PATHOPHYSIOLOGY, TREATMENT AND PROGNOSIS OF CEREBRAL HYPOXIC-ISCHEMICBRAIN-DAMAGE

Generally accepted treatment regimens of hypoxic-ischemic brain damage have not been established so far. Therefore, therapeutic measures are oriented to the pathophysiological mechanisms known at present, inclu ding ischemic calcium cascade, excitotoxicity, NO overformation, and d isturbances of re-circulation (e.g., no reflow phenomenon). Bioelectri c changes in the brain parenchyma evolving during hypoxia-ischemia bec ome successively apparent as hyperpolarization, failure of synaptic tr ansmission, massive depolarization of cells resembling the spreading d epression of Le (a) over cap o, neuronal K+ loss and uptake of large a mounts of Na+, Cl-, Ca++ accompanied by H2O, causing cell swelling. Up to now, the rapid progress of these pathological events has hardly pe rmitted an efficacious treatment. If any therapy, the combination of N MDA receptor antagonists, glucocorticosteroids, GABAergic drugs and he parin could be helpful in preventing the delayed postischemic injury t hat often occurs after initial apparent recovery. The therapeutic role of lazaroids, NO donators, and endothelin antagonists still has to be defined. An early assessment of the brain damage subsequent to hypoxi a-ischemia is possible by means of somatosensory evoked potentials (SS EP) and serum concentration of neuronspecific enolase (NSE), respectiv ely. NSE values exceeding 120 ng/ml during the first 5 days after hypo xia-ischemia point to an unfavorable outcome. In contrast, NSE concent rations below 35 ng/ml mostly indicate a good recovery.