Although the perinatal brain is more resistant towards hypoxia-ischemia than at any later stage of development, perinatal asphyxia still contributes to permanent brain damage in survivors. This short review focuses on the discussion of mechanisms of late neuronal death, i.e. cerebral damage related to lack of oxygen but caused by mechanisms during the stage of reoxygenation. Evidence is presented to indicate that the transient, dense glutamatergic innervation of basal structures of the perinatal brain may induce brain damage via overflow of excitatory amino acids during oxygen lack, causing a longstanding overstimulation of excitatory neurons. Oxygen derived free radicals may be generated during reoxygenation by several mechanisms, including the oxidation of hypoxanthine and arachidonic acid accumulated in the cerebral insterstitium during hypoxia. The increase of the intracellular concentration of free Ca-ions contributes to these events. Possible avenues for prevention of post-asphyxial brain damage include glutamate receptor antagonists, calcium antagonists, antioxidants, free radical scavengers, inhibitors of libid peroxidation and blockers of arachidonic acid metabolism.