| Background: White matter hyperintensities(WMH) and lacunar infarction are main MRI expressions of SVD; both are frequently observed in elderly subjects. WMH predict incident strokes and new lacunes, moreover, WMH may also affect infarct locations which may be associated with penumbra on the edge of WMH. Our aim was to examine spatial relationship between WMH and acute lacunar infarction.Methods: 590 patients with acute lacunar infarction in supratentorial region admitted to Beijing Chaoyang Hospital affiliated to Capital Medical University were included.Four situations between infarction and WMH were assessed by axial and coronal MRI: no contact(Grade 0), contact without overlap(Grade Ia), partial overlap(Grade Ib), and complete overlap(Grade II) with pre-existing WMH. Furthermore, we defined infarctions in Grade Ia and Ib as edge-localized infarctions and investigated their predictors and short term outcome.Results: 47.9%(283) of the infarctions were edge-localized infarctions(Grade Ia =27.6% and Grade Ib =20.3%), 51.5%(304) were Grade 0, only 0.5%(3) were Grade II. Patients with edge-localized infarction had larger infarct size( axial DWI :12.81±3.47 mm vs 11.45±3.22 mm, p=0.000; coronal FLAIR : 13.69±3.58 mm vs12.71±3.58 mm, p=0.001), more severe WMH(deep and periventricular WMH),higher NIHSS and lower barthel index score at admission than those with non-edge-localized infarction. They also had higher NIHSS and lower barthel index score at discharge. Infarction in subcortical white matter(OR=31.15; 95% CI14.13–68.69), DWI infarct size(OR=1.19; 95% CI 1.11–1.27), periventricular WMH(OR=1.42; 95% CI 1.05–1.91) and deep WMH(OR=1.95; 95% CI1.44–2.63) were predictors for edge-localized infarction.Conclusions: About half of lacunar infarctions were located to the edge of WMH.Both periventricular WMH and deep WMH were predictors for edge-localized infarction which indicates that WMH may have effect on the location of acute lacunarinfarctions.Background: Penumbra has been detected on the edge of white matter hyperintensities(WMH) which may have impact on imaging evolution of acute lacunar infarct. The aim of our study was to investigate whether cavity formation are different between acute infarcts on the edge of WMH and those out of the edge.Material and Methods: Ninety six subjects with acute lacunar infarct ≤ 25 mm in diameter were recruited. Subjects with infarct contacting or overlapping with WMH(on axial T2 or coronal FLAIR) were defined as edge group(on the edge of WMH).Those outside the edge of WMH were non-edge group. Vascular risk factors, clinical data, baseline infarct size, infarct sites and severity of WMH(by Fazekas scale) were recorded. In MR follow-up imaging, cavity formation was indentified. Risk factors for cavity formation were also investigated.Results: 37(38.5%) subjects were in edge group and 59(61.5%) were in non-edge group. 55(57.3%) subjects had cavity formation in follow-up imaging. Subjects in edge group had higher risk of developing cavities than those in non-edge group(78.4% vs 44.1%, p<0.05). The highest risk of cavity formation was in subcortical white matter(73.33%), followed by the thalamus(53.33%) and infratentorial region(48%), and the lowest risk of cavity formation was in basal ganglia(18.2%).In univariate analysis, subjects with cavity formation had larger infarct size and their infarcts were more often located in subcortical white matter. Vascular risk factors,clinical data and WMH did not differ between subjects with cavity formation and those without. In logistic regression, DWI infarct size(OR=1.13, 95% CI 1.01–1.25)and edge group(OR=4.30, 95% CI 1.65–11.19) were independent risk factors for cavity formation.Conclusions: Lacunar infarcts on the edge of WMH are more likely to develop cavities suggesting that WMH penumbra has impact on cavity formation.Backgrounds: Enlarged perivascular spaces(EPVS) correlate with cognitive impairment and incident dementia. However, basal ganglia EPVS(BG-EPVS)presents with heterogeneity and etiologies for severe BG-EPVS are still unclear. Our aim was to investigate the independent risk factors for severe BG-EPVS in patients with acute lacunar stroke.Methods: We prospectively identified patients with lacunar stroke(diameter on DWI< 20mm) from Jan 2011 to May 2015. Patients with severe BG-EPVS were identified on T2 weighted MRI. Age(+ 1 year) and sex matched controls were also recruited in the same population(two controls for one case). Vascular risk factors, clinical data,EPVS in centrum semiovale(rated 0 to 4), white matter hyperintensities(WMH)(by Fazekas scale), brain atrophy(rated 0 to 6) were compared between two groups.Logistic regression was performed to determine independent risk factors for severe BG-EPVS.Results: During study period, 89 patients with severe BG-EPVS and 178 matched controls were included. Vascular risk factors did not differ between two groups.Patients with severe BG-EPVS had lower level of Hb A1c(median: 6.0% vs 6.1%, p <0.05) and higher diastolic BP(86.20 + 13.03 mm Hg vs 82.61 + 11.35 mm Hg, p <0.05) at admission, but presented with larger infarct size(median: 12.18 mm vs 10.07 mm, p < 0.05), more severe WMH(including total WMH, periventricular WMH and deep WMH) and brain atrophy. In logistic regression, brain atrophy(OR=1.40;95%CI 1.13, 1.73) and deep WMH(OR=1.88; 95%CI 1.24, 2.83) were independent risk factors for severe BG-EPVS.Conclusions: Brain atrophy and deep WMH are independent risk factors for severe BG-EPVS, supporting the hypothesis that brain atrophy may be associated with the development of EPVS in basal ganglia. |
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