Patterns of neonatal hypoxic–ischemic brain injury

Neonatal hypoxic ischemic brain injuries can manifest in different patterns of involvement depending on the severity and timing of the insult. When considering the perinatal maturation process of the brain and the severity of an insult, it is possible to understand the various manifestations.

Typical patterns relative to timing of insult are as follows, with each condition described in detail in separate articles.

• before 28 weeks
  • hydranencephaly and porencephaly
    • the immature brain is not able to react with gliosis
    • liquefied brain parenchymal defect and enlargement of CSF spaces. Usually without hyperintensities on FLAIR
• 28 to 32 weeks
  • periventricular-intraventricular hemorrhage (PIVH)
    • origin in the subependymal germinal matrix, which is an extremely cellular area that gives rise to neurons and glia during gestation and involutes before term
    • there is a direct relation between prematurity and number of capillaries in this region
    • the hemorrhages are related to perinatal stress and usually the majority occurs after birth within the first week of life
• 32 to 36 weeks (pre or perinatal insult in preterm newborns)
  • partial asphyxia results in periventricular leukomalacia (PVL) and subcortical leukomalacia
    • there is some overlap with PIVH
    • bilateral coagulation necrosis with white matter loss, gliosis, and cavitated lesions adjacent to the external angles of lateral ventricles or diffuse white matter injury and hypomyelination
    • both periventricular and subcortical leukomalacia are a continuous disease spectrum: vascular border zones shift towards the periphery as the brain further matures; for this reason, white matter lesions move from the periventricular to the subcortical zone
  • profound asphyxia results in lesions of thalami, cerebellum, and brainstem
    • in contrast to term newborns, the basal ganglia and cortex are relatively spared due to later myelination compared with the thalami
• term newborn
  • acute profound asphyxia results in lesions in high-oxygen-demand areas, sometimes called the basal ganglia-thalamus pattern
    • ventrolateral thalamus
    • posterior putamen
    • corticospinal tract from perirolandic cortex to posterior limb of internal capsule (including absent posterior limb sign)
  • prolonged partial asphyxia results in lesions of white and grey matter in a watershed distribution, sometimes called a peripheral, parasagittal, or borderzone pattern
    • parieto-occipital and posterior temporal lobes are more often affected than frontal lobes
    • can lead to ulegyria, one of the leading causes of posterior cortex epilepsy