Cerebral blood flow and cranial magnetic resonance imaging in eclampsia and severe preeclampsia.

Objective: To measure cerebral blood flow in women with eclampsia and severe preeclampsia using phase-contrast magnetic resonance imaging (MRI).

Methods: Women with eclampsia and severe preeclampsia were studied and compared with normotensive cohorts. Magnetic resonance imaging studies were performed initially in hypertensive women after seizure treatment or prophylaxis was given. Magnetic resonance imaging flow measurements were made using a phase contrast velocity imaging technique in each middle and posterior cerebral artery. Conventional brain MRI and magnetic resonance angiography of the circle of Willis were performed at the time of flow measurement. Women with preeclampsia and eclampsia served as their own controls and were matched with normotensive cohorts. All of the hypertensive women were studied again 4-5 weeks postpartum. Paired t test analysis and an analysis of variance were performed. Considering a 20% minimum detectable difference in flow, the power was 0.80, 0.92, 0.86, and 0.96 for the left and right middle cerebral arteries and the left and right posterior cerebral arteries, respectively.

Results: All 28 women enrolled were studied initially within 24 hours of delivery or of their most recent seizure. There were no significant differences in blood flow in either the posterior or middle cerebral arteries in women with eclampsia or severe preeclampsia between the initial studies and those 4-5 weeks postpartum, or compared with their normal counterparts. No findings of vasospasm were seen. T2-weighted brain images were markedly abnormal in all eight women with eclampsia, mildly abnormal in two of ten with severe preeclampsia, and normal in all ten controls.

Conclusions: No flow changes were seen in the posterior or middle cerebral arteries of women with eclampsia and severe preeclampsia despite the presence of remarkable brain lesions in all women with eclampsia. These findings question the role of vasospasm and cerebral hypoperfusion, although a vasodilatory effect of magnesium could not be excluded.