Patterns of neonatal hypoxic–ischemic brain injury

Neonatal hypoxic ischaemic brain injuries can developmanifest in different lesion patterns patterns. Considering the perinatal maturation process of the brain and the severity of an insult it is possible to understand why of these differencesthe different manifestations.

Further information can be found in a broad discussion in each specific article:

• hydranencephaly and porencephaly
  • generally less than 28 weeks
  • the immature brain is not able to react with gliosis
  • liquefied brain parenchymal defect and enlargement of CSF spaces. Usually without hyperintensities on FLAIR
• periventricular-intraventricular haemorrhage (PIVH)
  • usually occurs between 28 and 32 weeks
  • origin in the subependymal germinal matrix, which is a highly cellular area that gives rise to neurons and glia during gestation and involutes before term 
  • there are a direct relation between prematurity and number of capillaries in this region
  • the haemorrhages are related to perinatal stress and usually the majority occurs after birth within the first week of life
• periventricular leukomalacia (PVL) and subcortical leukomalacia
  • usually between 32 and 36 weeks (pre or perinatal insult in preterm newborns)
  • 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
• hypoxic-ischaemic encephalopathy of the term newborn
  • profound asphyxia: multicystic encephalomalacia
  • less profound asphyxia: lesions in high oxygen demand areas such as the deep grey matter
  • ulegyria 
    •  one of the major causes of posterior cortex epilepsy ⁵