From the Neuroimaging of Epilepsy Laboratory (B.C.B., F.F., M.L., B.C., A.B., N.B.) and Multimodal Imaging and Connectome Analysis Laboratory (B.C.B.), McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Canada; Department of Bioengineering and Electrical and Systems Engineering (S.G., D.S.B.), University of Pennsylvania, Philadelphia; and York Neuroimaging Center (E.J., J.S.), University of York, UK.
Neurology. 2019 May 7;92(19):e2209-e2220. doi: 10.1212/WNL.0000000000007447. Epub 2019 Apr 19.
To assess whether hippocampal sclerosis (HS) severity is mirrored at the level of large-scale networks.
We studied preoperative high-resolution anatomical and diffusion-weighted MRI of 44 temporal lobe epilepsy (TLE) patients with histopathologic diagnosis of HS (n = 25; TLE-HS) and isolated gliosis (n = 19; TLE-G) and 25 healthy controls. Hippocampal measurements included surface-based subfield mapping of atrophy and T2 hyperintensity indexing cell loss and gliosis, respectively. Whole-brain connectomes were generated via diffusion tractography and examined using graph theory along with a novel network control theory paradigm that simulates functional dynamics from structural network data.
Compared to controls, we observed markedly increased path length and decreased clustering in TLE-HS compared to controls, indicating lower global and local network efficiency, while TLE-G showed only subtle alterations. Similarly, network controllability was lower in TLE-HS only, suggesting limited range of functional dynamics. Hippocampal imaging markers were positively associated with macroscale network alterations, particularly in ipsilateral CA1-3. Systematic assessment across several networks revealed maximal changes in the hippocampal circuity. Findings were consistent when correcting for cortical thickness, suggesting independence from gray matter atrophy.
Severe HS is associated with marked remodeling of connectome topology and structurally governed functional dynamics in TLE, as opposed to isolated gliosis, which has negligible effects. Cell loss, particularly in CA1-3, may exert a cascading effect on brain-wide connectomes, underlining coupled disease processes across multiple scales.
评估海马硬化（HS）严重程度是否在大规模网络层面上得到反映。
我们研究了 44 例颞叶癫痫（TLE）患者的术前高分辨率解剖和弥散加权 MRI，这些患者的组织病理学诊断为 HS（n=25；TLE-HS）和孤立性神经胶质增生（n=19；TLE-G），并纳入 25 名健康对照者。海马测量包括基于表面的萎缩亚区划分和 T2 高信号分别指数细胞丢失和神经胶质增生。全脑连接组通过弥散张量成像生成，并使用图论以及一种新的网络控制理论范式进行检查，该范式模拟来自结构网络数据的功能动力学。
与对照组相比，我们发现 TLE-HS 与对照组相比，路径长度明显增加，聚类减少，表明全局和局部网络效率降低，而 TLE-G 仅显示出细微的改变。同样，仅在 TLE-HS 中网络可控性较低，表明功能动力学范围有限。海马影像学标志物与宏观网络改变呈正相关，特别是在同侧 CA1-3。对多个网络进行系统评估显示，最大的变化发生在海马环路上。当校正皮质厚度时，发现结果一致，这表明与灰质萎缩无关。
严重的 HS 与 TLE 中海马连接组拓扑的显著重塑以及受结构控制的功能动力学相关，而孤立性神经胶质增生则几乎没有影响。细胞丢失，特别是在 CA1-3，可能对全脑连接组产生级联效应，强调了多个尺度上的耦合疾病过程。
