论文标题

体积和结构连通性异常在TLE中共定位

Volumetric and structural connectivity abnormalities co-localise in TLE

论文作者

Horsley, Jonathan J., Schroeder, Gabrielle M., Thomas, Rhys H., de Tisi, Jane, Vos, Sjoerd B., Winston, Gavin P., Duncan, John S., Wang, Yujiang, Taylor, Peter N.

论文摘要

颞叶癫痫(TLE)患者相对于健康对照组表现出容量和结构连通性异常。这些异常及其机制尚不清楚。我们计算了144例单侧TLE和96个健康对照患者的灰质体积变化和白质结构连通性异常。使用T1加权MRI计算区域体积,而结构连通性是使用来自扩散加权MRI的白质纤维拖拉机得出的。对于每个区域量和每个连接强度,我们计算了组级分析中患者和对照组之间的效果大小。然后,我们应用层次回归来研究个体的体积和结构连通性异常之间的关系。此外,我们通过计算骰子相似性评分来量化单个患者在单个患者中共定位的异常。在TLE中,在连接两个异常体积的灰质区域时,白质连通性异常更大。同样,当异常白质连接连接时,灰质的体积异常也更大。与癫痫持续时间有关的体积和连通性异常的程度,但共定位却没有。共定位主要是由同侧半球相邻异常驱动的。总体而言,体积和结构连通性异常与TLE有关。我们的结果表明,共同的机制可能是TLE患者的体积和连通性改变的基础。

Patients with temporal lobe epilepsy (TLE) exhibit both volumetric and structural connectivity abnormalities relative to healthy controls. How these abnormalities inter-relate and their mechanisms are unclear. We computed grey matter volumetric changes and white matter structural connectivity abnormalities in 144 patients with unilateral TLE and 96 healthy controls. Regional volumes were calculated using T1-weighted MRI, while structural connectivity was derived using white matter fibre tractography from diffusion-weighted MRI. For each regional volume and each connection strength, we calculated the effect size between patient and control groups in a group-level analysis. We then applied hierarchical regression to investigate the relationship between volumetric and structural connectivity abnormalities in individuals. Additionally, we quantified whether abnormalities co-localised within individual patients by computing Dice similarity scores. In TLE, white matter connectivity abnormalities were greater when joining two grey matter regions with abnormal volumes. Similarly, grey matter volumetric abnormalities were greater when joined by abnormal white matter connections. The extent of volumetric and connectivity abnormalities related to epilepsy duration, but co-localisation did not. Co-localisation was primarily driven by neighbouring abnormalities in the ipsilateral hemisphere. Overall, volumetric and structural connectivity abnormalities were related in TLE. Our results suggest that shared mechanisms may underlie changes in both volume and connectivity alterations in patients with TLE.

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