Risk factors for static encephalopathy vary with the period or timing of the insult. More than a century ago, Little described static encephalopathy and related it causally to difficulties in the birth process. However, data from several large population-based studies confirmed the subsequent theory, first advanced by Freud, that static encephalopathy in most children cannot be attributed to birth asphyxia and that “difficult birth in itself is merely a symptom of deeper effects that influenced the development of the fetus.” Intrapartum asphyxia is thought to be causely related in only 20% of cases of static encephalopathy. Congenital disorders may account for 30% to 40% of the total, and infections of the central nervous system account for another 5% to 10%. In fact, no specific cause can be identified for as many as 50% of infants in whom the condition develops. In infants born at term, neonatal events that previously have been attributed to asphyxia are at least as likely to occur in association with underlying congenital disease. These events include meconium in the amniotic fluid, low 10-minute Apgar scores, neonatal seizures, apnea, newborn neurologic abnormalities, and slow head growth. The term infant with low Apgar scores from a late asphyxial event who does not show signs of newborn encephalopathy will not develop static encephalopathy. Furthermore, epilepsy and mental retardation alone do not follow birth asphyxia as the sole cause. Prematurity, low birth weight, and placental dysfunction are increasingly important factors in the genesis of static encephalopathy. Risk factors in the very low-birth-weight infant include hypotension, acidosis, sepsis, seizures, pneumothorax, and prolonged ventilation.

Spastic diplegia most commonly is the result of prematurity and postnatal complications of premature birth, including periventricular leukomalacia and intraventricular hemorrhage. When it occurs in the full-term infant, spastic diplegia usually is the result of a complicated pregnancy and delivery. Spastic diplegia does not occur in the term infant whose only insult at birth is late asphyxia (i.e., antenatal risk factors must be considered).

Since 1960, infant mortality has decreased dramatically in the developed countries of the world. This decrease has been attributed to improved prenatal and perinatal care. That these improvements have not had a favorable effect on the frequency of static encephalopathy provides further support for causative factors other than the birth process itself in this disorder.
Extensive evaluation of electronic fetal monitoring revealed that this technique did not improve the outcome in terms of neurologic development in either term or preterm infants.

To define a causal relationship between intrapartum events and cerebral palsy more clearly, the International Cerebral Palsy Task Force developed a set of specific criteria that were refined further in 2003. These criteria are described in Box 398.1. Additionally, the investigators concluded that only cerebral palsy involving spastic quadriplegia is associated with significant intrapartum events and that purely dyskinetic or ataxic forms generally are genetic in origin. Infants injured during the prenatal period may have had time to recover before parturition and thus may not have perinatal encephalopathy. Their static problems can be assigned clearly to insults occurring at a time other than birth.