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Assessing Cerebral Autoregulation via Oscillatory Lower Body Negative Pressure and Projection Pursuit Regression
Published on: December 10, 2014
Cerebral autoregulation in normal pregnancy, preeclampsia, and 1-year postpartum
Niclas Carlberg1,2, Katja Junus3,4, Anna-Karin Wikström3,4
1Department of Anesthesiology and Intensive Care Medicine Sahlgrenska University Hospital Östra Gothenburg Sweden.
Introduction:
Cerebral complications of preeclampsia pose a significant threat to pregnant women worldwide. The underlying pathophysiology is unclear, but impaired cerebral autoregulation may contribute to adverse maternal outcomes. Long-term consequences of preeclampsia include cerebrovascular disease, and impairment of cerebral autoregulation could contribute to these outcomes. The aim of this study was to assess cerebral autoregulation in women with preeclampsia and normotensive pregnancies during pregnancy and 1-year postpartum to quantify impairment during disease and evaluate its persistence or recovery over time.
Methods:
This multicenter, prospective, observational cohort study included women from the UPMOST or GoPROVE studies. Women with preeclampsia were examined at diagnosis. Participants underwent transcranial Doppler examinations at inclusion and 1-year postpartum. Women were categorized as having normotensive pregnancies or preeclampsia with or without maternal complications. Cerebral autoregulation was assessed by the autoregulation index (ARI). Differences in mean ARI between and within groups were analyzed using regression models for repeated measures.
Results:
A total of 124 women were included in the analysis. During pregnancy, mean ARI was higher in normotensive pregnancies compared with preeclampsia (6.90 [SD, 0.77] vs. 6.12 [SD, 1.45]; mean difference 0.78 [95% CI, 0.37-1.19]), but no difference was observed 1-year postpartum (6.11 [SD, 1.14] vs. 6.15 [SD, 1.10]; mean difference -0.03 [95% CI, -0.47 to 0.54]). Mean ARI did not differ between preeclampsia with or without severe features, either during pregnancy (6.24 [SD, 1.49] vs. 5.98 [SD, 1.40]; mean difference 0.27 [95% CI, -0.43 to 0.96]), or 1-year postpartum (6.13 [SD, 1.23] vs. 6.18 [SD, 0.94]; mean difference -0.05 [95% CI, -0.64 to 0.54]).
Conclusion:
Preeclampsia impairs the autoregulatory advantage offered by pregnancy. This renders the maternal brain more vulnerable to neurovascular injury. This impairment appears to resolve by 1-year postpartum, suggesting that persistently depressed cerebral autoregulation is unlikely to account for long-term cerebrovascular consequences of preeclampsia.
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