CP but carry <3% absolute risk of CP. Indirect markers of chronic placental insufficiency such as fetal and placental growth patterns are associated with increased risk of CP, and risk of CP in infants with growth abnormalities born extremely preterm exceeds 10%. We synthesize these findings within a framework of risk accumulating across several defined pre- and perinatal developmental windows. Causal links remain incompletely understood, but genetic background, the intrauterine environment, general fetal health, and fetal neurologic health all appear to contribute.

Automated summary

Accumulating evidence has revealed that various seemingly unrelated factors are associated with the susceptibility to cerebral palsy, including prenatal and perinatal environmental factors and fetal health. These factors accumulate and increase the risk of cerebral palsy during different developmental stages.