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Treatment of vasospasm due to subarachnoid hemorrhage with calcium entry blockers
Cerebral vasospasm is the most important factor causing neurological deterioration later than 72 h after subarachnoid hemorrhage (SAH). The few clinical studies investigating the effect of calcium entry blockers on SAH demonstrate that patients treated with nimodipine have a better clinical outcome. The experimental data do not explain the mechanism of the observed clinical effect. Nimodipine does not reverse large vessel spasm, but it seems that it dilates microvessels and that it exerts a protective effect on nervous tissue by influencing metabolic processes not yet known.
Cerebral vasospasm is the most important factor causing neurological deterioration later than 72 h after subarachnoid hemorrhage (SAH). The few clinical studies investigating the effect of calcium entry blockers on SAH demonstrate that patients treated with nimodipine have a better clinical outcome. The experimental data do not explain the mechanism of the observed clinical effect. Nimodipine does not reverse large vessel spasm, but it seems that it dilates microvessels and that it exerts a protective effect on nervous tissue by influencing metabolic processes not yet known.