International journal of stroke : official journal of the International Stroke Society · 2026
Contrasting patterns of leptomeningeal and parenchymal gadolinium extravasation in cerebral amyloid angiopathy: An MRI-based evaluation.
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Voigt S, de Jong Jja, Voorter Phm, Koemans E A, Schipper M R, van der Plas M C, Kaushik K, van der Zwet Rgj, van Dort R, van den Brink H, van Veluw S J, van Osch Mjp, van Walderveen Maa, Backes W H, Wermer Mjh, Freeze W M
Аннотация
BACKGROUND: Previous studies suggest that blood-brain barrier (BBB) disruption may play a role in the pathophysiology of vessel rupture in cerebral amyloid angiopathy (CAA). Here, in a cross-sectional cohort study, we apply contrast-enhanced 3 Tesla magnetic resonance imaging (MRI) to test the hypothesis that the BBB is damaged in patients with CAA and to determine whether BBB leakage is associated with hemorrhagic brain injury in CAA.
METHODS: Parenchymal BBB leakage rate (Ki) was assessed in the cortex and white matter with dynamic contrast-enhanced (DCE)-MRI and quantified with pharmacokinetic modeling. Leptomeningeal BBB leakage was assessed visually on post-contrast heavily T2-weighted fluid attenuation inversion recovery (FLAIR) images. Cortical cerebral microbleeds (CMBs) and cortical superficial siderosis (cSS) were assessed on susceptibility-weighted images. Analyses included descriptive statistics, group comparisons using the Mann-Whitney U test and Spearman's rank correlation for associations with imaging markers.
RESULTS: In total, 25 patients with a clinical diagnosis of probable CAA without prior intracerebral hemorrhage and 19 age- and sex-matched controls were included. In patients with CAA, BBB leakage rates were lower in the cortex (4.2 × 10-4 min-1 vs 5.6 × 10-4 min-1; p = 0.004) and in the white matter (1.2 × 10-4 min-1 vs 2.1 × 10-4 min-1; p < 0.001) compared with controls. The presence of leptomeningeal enhancement was higher in patients with CAA (68%) compared with controls (47%) (p = 0.007). Within the group with CAA, we did not find a correlation between the number of cortical leakage and cortical CMBs (Spearman's ρ = 0.06, p = 0.79) or the number of foci of leptomeningeal enhancement and cSS hemisphere score (Spearman's ρ = 0.30, p = 0.15).
DISCUSSION: Our results suggest that global parenchymal gadolinium extravasation across the BBB is lower in patients with CAA compared with controls. This observation can be explained in terms of limited capillary blood perfusion and/or raising the possibility that vascular amyloid-β deposition impairing molecular transport across the BBB. In contrast, focal leptomeningeal enhancement was higher in CAA, reflecting vessel wall infiltration.
METHODS: Parenchymal BBB leakage rate (Ki) was assessed in the cortex and white matter with dynamic contrast-enhanced (DCE)-MRI and quantified with pharmacokinetic modeling. Leptomeningeal BBB leakage was assessed visually on post-contrast heavily T2-weighted fluid attenuation inversion recovery (FLAIR) images. Cortical cerebral microbleeds (CMBs) and cortical superficial siderosis (cSS) were assessed on susceptibility-weighted images. Analyses included descriptive statistics, group comparisons using the Mann-Whitney U test and Spearman's rank correlation for associations with imaging markers.
RESULTS: In total, 25 patients with a clinical diagnosis of probable CAA without prior intracerebral hemorrhage and 19 age- and sex-matched controls were included. In patients with CAA, BBB leakage rates were lower in the cortex (4.2 × 10-4 min-1 vs 5.6 × 10-4 min-1; p = 0.004) and in the white matter (1.2 × 10-4 min-1 vs 2.1 × 10-4 min-1; p < 0.001) compared with controls. The presence of leptomeningeal enhancement was higher in patients with CAA (68%) compared with controls (47%) (p = 0.007). Within the group with CAA, we did not find a correlation between the number of cortical leakage and cortical CMBs (Spearman's ρ = 0.06, p = 0.79) or the number of foci of leptomeningeal enhancement and cSS hemisphere score (Spearman's ρ = 0.30, p = 0.15).
DISCUSSION: Our results suggest that global parenchymal gadolinium extravasation across the BBB is lower in patients with CAA compared with controls. This observation can be explained in terms of limited capillary blood perfusion and/or raising the possibility that vascular amyloid-β deposition impairing molecular transport across the BBB. In contrast, focal leptomeningeal enhancement was higher in CAA, reflecting vessel wall infiltration.