Imaging studies of cerebral palsy have increasingly appeared and it has even been suggested, perhaps with excessive enthusiasm, that all such children undergo scanning. Cowan and colleagues (2003) used MRI to determine the proportion of infants with a neonatal encephalopathy who had antenatal brain injury. Excluding those with major congenital malformations or obvious chromosomal abnormalities, 80 percent of cases had no established lesion or brain atrophy. In contrast, those with only seizures and no neonatal encephalopathy in 69 percent of cases had evidence of antenatal damage on MRI; infarctions because of thrombophilic disorders were most common. An MRI–clinical correlative study of children with cerebral palsy by Bax and colleagues in The European Cerebral Palsy Study came to similar conclusions but found that periventricular leukomalacia of prematurity was the most common MRI change, present in 42 percent of infants, followed in frequency by basal ganglionic damage (13 percent), cortical-subcortical lesions (9 percent), malformations (9 percent), and focal infarcts (7 percent). These authors found a correspondence between the clinical and MRI findings. These studies demonstrate the utility of MRI in identifying neonatal forms of encephalopathy and indicate that few are the result of obstetric accidents. Added difficulty is caused by the fact that the clinical signs of perinatal injury may emerge only when the maturational process of the nervous system exposes them at a later period of life. Woodward and coworkers suggested that the MRI pattern is predictive of developmental outcome in preterm infants, but this requires corroboration.
Treatment Much of the resources of neonatal intensive care is devoted to sustaining oxygenation and blood pressure, and reducing hyperbilirubinemia in premature and full-term but ill infants. Techniques such as the predelivery administration of corticosteroids in premature births to promote lung maturity, attempting to bring early births to 34 to 36 weeks’ gestation, and the treatment of maternal infection have all contributed to improved outcomes in children. The American Academy of Pediatrics, based on a systematic review of randomized clinical trials (e.g, Azzopardi et al and Shankaran et al), has given guidance that hypothermia is an effective therapy for improving neurologic outcome in neonatal encephalopathy. Criteria for patient enrollment that simulate those used in clinical trials of this intervention must be followed to achieve an effect, including early institution of treatment (see
Committee on Fetus and Newborn in references). It must be acknowledged that clinical trials have given conflicting advice, have had short follow-up, and small differences between treated and untreated groups. Trials of cooling have generally excluded infants with major malformations, which are present in approximately one-third of children with cerebral palsy, as alluded to above.
The avoidance of the ostensible causes of cerebral palsy has been discussed in previous sections. None of the usually assigned causes of birth injury, particularly perinatal hypoxia-ischemia, explains most cases.
Clinical Syndromes of Congenital Spastic
The most frequent motor disorder evolving from the four major categories of neonatal cerebral disease—matrix hemorrhage, periventricular leukomalacia, hypoxic-ischemic encephalopathy, kernicterus (discussed further on)—is spastic diplegia; that is, a motor disturbance that is severe in the lower limbs and mild in the upper, as discussed below. In addition, hypoxic-ischemic injury occurring in the term or preterm infant may take the form of a hemiplegia, double hemiplegia (quadriplegia), or a mixed pyramidal–extrapyramidal or spastic–ataxic syndrome.