Hsieh Hsinyu, Xu Qiang, Zhang Qirui, Yang Fang, Xu Yin, Liu Gaoping, Liu Ruoting, Yu Qianqian, Zhang Zixuan, Lu Guangming, Gu Xing, Zhang Zhiqiang
Department of Diagnostic Radiology, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.
Department of Neurology, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.
Brain Res. 2024 Apr 1;1828:148766. doi: 10.1016/j.brainres.2024.148766. Epub 2024 Jan 17.
Mapping progressive patterns of structural damage in epilepsies with idiopathic and secondarily generalized tonic-clonic seizures with causal structural covariance networks and multiple analysis strategies.
Patients with idiopathic generalized tonic-clonic seizures (IGTCS) (n = 114) and secondarily generalized tonic-clonic seizures (SGTCS) (n = 125) were recruited. Morphometric parameter of gray matter volume was analyzed on structural MRI. Structural covariance network based on granger causality analysis (CaSCN) was performed on the cross-sectional morphometric data sorted by disease durations of patients. Seed-based CaSCN analysis was firstly carried out to map the progressive and influential patterns of damage to thalamus-related structures. A novel technique for voxel-based CaSCN density (CaSCNd) analysis was further proposed, enabling for identifying the epicenter of structural brain damage during the disease process.
The thalamus-associated CaSCNs demonstrated different patterns of progressive damage in two types of generalized tonic-clonic seizures. In IGTCS, the structural damage was predominantly driven from the thalamus, and expanded to the cortex, while in SGTCS, the damage was predominantly driven from the cortex, and expanded to the thalamus through the basal ganglia. CaSCNd analysis revealed that the IGTCS had an out-effect epicenter in the thalamus, whereas the SGTCS had equipotent in- and out-effects in the thalamus, cortex, and basal ganglia.
CaSCN revealed distinct damage patterns in the two types of GTCS, featuring with measurement of structural brain damage from the accumulating effect over a relatively long time period. Our work provided evidence for understanding network impairment mechanism underlying different GTCSs.
通过因果结构协方差网络和多种分析策略，描绘特发性和继发性全身性强直阵挛性癫痫结构性损伤的进展模式。
招募特发性全身性强直阵挛性癫痫（IGTCS）患者（n = 114）和继发性全身性强直阵挛性癫痫（SGTCS）患者（n = 125）。在结构磁共振成像上分析灰质体积形态学参数。对按患者病程分类的横断面形态学数据进行基于格兰杰因果分析的结构协方差网络（CaSCN）分析。首先进行基于种子点的CaSCN分析，以描绘丘脑相关结构损伤的进展和影响模式。进一步提出一种基于体素的CaSCN密度（CaSCNd）分析新技术，能够识别疾病过程中脑结构损伤的震中。
丘脑相关的CaSCN在两种全身性强直阵挛性癫痫中表现出不同的进展性损伤模式。在IGTCS中，结构损伤主要由丘脑驱动，并扩展到皮质，而在SGTCS中，损伤主要由皮质驱动，并通过基底神经节扩展到丘脑。CaSCNd分析显示，IGTCS在丘脑中存在向外效应震中，而SGTCS在丘脑、皮质和基底神经节中具有等效的向内和向外效应。
CaSCN揭示了两种全身性强直阵挛性癫痫不同的损伤模式，其特点是通过相对较长时间内的累积效应来测量脑结构损伤。我们的工作为理解不同全身性强直阵挛性癫痫潜在的网络损伤机制提供了证据。
