Most prophylactic measures for neonatal encephalopathy have been evaluated in preterm infants (Chap. 42, p. 824). One of these-postnatally induced hypothermia-may prevent death and mitigate moderate to severe neurological disability in term newborns (Garfinkle, 2015; Nelson, 2014; Shankaran, 2012). MR imaging studies have demonstrated a slowing of difusional abnormalities and fewer infarctions with hypothermia (Bednarek, 2012; Natarajan, 2016b). Most randomized trials have shown improved outcomes with induced hypothermia in those born at 36 weeks' gestation or older (Azzopardi, 2014; Guillet, 2012; Jacobs, 2011). In a metaanalysis of more than 1200 newborns, Tagin and colleagues (2012) concluded that hypothermia improves survival rates and neurodevelopment. Clinical trials to evaluate concomitant neonatal erythropoietin therapy for neuroprophylaxis have reported conlicting results (Fauchere, 2015; Ivf all a, 2017). Preliminary data from one multicenter trial of maternal alopurinol therapy indicate some mitigation of cerebral damage caused by hypoxia and ischemia (Kaandorp,r2013).
This term refers to a group of nonprogressive disorders of movement or posture caused by abnormal development or damage to brain centers for motor control. Cerebral palsy is further classiied by the type of neurological dysfunction-spastic, dyskinetic, or ataxic-and by the number and distribution of limbs involved-quadriplegia, diplegia, hemiplegia, or monoplegia. Together, the major types are spastic quadriplegia-the most common-which has a strong association with mental retardation and seizure disorders; diplegia, which is common in preterm or low-birthweight infants; hemiplegia; choreoathetoid ypes; and mixed varieties. Although epilepsy and mental retardation frequently accompany cerebral palsy, these two disorders seldom are associated with perinatal asphyxia in the absence of cerebral palsy.
According to Nelson and coworkers (2015), the prevalence of cerebral palsy in the United States averages 2 of every 1000 children. t is crucial to emphasize that this rate is derived rom al children-including those born preterm. Because of the remarkably greater survival rates of the latter currently, and despite the elevated cesarean delivery rate, the overall rate of cerebral palsy has remained essentially unchanged (Fig. 33-1). For example, follow-up studies of more than 900,000 Norwegian nonanomalo us term infants cite an incidence of 1 per 1000, but the incidence was 91 per 1000 for those born at 23 to 27 weeks (Moster, 2008). Similar indings have been reported for Australian births (Smithers-Sheedy, 2016). In absolute numbers, term newborns comprise half of cerebral palsy cases because there are proportionately far fewer preterm births. It is again emphasized that most studies of cerebral palsy rates have not made distinctions between term and preterm infants.
As noted earlier, Nelson and Ellenberg (1984, 1985, 1986a) made many fundamental observations concerning cerebral palsy. Their initial studies emanated from data from the Collaborative Perinatal Project. This included children from almost 54,000 pregnancies who were followed until age 7. hey found that the most frequently associated risk factors for cerebral palsy were: (1) evidence of genetic abnormalities