Abstract
Hypoxic-ischemic brain injury is a very important neurological problem of the perinatal period. This importance of hypoxic-ischemic brain injury relates to the general gravity of the lesions and to the relatively large number of affected infants. In this chapter, we review the neuropathology and pathogenesis of neonatal hypoxic-ischemic encephalopathy. The major neuropathological varieties include selective neuronal necrosis, which is the necrosis of neurons in a characteristic, often widespread distribution; it is very unusual to observe this in isolation. The topography of the neuronal injury depends in part on the severity and temporal characteristics of the insult and on the gestational age of the infant. Basic patterns observed best in term infants are diffuse neuronal injury, cerebrocortical–deep nuclear neuronal necrosis, pontosubicular neuronal injury, and cerebellar injury. Parasagittal cerebral injury is a lesion of the cerebral cortex and subcortical white matter with a distribution comprising parasagittal and superomedial aspects of the cerebral convexities; it is characteristic of the full-term infant with perinatal asphyxia. The predominant lesion in infants with hypoxic-ischemic encephalopathy may involve primarily cerebral white matter. Approximately 15% of infants exhibit this pattern of injury as the dominant abnormality. The similarities with periventricular leukomalacia of very premature infants are apparent. Important contributing pathogenetic factors in infants with hypoxic-ischemic encephalopathy are late preterm gestational age, neonatal hypoglycemia, and often chronic hemodynamic instability. The majority of term infants with congenital heart disease dying days after cardiac surgery exhibit at autopsy periventricular leukomalacia as a prominent lesion. Involvement of cerebral white matter is also the dominant neuroimaging feature of infants with complex congenital heart disease both before and after cardiac surgery.
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