ArticleNeuroimage. Reports2025
MRI signatures associated with active ischemia and disease severity in cerebral small vessel disease.
Article in Neuroimage. Reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: Cerebral small vessel disease, a leading cause of stroke and cognitive impairment, manifests on neuroimaging with white matter hyperintensities (WMH) and disrupted microstructure in normal-appearing white matter. WMH, by definition have high T2 FLAIR signal; however, both T2 FLAIR and T1 signal in WMH are highly variable. We hypothesized that signal intensity parameters would differ in cerebral small vessel disease compared to healthy controls and that signal heterogeneity would be associated with more severe ischemia. Methods: In this case-control cross-sectional study, participants with cerebral small vessel disease (n = 27) and controls (n = 35) underwent T1-weighted and T2 FLAIR MRI for signal intensity quantification as well as pseudocontinuous arterial spin labeling and asymmetric spin echo to measure cerebral blood flow, and oxygen extraction fraction, respectively, and diffusion tensor imaging to assess white matter microstructure. Following signal intensity normalization, we quantified white matter T1 and T2 FLAIR mean and heterogeneity and correlated them to biomarkers of disease severity and physiology (cerebral blood flow and oxygen extraction fraction) in order to understand how signal variability relates to tissue hypoxia-ischemia. Results: The cerebral small vessel disease group had increased T2 FLAIR intensity ( Interpretation: In conclusion, we found evidence that T1 and T2 FLAIR signal is heterogeneous in cerebral small vessel disease and is associated with disease severity. Within WMH, focal T1 hypointensity and variability, as well as T2 FLAIR hyperintensity and variability is associated with ischemia, but not infarction, particularly in larger lesions, suggesting that these patterns of MRI signal follow both disease severity and aberrant physiology. Finally, WMH clustered by structural properties align with specific physiologic patterns suggesting that imaging appearance may reveal underlying ischemic vulnerability. Although these data are exploratory, they suggest that certain categories of WMH with highly ischemic but non-infarcted physiology may represent high-risk tissue that is reversibly injured. Future work will investigate the role these imaging parameters have on clinically relevant outcomes such as incident stroke and cognitive impairment.
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