Cerebrovascular (Patho)Physiology in Preeclampsia/Eclampsia

This chapter coorelates neuropathological observations of eclampsia with the noninvasive imaging findings derived from CT scanning and MR imaging. It also correlates cerebrovascular abnormalities induced by preeclampsia–eclampsia and measured with direct and indirect noninvasive methods such as MR technology and Doppler velocimetry. The brain has a central role in the preeclampsia–eclampsia syndrome. There are two general theories to explain cerebral abnormalities associated with eclampsia. Importantly—and as emphasized throughout this edition—endothelial cell dysfunction that characterizes the preeclampsia syndrome may play a key role in both theories. The first theory suggests that in response to acute severe hypertension cerebrovascular overregulation leads to vasospasm. This presumption was based on the angiographic appearance of diffuse or multifocal segmental narrowings suggestive of vasospasm of the cerebral vasculature in women with severe preeclampsia and eclampsia. The second theory is that sudden elevations in systemic blood pressure exceed the normal cerebrovascular autoregulatory capacity. Regions of forced vasodilation and vasoconstriction develop, especially in arterial boundary zones. At the capillary level, disruption of the end-capillary pressure causes increased hydrostatic pressure, hyperperfusion, and extravasation of plasma and red cells through opening of the endothelial tight junctions leading to the accumulation of vasogenic edema.