On the Brain in Eclampsia

Abstract

Eclampsia is a syndrome of unknown etiology that is unique to human pregnancy. The pathophysiologic abnormalities of eclampsia have been the subject of extensive investigation and speculation. Reported abnormalities include vasospasm, disturbed hemodynamics, activation of the coagulation system, endothelial cell injury, mitochondria injury, and uteroplacental ischemia (1). Endothelial cell dysfunction or injury plays a central role in its pathogenesis (2). Endothelial cell injury results in altered balance between the release of potent vasoconstricting substances such as endothelin and lack of potent vasodilating substances such as prostacyclin and endothelium-derived relaxing factors. In addition, platelet activation results in abnormal production of vasoconstricting and platelet aggregating agents such as thromboxane A₂ and serotonin. A combination of the above may lead to pathophysiologic ischemic lesions within multiple organ systems including the uteroplacental vascular beds, kidneys, liver, and brain.

The precise etiology of eclamptic convulsions remains an enigma. Reported mechanisms have included vasospasm, hypertensive encephalopathy, cerebral edema, infarction, and hemorrhage (3). Overall, the results of clinical studies and neurodiagnostic findings in eclamptic women suggest that cerebral vasospasm play a central role in the etiology of eclamptic convulsions (4-10).