Bo Wu1, Xiaoying Yao1, Chunyan Lei1, Ming Liu1, Magdy H Selim2. 1. From the Center of Cerebrovascular Diseases (B.W., C.L., M.L.), Department of Neurology, West China Hospital, Sichuan University, Chengdu, China; Stroke Division (B.W., X.Y., M.H.S.), Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; and the Department of Neurology (X.Y.), Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, China. 2. From the Center of Cerebrovascular Diseases (B.W., C.L., M.L.), Department of Neurology, West China Hospital, Sichuan University, Chengdu, China; Stroke Division (B.W., X.Y., M.H.S.), Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; and the Department of Neurology (X.Y.), Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, China. mselim@bidmc.harvard.edu.
Abstract
OBJECTIVE: To examine the association between enlarged perivascular spaces (EPVS) and the prevalence and extent of small acute diffusion-weighted imaging (DWI) lesions (SA-DWIL) in patients with spontaneous supratentorial intracerebral hemorrhage (ICH). METHODS: We conducted a retrospective review of a consecutive cohort of 201 patients with spontaneous supratentorial ICH who had brain MRI with DWI within 1 month of ICH onset. We compared the clinical and imaging characteristics, including EPVS, of patients with and without SA-DWIL. We used univariate and multivariate logistic regression analyses to determine the variables associated with SA-DWIL. RESULTS: Small acute DWI lesions were detected in 27.9% (n = 56) of patients. Intraventricular and subarachnoid extension of ICH (p ≤ 0.001), high centrum semiovale (CSO)-EPVS (p < 0.001), high basal ganglia-EPVS (p = 0.007), overall extent of white matter hyperintensity (p = 0.018), initial ICH volume (p < 0.001), and mean change in mean arterial blood pressure (δ MAP = MAP at admission - the lowest MAP before MRI scan) (p = 0.027) were associated with SA-DWIL on univariate analyses. On multivariate logistic regression analyses, larger ICH volume (odds ratio [OR] 1.03; 95% confidence interval [CI] 1.01-1.06; p = 0.006) and high CSO-EPVS (OR 12.56; 95% CI 4.40-35.85; p < 0.001) were independently associated with the presence of SA-DWIL. CONCLUSIONS: In our cohort, high EPVS, in particular CSO-EPVS, and larger hematoma volume emerged as independent predictors for SA-DWIL after ICH. Our findings might provide a new explanation for the pathophysiologic mechanisms predisposing to SA-DWIL after ICH.
OBJECTIVE: To examine the association between enlarged perivascular spaces (EPVS) and the prevalence and extent of small acute diffusion-weighted imaging (DWI) lesions (SA-DWIL) in patients with spontaneous supratentorial intracerebral hemorrhage (ICH). METHODS: We conducted a retrospective review of a consecutive cohort of 201 patients with spontaneous supratentorial ICH who had brain MRI with DWI within 1 month of ICH onset. We compared the clinical and imaging characteristics, including EPVS, of patients with and without SA-DWIL. We used univariate and multivariate logistic regression analyses to determine the variables associated with SA-DWIL. RESULTS: Small acute DWI lesions were detected in 27.9% (n = 56) of patients. Intraventricular and subarachnoid extension of ICH (p ≤ 0.001), high centrum semiovale (CSO)-EPVS (p < 0.001), high basal ganglia-EPVS (p = 0.007), overall extent of white matter hyperintensity (p = 0.018), initial ICH volume (p < 0.001), and mean change in mean arterial blood pressure (δ MAP = MAP at admission - the lowest MAP before MRI scan) (p = 0.027) were associated with SA-DWIL on univariate analyses. On multivariate logistic regression analyses, larger ICH volume (odds ratio [OR] 1.03; 95% confidence interval [CI] 1.01-1.06; p = 0.006) and high CSO-EPVS (OR 12.56; 95% CI 4.40-35.85; p < 0.001) were independently associated with the presence of SA-DWIL. CONCLUSIONS: In our cohort, high EPVS, in particular CSO-EPVS, and larger hematoma volume emerged as independent predictors for SA-DWIL after ICH. Our findings might provide a new explanation for the pathophysiologic mechanisms predisposing to SA-DWIL after ICH.
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