Prenatal risk factors causing cerebral palsy (CP), here defined as a non-progressive motor abnormality of tone or posture, are much more numerous than once believed, when a great deal of brain injury was attributed to factors surrounding delivery. Scientific advances in genetics and biochemistry, as well as clinical technical advances in, for example, amniotic fluid examination or fetal neuroimaging, has permitted us to find a multiplicity of new etiologies causing neonatal encephalopathy, most of which were formerly attributed to perinatal hypoxia-ischemia. This article reviews an expanded list of etiologies, including asphyxia, which has been found to cause only 6-10% of CP in full term infants, and periventricular leukomalacia, which is associated with 30-50% of CP in premature births. We also review a few of the genetic causes of CP, which lead to metabolic encephalopathies in come cases, to congenital anomalies in others, and sometimes to both. We discuss maternal gestational or intrapartum infections which may affect the fetus by direct in utero contagion or by other less direct means. Inborn metabolic errors affecting the fetus, such as diabetes, are touched on, as are the effects of maternal medications or recreational drugs on the fetus. Finally, we briefly cite the curious phenomenon occurring in multiple births, namely the potential of CP in the surviving infant or infants were the others have died in utero.
