Background and Purpose-Lacunar stroke is associated with endothelial dysfunction and histologically with intrinsic cerebral microvascular disease of unknown cause. Endothelial dysfunction could impair blood-brain barrier integrity.We assessed background blood-brain barrier leakage in patients with lacunar ischemic stroke compared with cortical stroke controls. Methods-We recruited patients with lacunar or mild cortical ischemic stroke and assessed generalized cerebral blood-brain barrier leak with MRI and intravenous gadolinium at least 1 month after stroke. We used detailed image processing to compare signal change before and for 30 minutes postcontrast throughout gray matter, white matter, and cerebrospinal fluid with summary analyses and general linear modeling. Results-Among 48 patients (29 lacunar, 19 cortical), postcontrast enhancement was significantly higher in cerebrospinal fluid (Pϭ0.04, Mann-Whitney U), and nonsignificantly higher in white matter, in lacunar than in cortical strokes, with no difference in gray matter. General linear modeling confirmed significantly greater postcontrast enhancement in cerebrospinal fluid in lacunar patients than in cortical controls (tϭ3.37, PϽ0.0008). Conclusion-These preliminary data suggest that the blood-brain barrier may be dysfunctional throughout subcortical white matter (white matter drains via interstitial spaces to cerebrospinal fluid) in patients with lacunar stroke. Further studies are required to confirm these findings and determine whether abnormal blood-brain barrier might predate development of lacunar disease. Blood-brain barrier dysfunction may be an important mechanism for brain damage in cerebral microvascular disease.
Aim: Early infarct signs predict symptomatic intracranial haemorrhage (SICH) and poor outcome after stroke. Structural brain features increase with age. It is unclear if, or when, any of these imaging signs should influence decisions to use rt-PA. We assessed imaging, SICH, 6-month outcome and rt-PA effects in 3035 patients randomised in IST-3. Methods: IST-3 was a randomised trial of iv rt-PA (0.9mg/kg) <6 hours of ischaemic stroke ( ISRCTN25765518 ). All pre- and post-randomisation imaging was read centrally, masked, by international experts for early infarct signs (tissue hypodensity site/size, swelling, hyperdense artery) and structural brain changes (atrophy, leukoaraiosis, prior infarct) using validated scales. We tested associations between pre-treatment imaging, SICH, 6-month outcome and rt-PA effects, adjusted for time, NIHSS, age, with logistic regression. Results: Of 3035 patients, (1515 rt-PA, 1520 control; baseline imaging CT 2848, 98%, MR 54, 2%), 1616 aged >80; 851 treated <3hr, 1177 3-4.5 and 1007 4.5-6hr; 40% had tissue hypodensity/swelling (ASPECTS <7 in 25%, 8-10 in 75%); 24% had hyperdense artery; 50% had leukoaraiosis, atrophy or prior infarct; 9% were totally normal. On adjusted analyses, no imaging feature alone modified rt-PA effects. SICH increased with prior infarct (OR 1.66, p=0.009), tissue hypodensity (1.51, p=0.04), hyperdense artery (1.51, p=0.04). 6-month independent survival decreased with hypodensity (0.66, p=0.000), swelling (0.59, p=0.000), hyperdense artery (0.59, p=0.000), leukoaraiosis (0.72, p=0.0008) and atrophy (0.74, p=0.01). On elimination modelling, prior infarct predicted 54% of SICH risk; swelling, hyperdense artery, leukoaraiosis each predicted 33% of poor outcome risk. Conclusion: Amongst these 3035 patients, neither structural nor early ischaemic imaging features alone modify rt-PA effects, but can inform rt-PA treatment decisions where benefits are likely to be marginal by predicting risk of rt-PA-associated SICH and poor functional outcome. The results are also relevant to older as well as younger patients and to rt-PA given <3 as well as up to 6 hours after stroke.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.