ArticleNeuroradiology2026
Multimodal MRI assessment of cerebral small vessel disease-related brain injury in the context of unilateral severe carotid artery stenosis.
Article in Neuroradiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
purposeTo investigate the transhemispheric effects of unilateral severe carotid artery stenosis (CAS) on brain structure and hemodynamics, and their association with cerebral small vessel disease (CSVD) markers.
methodsFifty-one patients with unilateral severe CAS and 48 matched healthy controls underwent multimodal MRI. Quantified metrics included cortical thickness, white matter hyperintensity (WMH) volume, free water fraction in white matter (FW-WM), peak width of skeletonized mean diffusivity (PSMD), and lateralization index for cerebral blood flow (LI-CBF). Group comparisons, interhemispheric comparisons, partial correlation analyses, and multivariable linear regression models were performed.
resultsCompared with controls, CAS patients exhibited reduced cortical thickness (2.32 ± 0.08 vs. 2.36 ± 0.08 mm, P = 0.015), elevated PSMD (median 2.56 × 10⁻⁴ vs. 2.35 × 10⁻⁴, P = 0.006), increased WMH volume (median 4.65 vs. 2.37 cm³, P < 0.001), higher FW-WM (0.21 ± 0.03 vs. 0.17 ± 0.02, P < 0.001), and pronounced CBF lateralization (P < 0.001). Ipsilateral FW-WM was significantly higher than contralateral FW-WM (P < 0.001). Both FW-WM (β'=0.347, P = 0.019) and PSMD (β'=0.426, P = 0.002) were independently associated with global WMH volume. Age and anterior cerebral artery LI-CBF independently predicted FW-WM and PSMD. Ipsilateral WMH volume (β'=-0.264, P = 0.044) and age (β'=-0.371, P = 0.005) were independently associated with MoCA scores.
conclusionUnilateral severe CAS induces structural and hemodynamic alterations overlapping with CSVD features. Hemodynamic disturbance is associated with diffuse white matter injury, which may contribute to WMH formation. Multimodal MRI metrics provide imaging evidence linking macrovascular stenosis to CSVD.
Indexed as
Identifiers
42429942What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.