Seizures associated with eclampsia

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
C P Panayiotopoulos MD PhD, editor. (

Dr. Panayiotopoulos of St. Thomas' Hospital had no relevant financial relationships to disclose.

Originally released September 22, 2005; last updated March 27, 2020; expires March 27, 2023

This article includes discussion of seizures associated with eclampsia, eclamptic amaurosis, eclamptic encephalopathy, eclamptogenic toxemia, peripartum seizures, postpartum eclampsia, and toxemia of pregnancy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Preeclampsia or eclampsia is a multisystem disorder of pregnancy and the puerperium. Eclampsia is defined as the occurrence of generalized seizures in a woman with preexisting preeclampsia. Approximately 10% to 15% of maternal deaths are associated with preeclampsia and eclampsia. Although the incidence of eclampsia and its complications have decreased significantly in developed countries, the incidence is still high in poor countries. Eclampsia occurring more than 48 hours, but less than 4 weeks, after delivery is known as late postpartum eclampsia. Postpartum preeclampsia or eclampsia may present without a history of preeclampsia during the pregnancy. Visual disturbances, epigastric pain, headache, and edema are 4 of the most frequent symptoms that can predict imminent eclampsia in ladies with preeclampsia. In eclampsia, reversible posterior leukoencephalopathy syndrome is an increasingly recognized cause of seizures, cortical blindness, and encephalopathy. In addition to posterior leukoencephalopathy syndrome, neuroimaging may reveal cerebral edema, infarction, cerebral venous thrombosis, and cerebral hemorrhage. Magnesium sulfate is the treatment of choice for the control of recurrent eclamptic seizures in pregnant women. In a study, a low-dose regimen of magnesium sulfate appeared comparable to the “standard” dose regimen. The American College of Obstetricians and Gynecologists and the Society for Maternal-Fetal Medicine recommends only short-term (usually less than 48 hours) use of magnesium sulfate. Early combined treatment of critically raised blood pressure with intravenous antihypertensive drugs and magnesium sulfate is associated with a reduction in frequency of eclampsia and severe maternal morbidity. The long-term risk of seizures in an eclamptic patient is low. In this article, the author reviews the clinical features, epidemiology, pathophysiology, differential diagnosis, complications, and principles of treatment.

Key points


• Preeclampsia is a multisystem disorder occurring after the 20th week of gestation that is characterized by hypertension, proteinuria, and pathologic edema.


• Eclampsia is defined as the occurrence of generalized seizures in a woman with preexisting preeclampsia.


• The onset of eclamptic convulsions can be antepartum, intrapartum, postpartum, or late postpartum (48 hours after delivery).


MRI of brain reveals bilateral, symmetrical, reversible hypodense lesions in the white matter of parietooccipital regions of brain.


• Magnesium sulphate is considered the treatment of choice.


• Reduction in eclampsia can be achieved by good prenatal care, early detection of preeclampsia, and prophylactic use of magnesium sulfate in preeclampsia.

Historical note and terminology

Ancient accounts of eclampsia and childbirth are available in medical writings of Egyptian, Indian, Chinese, and Greek civilizations. The term “eclampsia” was used by ancient Greeks. Prior to the 18th century, the term “eclampsia” was used to refer to the visual phenomenon associated with this disorder. Mauriceau, a noted French obstetrician, in 1673 gave a detailed description of the subject in his book, and he believed that eclampsia improved after delivery (Chesley 1984; Kaplan 2004). The view that salt plays a crucial role in eclampsia was given by De Snoo (1877-1949), a Dutch obstetrician. In 1840, PF Rayer, a French pathologist, for the first time noted proteinuria in pregnant women. However, the discovery of proteinuria in eclampsia was made by LC Lever of London and JY Simpson of Scotland in 1843. Lever recommended periodic testing of urine for proteinuria in pregnancy. Georg Schmorl, in 1893, first demonstrated the presence of fetal cells in the maternal body and emphasized the importance of the placenta in eclampsia (Lapaire et al 2007). Until the middle of the 19th century, treatment of eclampsia was mostly by physical methods and expediting the delivery. Physical methods were bleeding by venesection, blistering, immersion in hot water, and hot compress in kidney regions. Bleeding was considered an important procedure to get rid of toxins, and a large amount of blood used to be let out. Opening of temporal artery had been advocated for bloodletting. By the end of the 19th century, bloodletting for eclampsia had generally been abandoned, replaced chiefly by expeditious delivery as the treatment of choice. Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulfate as an anticonvulsant in humans. As early as 1906, magnesium sulfate was injected intrathecally to prevent eclamptic seizures. Because of reports that intramuscular magnesium sulfate–controlled convulsions associated with tetanus, a similar regimen was used by Lazard and Dorsett in 1926 to prevent recurrent seizures in women with eclampsia. In 1933, the drug was given intravenously to hundreds of women with preeclampsia and eclampsia at the Los Angeles General Hospital (Chesley 1984; Purkerson and Vekerdy 1999).

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