In addition, such infants may have been exposed to certain prenatal risk factors (toxemia of pregnancy, antepartum uterine hemorrhage, maternal hypotension, and certain epidemiologic associations such as hypothyroidism or fertility treatment), or their growth may have been abnormal (small-for-date babies). Some of these babies are born at term; others are premature, and the birth process may or may not have been abnormal. One must then consider the possibility, originally pointed out by Sigmund Freud, that the abnormality of the birth process, instead of being causal, was actually the consequence of prenatal pathology. The latter might include preterm intrauterine hypoxia-ischemia.
Other evidence of multifactorial etiology in the “causation” of cerebral palsy has been provided by Nelson and Ellenberg, who found that maternal developmental delay, birth weight below 2,000 g, and fetal malformation were among the leading predictors. Breech presentation was another factor, and one-third of these cases also had some noncerebral malformation. Twenty-one percent of the 189 children in their series had also suffered some degree of asphyxia. Additional determinants were maternal seizures, a motor deficit in an older sibling, two or more prior fetal deaths, hyperthyroidism in the mother, preeclampsia, and eclampsia. In children with cerebral diplegia born at term, likely contributory factors that were operative in nearly half included toxemia of pregnancy, low birth weight for age, placental infarction, and intrauterine asphyxia.
The factors enumerated above are involved to different degrees in the outcome of pregnancies but are informative because they bring to light the significant proportion of cases of cerebral birth injury in which hypoxia-ischemia, matrix hemorrhages, and leukomalacia were not operative. In this group, can be included the symmetrical porencephalies and hydranencephalies.
Thus the complexity of assigning a cause for cerebral palsy is evident. In respect to the motor disorders discussed below, hypoxic-ischemic perinatal injury is still the most commonly specified cause of neonatal encephalopathy but is often unrelated to a permanent defect of cerebral palsy. This statement has been amply confirmed by a large and often cited study from Western Australia that detected neonatal encephalopathy in 3.8 of 1,000 live term births but was able to identify causative intrapartum factors alone in only 5 percent (Badawi et al). Furthermore, only 10 percent of all the infants with neonatal encephalopathy developed spastic quadriplegia, according to Evans and colleagues.