Marco Duering1, Ruthger Righart1, Frank Arne Wollenweber1, Vera Zietemann1, Benno Gesierich1, Martin Dichgans2. 1. From the Institute for Stroke and Dementia Research (M.D., R.R., F.A.W., V.Z., B.G., M.D.), Klinikum der Universität München, Ludwig-Maximilians University, Munich; German Center for Neurodegenerative Diseases (DZNE, Munich) (R.R., M.D.), Munich; and Munich Cluster for Systems Neurology (SyNergy) (M.D.), Munich, Germany. R.R. is currently with the Department of Neurology, Technische Universität München, Munich, Germany. 2. From the Institute for Stroke and Dementia Research (M.D., R.R., F.A.W., V.Z., B.G., M.D.), Klinikum der Universität München, Ludwig-Maximilians University, Munich; German Center for Neurodegenerative Diseases (DZNE, Munich) (R.R., M.D.), Munich; and Munich Cluster for Systems Neurology (SyNergy) (M.D.), Munich, Germany. R.R. is currently with the Department of Neurology, Technische Universität München, Munich, Germany. martin.dichgans@med.uni-muenchen.de.
Abstract
OBJECTIVE: To study remote effects distant from acute ischemic infarcts by measuring longitudinal changes of cortical thickness in connected brain regions as well as changes in microstructural integrity in connecting fiber tracts. METHODS: Thirty-two patients (mean age 71 years) underwent a standardized protocol including multimodal MRI and clinical assessment both at stroke onset and 6 months after the event. Cortex connected to acute infarcts was identified by probabilistic diffusion tensor tractography starting from the acute lesion. Changes of cortical thickness were measured using the longitudinal stream of FreeSurfer. Microstructural damage in white matter tracts was assessed by changes of mean diffusivity. RESULTS: We found focal cortical thinning specifically in areas connected to acute infarcts (p < 0.001). Thinning was more pronounced in regions showing a high probability of connectivity to infarcts. Microstructural damage in white matter tracts connecting acute infarcts with distant cortex significantly correlated with thickness changes in that region (ρ = -0.39, p = 0.028). There was no indication of an influence of cavitation status or infarct etiology on the observed changes in cortex and white matter. CONCLUSIONS: These findings identify secondary degeneration of connected white matter tracts and remote cortex as key features of acute ischemic infarcts. Our observations may have implications for the understanding of structural and functional reorganization after stroke.
OBJECTIVE: To study remote effects distant from acute ischemic infarcts by measuring longitudinal changes of cortical thickness in connected brain regions as well as changes in microstructural integrity in connecting fiber tracts. METHODS: Thirty-two patients (mean age 71 years) underwent a standardized protocol including multimodal MRI and clinical assessment both at stroke onset and 6 months after the event. Cortex connected to acute infarcts was identified by probabilistic diffusion tensor tractography starting from the acute lesion. Changes of cortical thickness were measured using the longitudinal stream of FreeSurfer. Microstructural damage in white matter tracts was assessed by changes of mean diffusivity. RESULTS: We found focal cortical thinning specifically in areas connected to acute infarcts (p < 0.001). Thinning was more pronounced in regions showing a high probability of connectivity to infarcts. Microstructural damage in white matter tracts connecting acute infarcts with distant cortex significantly correlated with thickness changes in that region (ρ = -0.39, p = 0.028). There was no indication of an influence of cavitation status or infarct etiology on the observed changes in cortex and white matter. CONCLUSIONS: These findings identify secondary degeneration of connected white matter tracts and remote cortex as key features of acute ischemic infarcts. Our observations may have implications for the understanding of structural and functional reorganization after stroke.
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