Cerebrovascular disease in pregnancy and puerperium: perspectives from neuroradiologists

Abstract

Pregnancy-related cerebrovascular disease is a serious complication of pregnancy and puerperium. The etiology and pathological mechanisms of cerebrovascular disease are complex, involving changes in the cardiovascular, endocrine, and immune systems. Vascular risk factors during pregnancy and puerperium may cause vasospasm and endothelial cell damage leading to cerebral ischemia, hemorrhage, posterior reversible encephalopathy syndrome (PRES), and reversible cerebral vasoconstriction syndrome. Arterial or venous obstruction may damage the blood-brain barrier (BBB) and impede venous return, resulting in cerebral edema, hemorrhage, and intracranial hypertension. Pregnancy with hypercoagulability may threaten the lives of both the mother and the developing fetus. With improvements in stroke treatment during pregnancy and puerperium, neuroradiologists have gained new insights into this problem. This article reviews the pathogenesis, imaging findings, and risk factors of stroke during pregnancy and puerperium, focusing on imaging diagnosis and prognostic assessment.

Keywords: Cerebrovascular circulation; imaging; pregnancy; puerperium; stroke.

Figure 1

A 20-year-old woman, 34 weeks pregnant, presenting with headaches, dizziness, and progressive left-side weakness. T2-weighted image (T2WI) reveals areas of hyperintensity in the right basal ganglia and occipital periventricular region (A), with corresponding hyperintensity on diffusion weighted imaging (DWI) (B) and diffusion restriction evident on apparent diffusion coefficient (ADC) map (C) suggestive of acute cerebral infarction in these areas. Magnetic resonance angiography (MRA) (D) shows normal cerebral vessels.

Figure 2

A 25-year-old woman presenting persistent headache and dizziness at 37 weeks gestation. T1-weighted images (T1WI) (A) shows hyperintensities in the right frontal lobe with a hypointense ring around the lesion on sagittal T2-weighted image (T2WI) (B, black arrow), and susceptibility weighted images (SWI) (C) demonstrate susceptibility artifact consistent with chronic hemorrhage. Source image of magnetic resonance angiography (MRA) (D) demonstrates presence of underlying arteriovenous malformation (AVM) (white arrow).

Figure 3

A 28-year-old woman with a history of cardiac insufficiency suddenly developed aphasia and weakness of right limbs 4 days after cesarean section. CT (A) shows a small area of mild high-attenuation in the left basal ganglia with a large area of low-attenuation. Diffusion weighted imaging (DWI) (B) shows slight hypo-intensity in the left basal ganglia and a large hyperintensity area in middle cerebral arteries (MCA) territory suggestive of cerebral infarction. Susceptibility weighted images (SWI) (C) shows marked hypo-intensity consistent with hemorrhage complicating ischemic infarction. Contrast enhanced CT (D) shows low-attenuation thrombosis in the left atrium (black arrow), likely representing the source of infarction from cardiac emboli.

Figure 4

A 25-year-old woman with history of preeclampsia presenting with headaches at 1 week postpartum. Post-contrast T1-weighted images (T1WI) and sagittal reformat maximum intensity projection (MIP) (A,B) show extensive filling defects in the superior sagittal sinus (arrow); diffusion weighted imaging (DWI) (C) and apparent diffusion coefficient (ADC) map (D) demonstrate multiple focal infarcts in the bilateral cerebral cortex. Post-contrast T1WI and reformat MIP (E,F) show thrombus recanalization after active treatment.

Figure 5

A 21-year-old woman with history of eclampsia presenting with headaches and convulsions. CT (A) shows low-attenuation in the subcortical white matter of the bilateral parietal and occipital lobes. Magnetic resonance imaging (MRI) (B,C) show hyperintensities on T2-Fluid-Attenuated Inversion Recovery (FLAIR) and iso-intensity on diffusion weighted imaging (DWI) (D). The lesions resolve after active treatment (D).