Update on perinatal hypoxic insult: mechanism, diagnosis and interventions

Cerebral hypoxia-ischaemia in the neonate can produce irreversible tissue injury and is always associated with major perturbations in the energy status of the brain. The major neurological manifestations of brain injury in these babies are spastic motor deficits. Different pathogenetic mechanisms may underlie hypoxic-ischaemic injury of the brain such as decreased blood flow autoregulation, altered cerebral metabolism, thrombosis, haemorrhage, accumulation of toxic metabolites such as glutamate, impaired intracellular calcium turnover, release of interleukins and prostaglandins, iron accumulation and overproduction of free-radicals. In summary, hypoxia-ischaemia in neonates triggers a cascade of biological processes culminating in cell death. Important advances in the assessment of cerebral injuries in neonates have been made in the area of neuroimaging, especially in magnetic resonance imaging which may provide useful prognostic information when obtained in the course of brain injury. Future studies may focus on new therapeutic pharmacological and non-pharmacological strategies aimed at the reversal of the pathophysiological mechanisms activated by perinatal hypoxia-ischaemia.