Susanne J van Veluw1, Arne Lauer2, Andreas Charidimou2, Narimene Bounemia2, Li Xiong2, Gregoire Boulouis2, Panagiotis Fotiadis2, Alison Ayres2, M Edip Gurol2, Anand Viswanathan2, Steven M Greenberg2, Meike W Vernooij2. 1. From the Hemorrhagic Stroke Research Program, Department of Neurology (S.J.v.V., A.L., A.C., N.B., L.X., G.B., P.F., A.A., M.E.G., A.V., S.M.G., M.W.V.), Massachusetts General Hospital, Harvard Medical School, Boston; and Departments of Radiology and Nuclear Medicine (M.W.V.) and Epidemiology (M.W.V.), Erasmus MC, Rotterdam, the Netherlands. svanveluw@mgh.harvard.edu. 2. From the Hemorrhagic Stroke Research Program, Department of Neurology (S.J.v.V., A.L., A.C., N.B., L.X., G.B., P.F., A.A., M.E.G., A.V., S.M.G., M.W.V.), Massachusetts General Hospital, Harvard Medical School, Boston; and Departments of Radiology and Nuclear Medicine (M.W.V.) and Epidemiology (M.W.V.), Erasmus MC, Rotterdam, the Netherlands.
Abstract
OBJECTIVE: To address the pathophysiologic nature of small diffusion-weighted imaging (DWI) lesions in patients with cerebral amyloid angiopathy (CAA) who underwent serial MRI. Specifically, we tested (1) whether DWI lesions occurred preferentially in individuals with prior DWI lesions, (2) the cross-sectional association with chronic cortical cerebral microinfarcts (CMIs), and (3) the evolution of DWI lesions over time. METHODS: Patients with probable CAA (n = 79) who underwent at least 2 MRI sessions were included. DWI lesions were assessed at each available time point. Lesion appearance and characteristics were assessed on available structural follow-up images. Presence and burden of other neuroimaging markers of small vessel disease (white matter hyperintensities, cerebral microbleeds, cortical superficial siderosis, and chronic cortical CMIs) were assessed as well. RESULTS: Among 221 DWI scans (79 patients with 2 DWI scans; 40 with ≥3), 60 DWI lesions were found in 28 patients. Patients with DWI lesions at baseline were not more likely to have additional DWI lesions on follow-up compared to patients without DWI lesions at baseline. DWI lesions were associated with chronic cortical CMIs and cortical superficial siderosis, but not with other markers. For 39/60 DWI lesions, >1 MRI sequence was available at follow-up to determine lesion evolution. Twenty-four (62%) were demarcated as chronic lesions on follow-up MRI. Five appeared as cavitations, 18 as noncavitated infarcts, and 1 underwent hemorrhagic transformation. CONCLUSIONS: Based on their neuroimaging signature as well as their association with chronic cortical CMIs, DWI lesions appear to have an ischemic origin and represent one part of the CMI spectrum.
OBJECTIVE: To address the pathophysiologic nature of small diffusion-weighted imaging (DWI) lesions in patients with cerebral amyloid angiopathy (CAA) who underwent serial MRI. Specifically, we tested (1) whether DWI lesions occurred preferentially in individuals with prior DWI lesions, (2) the cross-sectional association with chronic cortical cerebral microinfarcts (CMIs), and (3) the evolution of DWI lesions over time. METHODS: Patients with probable CAA (n = 79) who underwent at least 2 MRI sessions were included. DWI lesions were assessed at each available time point. Lesion appearance and characteristics were assessed on available structural follow-up images. Presence and burden of other neuroimaging markers of small vessel disease (white matter hyperintensities, cerebral microbleeds, cortical superficial siderosis, and chronic cortical CMIs) were assessed as well. RESULTS: Among 221 DWI scans (79 patients with 2 DWI scans; 40 with ≥3), 60 DWI lesions were found in 28 patients. Patients with DWI lesions at baseline were not more likely to have additional DWI lesions on follow-up compared to patients without DWI lesions at baseline. DWI lesions were associated with chronic cortical CMIs and cortical superficial siderosis, but not with other markers. For 39/60 DWI lesions, >1 MRI sequence was available at follow-up to determine lesion evolution. Twenty-four (62%) were demarcated as chronic lesions on follow-up MRI. Five appeared as cavitations, 18 as noncavitated infarcts, and 1 underwent hemorrhagic transformation. CONCLUSIONS: Based on their neuroimaging signature as well as their association with chronic cortical CMIs, DWI lesions appear to have an ischemic origin and represent one part of the CMI spectrum.
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