动静脉畸形患者上纵束语言功能的自动纤维定量研究。

Fangrong Zong, Zhaoyi You, Leqing Zhou, Xiaofeng Deng
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引用次数: 0

摘要

上纵束(SLF)是参与语言加工的主要纤维束,已被用于研究许多神经系统疾病的语言障碍和可塑性。SLF分为四个主要分支,与不同的皮层区域相连,其中两个分支(SLF II、SLF III)与语言直接相关。然而,大多数白质分析将SLF视为单个束,这可能低估了这些纤维束与语言功能之间的关系。在这项研究中,我们研究了动静脉畸形(AVM)患者SLF分支的差异,这是研究语言重组的独特模型。我们分析AVM患者和健康对照的弥散张量成像数据,生成全脑纤维束图,然后根据不同的路点区域将SLF划分为SLF II和SLF III。进一步量化SLF、SLF II和SLF III,比较avm与对照组3支4项扩散参数。两组间整个SLF的扩散率无显著差异,但与对照组相比,avm的右侧SLF II和III表现出明显的重组或损伤模式。结果表明,在研究具有SLF损伤的神经疾病的结构-功能关系时,需要减去SLF分支。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Language function of the superior longitudinal fasciculus in patients with arteriovenous malformation as evidenced by automatic fiber quantification.

The superior longitudinal fasciculus (SLF) is a major fiber tract involved in language processing and has been used to investigate language impairments and plasticity in many neurological diseases. The SLF is divided into four main branches that connect with different cortex regions, with two branches (SLF II, SLF III) being directly related to language. However, most white matter analyses consider the SLF as a single bundle, which may underestimate the relationship between these fiber bundles and language function. In this study, we investigated the differences between branches of the SLF in patients with arteriovenous malformation (AVM), which is a unique model to investigate language reorganization. We analyzed diffusion tensor imaging data of AVM patients and healthy controls to generate whole-brain fiber tractography, and then segmented the SLF into SLF II and III based on their distinctive waypoint regions. The SLF, SLF II, and III were further quantified, and four diffusion parameters of three branches were compared between the AVMs and controls. No significant diffusivity differences of the whole SLF were observed between two groups, however, the right SLF II and III in AVMs showed significant reorganization or impairment patterns as compared to the controls. Results demonstrating the need to subtracting SLF branches when studying structure-function relationship in neurological diseases that have SLF damage.

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