Cerebral infarcts, edema, hypoperfusion and vasospasm in preeclampsia and eclampsia.

Abstract

Background: Eclampsia, a serious pregnancy complication, is associated with cerebral edema and infarctions but the underlying pathophysiology remains largely unexplored.

Objectives: To assess the pathophysiology of eclampsia using specialized magnetic resonance imaging that measures diffusion, perfusion, and vasospasm.

Study design: This was a cross-sectional study recruiting consecutive pregnant women between April 2018 to November 2021 at Tygerberg Hospital, Cape Town, South Africa. We recruited women with eclampsia, preeclampsia, and normotensive pregnancies who underwent magnetic resonance imaging after birth. Main outcome measures were cerebral infarcts, edema, and perfusion using intravoxel incoherent motion imaging and vasospasm using magnetic resonance imaging angiography. The imaging protocol was established before inclusion.

Results: Forty-nine women with eclampsia, 20 with preeclampsia and 10 normotensive women were included. Cerebral infarcts were identified in 34% of eclamptic, 5% of preeclamptic (risk difference (RD) 0.29; 95% confidence interval (CI) 0.06 to 0.52, p=0.012) and in no normotensive controls. Eclamptic women were more likely to have vasogenic cerebral edema compared to preeclamptic (80% vs 20%, RD 0.60; CI 0.34 to 0.85, p<.001) and normotensive women (RD 0.80; CI 0.47 to 1.00, p<.001). Diffusion was increased in eclampsia in the parietooccipital white matter (mean difference (MD) 0.02 x10^-3 mm²/s, CI 0.00 to 0.05, p=0.045) and the caudate nucleus (MD 0.02 x10^-3 mm²/s, CI 0.00 to 0.04, p=0.033) when compared to preeclamptic women. Diffusion was also increased in eclamptic women in the frontal (MD 0.07 x10^-3 mm²/s, CI 0.02 to 0.12, p=0.012) and parietooccipital white matter (MD 0.05 x10^-3 mm²/s, CI 0.02 to 0.07, p=0.03) and the caudate nucleus (MD 0.04 x10^-3 mm²/s, CI 0.00 to 0.07, p=0.028) when compared to normotensive women. Perfusion was decreased in edematous regions. Hypoperfusion was present in the caudate nucleus in eclampsia (MD -0.17 x10^-3 mm²/s, CI -0.27 to -0.06, p=0.003) when compared to preeclampsia. There were no signs of hyperperfusion. Vasospasm was present in 18% of eclamptic, 6% of preeclamptic and none of the controls.

Conclusions: Eclampsia is associated with cerebral infarcts, vasogenic cerebral edema, vasospasm and decreased perfusion, all not usually evident on standard clinical imaging. This may explain why some have cerebral symptoms and signs despite having normal conventional imaging.