PATHOPHYSIOLOGY, TREATMENT AND PROGNOSIS OF CEREBRAL HYPOXIC-ISCHEMIC BRAIN-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, including ischemic calcium cascade, excitotoxicity, NO overformation, and disturbances of re-circulation (e.g., no reflow phenomenon). Bioelectric changes in the brain parenchyma evolving during hypoxia-ischemia become successively apparent as hyperpolarization, failure of synaptic transmission, massive depolarization of cells resembling the spreading depression of Le (a) over cap o, neuronal K+ loss and uptake of large amounts of Na+, Cl-, Ca++ accompanied by H2O, causing cell swelling. Up to now, the rapid progress of these pathological events has hardly permitted an efficacious treatment. If any therapy, the combination of NMDA receptor antagonists, glucocorticosteroids, GABAergic drugs and heparin could be helpful in preventing the delayed postischemic injury that 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 hypoxia-ischemia is possible by means of somatosensory evoked potentials (SSEP) and serum concentration of neuronspecific enolase (NSE), respectively. NSE values exceeding 120 ng/ml during the first 5 days after hypoxia-ischemia point to an unfavorable outcome. In contrast, NSE concentrations below 35 ng/ml mostly indicate a good recovery.