Transcallosal Fiber Disruption and its Relationship with Corresponding Gray Matter Alteration in Patients with Diffuse Axonal Injury
Transcallosal Fiber Disruption and its Relationship with Corresponding Gray Matter Alteration in Patients with Diffuse Axonal Injury
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弥漫性轴突损伤患者的胼胝体纤维断裂及其与相应灰质改变的关系
DOI：
10.1089/neu.2018.5823
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发表时间：
2018
影响因子：
4.2
通讯作者：
Ueda Keita
中科院分区：
文献类型：
--
作者：
Ubukata Shiho;Oishi Naoya;Sugihara Genichi;Aso Toshihiko;Fukuyama Hidenao;Murai Toshiya;Ueda Keita
弥漫性轴索损伤(DAI)以脑部剪切力引起的弥漫性白质(WM)破坏为特征。皮质萎缩可伴有WM破坏，这被认为反映了邻近WM破坏的灰质(GM)区神经元胞体的丢失。目前尚不清楚西药中断是否会导致DAI的区域性GM改变。本研究的目的是使用基于连接组的方法评估DAI患者的WM中断和相应的GM改变。对24例患者和24例健康对照进行磁共振弥散张量成像(DTI)。确定性纤维追踪被用来研究胼胝体(CC)和每个预先定义的区域皮质区之间的结构连接。我们计算了分数各向异性(FA)的85 × 85连接性矩阵。进行组内比较，以确定患者中的异常连接。此外，还比较了患者和对照组之间每个连接矩阵的区域皮质体积。最后，在患者组内进行了矩阵和区域皮质体积之间的相关性分析。连接组分析显示，与对照组相比，患者通过CC连接到32个皮质区域的FA减少，包括额叶、顶叶和枕叶皮质。在这些地区中，32个地区中有19个地区的转基因汽车销量减少。在发现连接异常的WM中断与相应的GM改变之间没有显著的相关性。这些结果表明，至少部分地，GM病理与DAI相应的WM损伤无关。
Diffuse axonal injury (DAI) is characterized by diffuse white matter (WM) disruption caused by shearing forces acting on the brain. Cortical atrophy can be accompanied by WM disruption, which is assumed to reflect the loss of neuron cell bodies in gray matter (GM) regions adjacent to disrupted WM. It remains unclear whether WM disruption leads to regional GM alteration in DAI. The aim of the present study was to assess WM disruption and corresponding GM alterations in patients with DAI using a connectome-based approach. Twenty-four patients and 24 healthy controls underwent magnetic resonance imaging with diffusion tensor imaging (DTI). Deterministic fiber tracking was conducted to investigate structural connectivity between the corpus callosum (CC) and each pre-defined regional cortical area. We calculated 85 × 85 connectivity matrices for fractional anisotropy (FA). Group comparisons were conducted to identify abnormal connectivity in patients. Further, the regional cortical volume of each connectivity matrix was compared between patients and controls. Finally, correlation analyses between the matrices and regional cortical volumes were performed within the patient group. Connectome analyses revealed that, compared with controls, patients exhibited a FA reduction in connectivity via CC to 32 cortical regions including the frontal, parietal, and occipital cortices. Among these regions, GM volume was reduced in 19 of 32 regions. There were no significant correlations between WM disruption in which abnormal connectivity was identified and the corresponding GM alterations. These results suggest that GM pathology is, at least in part, independent of the corresponding WM damage in DAI.