Duering Marco, Righart Ruthger, Wollenweber Frank Arne, Zietemann Vera, Gesierich Benno, Dichgans Martin
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.
Neurology. 2015 Apr 21;84(16):1685-92. doi: 10.1212/WNL.0000000000001502. Epub 2015 Mar 25.
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.
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.
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.
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.
通过测量相连脑区皮质厚度的纵向变化以及连接纤维束微观结构完整性的变化，研究急性缺血性梗死灶远处的远程效应。
32例患者（平均年龄71岁）在卒中发作时及发病6个月后接受了包括多模态磁共振成像和临床评估的标准化方案。从急性病变开始，通过概率性扩散张量纤维束成像确定与急性梗死灶相连的皮质。使用FreeSurfer的纵向流程测量皮质厚度的变化。通过平均扩散率的变化评估白质纤维束的微观结构损伤。
我们发现，在与急性梗死灶相连的区域出现了局灶性皮质变薄（p < 0.001）。在与梗死灶连接可能性高的区域，变薄更为明显。连接急性梗死灶与远处皮质的白质纤维束的微观结构损伤与该区域的厚度变化显著相关（ρ = -0.39，p = 0.028）。没有迹象表明空洞状态或梗死病因对观察到的皮质和白质变化有影响。
这些发现确定相连白质纤维束和远处皮质的继发性变性是急性缺血性梗死的关键特征。我们的观察结果可能对理解卒中后的结构和功能重组有启示意义。
