Treatment Control of the respiratory distress of prematurity may reduce the incidence of matrix hemorrhages and periventricular leukomalacia. Claims have been made that the administration of indomethacin ethamsylate, a drug that reduces capillary bleeding, and the intramuscular injection of vitamin E for the first 3 days after birth and possibly the use of betamethasone or other corticosteroids appears to be of value in reducing the incidence of periventricular hemorrhage (Benson et al; Sinha et al; see also Volpe [1989] for discussion of control of cerebral hemodynamics and effects of medications in the neonatal period). Acetazolamide and furosemide, which reduce the formation of spinal fluid, have been widely used in the treatment of posthemorrhagic hydrocephalus. However, in a large-scale controlled study, the effects were negligible and shunt placement was required to control worsening hydrocephalus (see International PHVD Drug Trial Group in the references).
These are zones of necrosis of white matter in the deep territories of cortical and central arteries. They lie lateral and posterolateral to the lateral ventricles, in a position to involve the occipital radiations and the sensorimotor fibers in the corona radiata (first described by Banker and Larroche; see also Shuman and Selednik). The white matter lesions occur in about one-third of cases of subependymal hemorrhage as mentioned, but they may develop independently in both premature and full-term infants who have suffered hypotension and apnea. In a study of 753 preterm infants, those born at 28 weeks’ gestation or less were at highest risk of this complication; the combination of intrauterine infection and premature rupture of membranes carried a 22 percent risk (Zupan et al). Survivors often manifest cerebral hemiplegia or diplegia and variable degrees of cognitive impairment. The motor disorder is usually more severe than the cognitive and language impairment. Increasingly, small lesions of this nature are being identified in term infants by cerebral imaging including ultrasound.
The mechanism of this type of periventricular infarction has been debated, and the terminology and clinical features, insofar as they overlap with germinal matrix hemorrhage, have been confusing. In recent years, most theories and experimental evidence converge on the notion that these represent regions of venous ischemia and infarction.
It has been estimated that in the range of 1 to 6 of every 1,000 live births manifests a neonatal encephalopathy (as quoted in the review by Ferriero). The seriousness of the condition is further emphasized by the associated mortality rate of 20 percent in the newborn period and the 25 percent rate of neurodevelopmental disability in survivors. Little’s conception of the hypoxic-ischemic form of “birth injury,” enunciated in 1862, has been reconsidered over the years. Although it is evident that many newborns suffer some degree of perinatal asphyxia, relatively few seem to manifest brain damage. Moreover, many, if not most, infants with a variety of cerebral motor syndromes appear to have passed the parturitional (perinatal) period without mishap, indicating the greater importance of other prenatal and postnatal causative factors. Nonetheless, severe neonatal asphyxia of term or preterm babies can be an important cause of spastic, dystonic and ataxic syndromes, often accompanied by seizures and mental delay in development.
This field has been sullied by an unprecedented rise in malpractice litigation, spawned in part by the belief that early detection of asphyxia and rapid delivery would have prevented the motor, epileptic, and cognitive problems of birth injury. The fallacy of this assumption is highlighted both by the below comments and by the observation that the incidence of cerebral palsy has not changed in term infants over the past few decades, despite the institution of fetal monitoring and more frequent cesarean sections.