Is High Cerebral Perfusion Pressure and Cerebral Flow Predictive of Impending Seizures in Preeclampsia? A Case Report

Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of Utah, Salt Lake City 84132, USA.
Hypertension in Pregnancy (Impact Factor: 1.41). 02/2005; 24(1):59-63. DOI: 10.1081/PRG-45776
Source: PubMed


Transcranial Doppler ultrasound was used to demonstrate elevated estimated cerebral perfusion pressure (CPP) and cerebral flow index (CFI) in a preeclamptic patient. She subsequently developed eclampsia. After magnesium sulfate therapy her CPP and CFI were within the normal range and she did not experience further seizures. This finding suggests that cerebral overperfusion may be at least one of the etiologies involved in the pathogenesis of eclampsia.

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    ABSTRACT: The objective of the study was to evaluate neurocognitive function in preeclampsia and normal pregnancy. Three groups (each n = 15) were studied before and after delivery using standard neurocognitive test techniques. Group A consisted of normal laboring patients; group B, preeclamptics receiving magnesium; and group C, women in preterm labor receiving MgSO4 tocolysis (Mg control). The tests, examining attention, working memory, explicit memory, auditory comprehension, and measures for emotional distress, pain, and fatigue were analyzed via 4-way multivariate analysis of variance and multiple t tests. Preeclamptics receiving MgSO4 had better attention and working memory (P = .05), compared with normal laboring women and the preterm patients. Explicit memory was impaired in all groups, and this could not be accounted for by pain or emotional distress. We could detect no cognitive defects in preeclamptics, compared with normotensive gravidas, at least while the cerebral vasodilator MgSO4 is being infused.
    No preview · Article · Aug 2006 · American journal of obstetrics and gynecology
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    ABSTRACT: Thesis (Ph. D. )--University of Vermont, 2007. Includes bibliographical references (leaves 191-240).
    Preview · Article · Jan 2007
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    ABSTRACT: Eclampsia is considered a form of hypertensive encephalopathy in which an acute elevation in blood pressure causes autoregulatory breakthrough, blood-brain barrier disruption, and edema formation. We hypothesized that pregnancy predisposes the brain to eclampsia by lowering the pressure of autoregulatory breakthrough and enhancing cerebral edema formation. Because NO production is increased in pregnancy, we also investigated the role of NO in modulating autoregulation. Cerebral blood flow autoregulation was determined by phenylephrine infusion and laser Doppler flowmetry. Four groups were studied: untreated nonpregnant (n=7) and late-pregnant (days 19 to 21; n=8) Sprague-Dawley rats and nonpregnant (n=8) and late-pregnant (n=8) animals treated with an NO synthase inhibitor (N(G)-nitro-l-arginine methyl ester; 0.5 to 0.7 g/L). Brain water content and blood-brain barrier permeability to sodium fluorescein were determined after breakthrough. Pregnancy caused no change in autoregulation or the pressure of breakthrough. However, treatment with the NO synthase inhibitor significantly increased the pressure of autoregulatory breakthrough (nonpregnant: 183.6+/-3.0 mm Hg versus 212.0+/-2.8 mm Hg, P<0.05; late-pregnant: 180.8+/-3.2 mm Hg versus 209.3+/-4.7 mm Hg, P<0.05). After autoregulatory breakthrough, only late-pregnant animals showed a significant increase in cerebral edema formation, which was attenuated by NO synthase inhibition. There was no difference in blood-brain barrier permeability between nonpregnant and late-pregnant animals in response to acute hypertension, suggesting that pregnancy may predispose the brain to eclampsia by increasing cerebral edema through increased hydraulic conductivity.
    Preview · Article · Mar 2007 · Hypertension
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