"The pattern of cerebral damage that results from perinatal/neonatal hypoxic-ischaemia depends on both gestational age (preterm or term) as well as the degree of insult (acute profound versus sustained partial asphyxia) 4. See patterns of neonatal hypoxic–ischaemic brain injury."
"In general, pre-term infants with sustained partial asphyxia generally develop periventricular leukomalacia 4. Term infants with sustained partial asphyxia generally develop border zone ischaemia typically between the territories of the posterior cerebral artery and middle cerebral artery, commonly resulting in ulegyria 4. In contrast, term infants with profound asphyxia typically develop infarcts of the basal ganglia and areas of the cerebral cortex (e.g. precentral and postcentral gyri) 4."
"The exact nature of the injury depends on the severity of hypotension and the degree of brain maturation. In general, the myelinated areas are more metabolically active and express more glutamate receptors (NMDA receptors), which make them more vulnerable to HIE due to excitotoxicity."
"In term infants blood flow is ventriculofugal and changes are mainly, like in older children, in watershed-border zones; namely, parasagittal grey matter and subcortical white matter. Profound HIE in term babies results in thalamic and basal ganglia as well as sensorimotor cortex (perirolandic region) injury."
"Studies estimate a short therapeutic window of 2-6 hours during which interventions may be efficacious in reducing the severity of ultimate brain injury; thus, early identification of a neonate who has sustained a hypoxic-ischaemic insult is a paramount objective for optimal management and treatment."