Antenatal risk factors for cerebral palsy

Two of every 1000 live-born children develop cerebral palsy (CP). The aetiology of CP is often unclear and because CP is a symptom complex rather than a disease, clinically defined at 4–5 years of age, it is not surprising that there are considerable problems associated with epidemiological studies of its aetiology. The only reason for the CP concept is that it emanates from an insult to a growing, developing brain and a dynamic clinical picture from static pathology. Evidence suggests that 70–80% of CP cases are due to prenatal factors and that birth asphyxia plays a relatively minor role (<10%). Some antenatal risk factors are repeatedly observed to be related to CP: low gestational age, male gender, multiple gestation, intrauterine viral infections and maternal thyroid abnormalities. Recently, intrauterine infection/inflammation with a maternal response (consisting of chorioamnionitis) and a fetal inflammatory response (consisting of funicitis or elevated interleukin-6 in fetal plasma) has been found to be related to white matter injury and CP. Some risk factors are associated with CP at all gestational ages whereas others mostly affect term or preterm infants, e.g. intrauterine growth restriction seems to be a risk factor in term infants. There also seems to be an association between autoimmune and coagulation disorders and CP.