Abstract

Data from animal stroke models looked promising with regard to neuroprotection for human stroke, but results from clinical trials so far have been disappointing. Various issues that may explain discrepancies between experimental results and clinical neuroprotection trials are discussed. Furthermore, clinical trial methods may not have been optimal to detect small but clinically relevant improvement in patient outcome. Therefore, trial methods should be improved. Besides, alternative strategies to identify potentially neuroprotective drugs in stroke may be explored, whereas testing of optimizing early glucose levels, regulation of blood pressure, and lowering of body temperature should be put to clinical testing. The concept of neuroprotection in human stroke remains valid, but needs a more rational exploration in the future.

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