Eclampsia continues to be a major cause of maternal morbidity and mortality rates, especially in underdeveloped nations. Our data indicate that eclampsia may represent the end stage of at least two very different pathophysiological pathways: one in which cerebral perfusion is low because of vasospasm and another in which cerebral perfusion is increased because of abnormal autoregulation and a failure of the normal protective mechanisms. Magnesium sulfate has been extensively used in the management and prevention of eclamptic seizures in the United States and has been recently shown to be superior to both diphenylhydantoin and diazepam. We have shown that magnesium sulfate is a potent vasorelaxant and that its action may depend on improving cerebral perfusion. Nimodipine, a calcium channel blocker with selective cerebrovascular effect, is currently under investigation in severe preeclampsia. The data show that it is as effective as magnesium sulfate in preventing eclampsia, with less maternal and fetal side effects. Magnesium sulfate and nimodipine have opposite effects on the estimated cerebral perfusion pressure as determined with the Doppler ultrasound. We speculate that the estimated cerebral perfusion pressure may be used to determine the type of cerebrovascular abnormality and the most appropriate treatment in each individual patient with preeclampsia.