The pathogenesis of eclamptic convulsions remains unknown. Cerebral imaging suggests that cerebral abnormalities in eclampsia (mostly vasogenic edema) are similar to those found in hypertensive encephalopathy. However, cerebral imaging is not necessary for the diagnosis or management of most women with eclampsia. The onset of eclamptic convulsions can be antepartum (38–53%), intrapartum (18–36%), or postpartum (11–44%). Recent data reveal an increase in the proportion of women who develop eclampsia beyond 48 hours after delivery. Other than early detection of preeclampsia, there are no reliable tests or symptoms for predicting the development of eclampsia. In developed countries, the majority of cases reported in recent series are considered unpreventable. Magnesium sulfate is the drug of choice for reducing the rate of eclampsia developing intrapartum and immediately postpartum. There are 4 large randomized trials comparing magnesium sulfate with no treatment or placebo in patients with severe preeclampsia. The rate of eclampsia was significantly lower in those assigned to magnesium sulfate (0.6% versus 2.0%, relative risk 0.39, 95% confidence interval 0.28–0.55). Thus, the number of women needed to treat to prevent one case of eclampsia is 71. Magnesium sulfate is the drug of choice to prevent recurrent convulsions in eclampsia. The development of eclampsia is associated with increased risk of adverse outcome for both mother and fetus, particularly in the developing nations. Pregnancies complicated by eclampsia require a well-formulated management plan. Women with a history of eclampsia are at increased risk of eclampsia (1–2%) and preeclampsia (22–35%) in subsequent pregnancies. Recommendations for diagnosis, prevention, management, and counseling of these women are provided based on results of recent studies and my own clinical experience.