HYPOXIC-ISCHEMIC BRAIN INJURY IN THE NEONATALPERIOD – CURRENT CONCEPTS, NOVEL DIAGNOSTICAPPROACHES AND NEUROPROTECTIVE STRATEGIES*

Abstract

In the presenting paper, we describe mechanisms of brain injury following a hypoxicischemic event in the neonatal period. Neuronal death occurs in two major phases, theprimary neuronal cell loss at the time of the insult and the delayed neuronal cell loss, occurring about 6 hours – 4 days after the injury. We describe different cellular mechanismsresponsible for the neuronal death. The main patterns of brain injury that can be readilyrecognized with the newer neuroimaging techniques are dependent on the gestationalage of the newborn. In order to apply novel neuroprotective treatments to the newbornswith hypoxic-ischemic encephalopathy (HIE), the newborns at risk have to be identified asearly as possible. Among the most useful diagnostic methods are amplitude-integrated EEG,new markers of brain lesions and different modalities of magnetic-resonance imaging.During resuscitation of neonates with HIE the importance of prevention of hyperoxia,and, during intensive care, of hypocapnia and hyperglycemia is stressed. In the treatmentof newborns with HIE hypothermia, by means of both selective head cooling or whole bodyhypothermia, reduced the risk of death and disability according to three multicenterrandomized controlled studies. It is therefore recommended for treatment of HIE in thenewborn. One of the potentially beneficial effects of therapeutic hypothermia is also widening of the therapeutic window for intervention with other neuroprotective regimens. Amongthese, treatments with erythropoietin or minocycline seem to be clinically promising.