Cerebrovascular Changes in Hypertensive Pregnancy Disorders

Hypertensive disorders of pregnancy, most notably preeclampsia and its progression to eclampsia, represent a significant cause of maternal morbidity worldwide. These conditions are characterised by systemic endothelial dysfunction that extends to the cerebral vasculature, leading to impaired autoregulation of blood flow, disruption of the blood–brain barrier and an increased risk of cerebral oedema and haemorrhage. Animal models of placental ischemia demonstrate that reduced uteroplacental perfusion impairs myogenic reactivity in cerebral arteries, transmits elevated pressures to the microcirculation and increases permeability of cerebral capillaries. In women, neuroimaging and biomarker studies have revealed alterations in white matter integrity, subtle reductions in cortical volumes and elevated concentrations of neuronal proteins in plasma even before clinical onset. Although gross brain volumes may remain unchanged in the first decades after an affected pregnancy, microstructural changes accumulate over time and correlate with cognitive symptoms in some cohorts. Understanding these cerebrovascular sequelae has global importance for risk stratification, early detection of neurological complications and the development of targeted therapeutic strategies, such as agents that stabilise endothelial function or prevent neuroinflammation.

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Cerebrovascular Changes in Hypertensive Pregnancy Disorders publication trend

The graph below shows the total number of articles in cerebrovascular changes in hypertensive pregnancy disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Cerebral autoregulation: The intrinsic ability of cerebral blood vessels to maintain relatively constant blood flow despite changes in systemic blood pressure.

Blood–brain barrier (BBB): A selective endothelial interface that restricts passage of molecules and cells from the bloodstream into the brain parenchyma.

White matter hyperintensities (WMHs): Areas of increased signal on T2‐weighted MRI reflecting demyelination, gliosis or small‐vessel disease in cerebral white matter.

Cerebral oedema: The accumulation of excess fluid in brain tissue, leading to increased intracranial pressure and potential neuronal injury.

Myogenic reactivity: The inherent contractile response of small arteries and arterioles to changes in intravascular pressure, contributing to vascular tone and autoregulation.

References

1. Cerebral volume is unaffected after pre‐eclampsia. Ultrasound in Obstetrics and Gynecology (2023).
2. Long-term cerebral white and gray matter changes after preeclampsia. Neurology (2017).
3. Placental ischemia in pregnant rats impairs cerebral blood flow autoregulation and increases blood–brain barrier permeability. Physiological Reports (2014).
4. Blood-based cerebral biomarkers in preeclampsia: Plasma concentrations of NfL, tau, S100B and NSE during pregnancy in women who later develop preeclampsia - A nested case control study. PLOS ONE (2018).
5. Cerebral Blood Flow Regulation in Pregnancy, Hypertension, and Hypertensive Disorders of Pregnancy. Brain Sciences (2019).