Volumetric and structural connectivity abnormalities co-localise in TLE.

Volumetric and structural connectivity abnormalities co-localise in TLE.
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DOI:
10.1016/j.nicl.2022.103105
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发表时间:
2022
影响因子:
4.2
通讯作者:
Taylor, Peter N.
Taylor, Peter N.
中科院分区:
医学2区
文献类型:
--
作者:
Horsley, Jonathan J.;Schroeder, Gabrielle M.;Thomas, Rhys H.;de Tisi, Jane;Vos, Sjoerd B.;Winston, Gavin P.;Wang, Yujiang;Taylor, Peter N.

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TLE中存在结构连接异常。灰质体积异常也存在于TLE。96名对照和144名患者研究异常共定位。在个体和群体层面上,绝对共同定位。癫痫持续时间越长,异常越多。颞叶癫痫(TLE)患者表现出体积和结构连接异常相对于健康对照。这些异常是如何相互关联的,其机制尚不清楚。我们计算了144例单侧TLE患者和96例健康对照者的灰质体积变化和白色物质结构连接异常。使用T1加权MRI计算区域体积,而使用弥散加权MRI的白色物质纤维束成像推导结构连接。对于每个区域体积和每个连接强度,我们在组水平分析中计算了患者组和对照组之间的效应量。然后,我们应用分层回归研究个体的体积和结构连接异常之间的关系。此外,我们通过计算Dice相似性分数来量化个体患者内是否存在异常共定位。在颞叶癫痫,白色物质连接异常时,加入两个灰质区域异常体积更大。同样,当灰质体积异常与异常的白色物质连接相连时,灰质体积异常更大。体积和连接异常的程度与癫痫持续时间有关,但共定位没有。共定位主要是由同侧半球的相邻异常驱动的。总的来说,体积和结构连接异常相关的TLE。我们的研究结果表明,共享的机制可能是TLE患者的体积和连接改变的基础。
Structural connectivity abnormalities present in TLE. Grey matter volume abnormalities also present in TLE. 96 controls & 144 patients to investigate abnormality co-localisation. Abnormalities co-localise in individuals, and at group level. More abnormalities related to longer epilepsy duration. 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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