Abstract：
BACKGROUND: Alterations in white matter microstructure and functional activity have been demonstrated to be involved in the central nervous system mechanism of classic trigeminal neuralgia (CTN). However, the rich-club organization and related topological alterations in the CTN brain networks remain unclear.
METHODS: We simultaneously collected diffusion-tensor imaging (DTI) and resting state functional magnetic resonance imaging (rs-fMRI) data from 29 patients with CTN (9 males, mean age = 54.59 years) and 34 matched healthy controls (HCs) (12 males, mean age = 54.97 years) to construct structural networks (SNs) and functional networks (FNs). Rich-club organization was determined separately based on each group\'s SN and different kinds of connections. For both network types, we calculated the basic connectivity properties (network density and strength) and topological properties (global/local/nodal efficiency and small worldness). Moreover, SN-FN coupling was obtained. The relationships between all those properties and clinical measures were evaluated.
RESULTS: Compared to their FN, the SN of CTN patients was disrupted more severely, including its topological properties (reduced network efficiency and small-worldness), and a decrease in network density and strength was observed. Patients showed reorganization of the rich-club architecture, wherein the nodes with decreased nodal efficiency in the SN were mainly non-hub regions, and the local connections were closely related to altered global efficiency and whole brain coupling. While the cortical-subcortical connections of feeder were found to be strengthened in the SN of patients, the coupling between networks increased in all types of connections. Finally, disease severity (duration, pain intensity, and affective alterations) was negatively correlated with coupling (rich-club, feeder, and whole brain) and network strength (the rich-club of the SN and local connections of the FN). A positive correlation was only found between pain intensity and the coupling of local connections.
CONCLUSIONS: The SN of patients with CTN may be more vulnerable. Accompanied by the reorganization of the rich-club, the less efficient network communication and the impaired functional dynamics were largely attributable to the dysfunction of non-hub regions. As compensation, the pain transmission pathway of feeder connections involving in pain processing and emotional regulation may strengthen. The local and feeder sub-networks may serve as potential biomarkers for diagnosis or prognosis.
METHODS: We simultaneously collected diffusion-tensor imaging (DTI) and resting state functional magnetic resonance imaging (rs-fMRI) data from 29 patients with CTN (9 males, mean age = 54.59 years) and 34 matched healthy controls (HCs) (12 males, mean age = 54.97 years) to construct structural networks (SNs) and functional networks (FNs). Rich-club organization was determined separately based on each group\'s SN and different kinds of connections. For both network types, we calculated the basic connectivity properties (network density and strength) and topological properties (global/local/nodal efficiency and small worldness). Moreover, SN-FN coupling was obtained. The relationships between all those properties and clinical measures were evaluated.
RESULTS: Compared to their FN, the SN of CTN patients was disrupted more severely, including its topological properties (reduced network efficiency and small-worldness), and a decrease in network density and strength was observed. Patients showed reorganization of the rich-club architecture, wherein the nodes with decreased nodal efficiency in the SN were mainly non-hub regions, and the local connections were closely related to altered global efficiency and whole brain coupling. While the cortical-subcortical connections of feeder were found to be strengthened in the SN of patients, the coupling between networks increased in all types of connections. Finally, disease severity (duration, pain intensity, and affective alterations) was negatively correlated with coupling (rich-club, feeder, and whole brain) and network strength (the rich-club of the SN and local connections of the FN). A positive correlation was only found between pain intensity and the coupling of local connections.
CONCLUSIONS: The SN of patients with CTN may be more vulnerable. Accompanied by the reorganization of the rich-club, the less efficient network communication and the impaired functional dynamics were largely attributable to the dysfunction of non-hub regions. As compensation, the pain transmission pathway of feeder connections involving in pain processing and emotional regulation may strengthen. The local and feeder sub-networks may serve as potential biomarkers for diagnosis or prognosis.
摘要：
背景：已证明白质微结构和功能活动的改变与经典三叉神经痛（CTN）的中枢神经系统机制有关。然而,CTN脑网络中的富俱乐部组织和相关拓扑改变仍不清楚。
方法：我们同时收集了29例CTN患者（9例男性，平均年龄=54.59岁)和34个匹配的健康对照(HCs)(12名男性，平均年龄=54.97岁)来构建结构网络(SNs)和功能网络(FNs)。根据每个组的SN和不同的连接类型，分别确定了丰富的俱乐部组织。对于这两种网络类型，我们计算了基本连通性属性（网络密度和强度）和拓扑属性（全局/局部/节点效率和小世界性）。此外，获得SN-FN偶联。评估了所有这些特性与临床措施之间的关系。
结果：与其FN相比，CTN患者的SN受到更严重的干扰，包括其拓扑属性(降低的网络效率和小世界)，并且观察到网络密度和强度的降低。患者表现出富人俱乐部建筑的重组，其中SN中节点效率降低的节点主要是非集线器区域，局部连接与改变的整体效率和全脑耦合密切相关。虽然发现饲养者的皮质-皮质下连接在患者的SN中得到加强，在所有类型的连接中，网络之间的耦合都增加了。最后,疾病严重程度(持续时间，疼痛强度，和情感改变)与耦合(丰富的俱乐部，馈线,和整个大脑）和网络强度（SN的丰富俱乐部和FN的本地连接）。仅在疼痛强度与局部连接的耦合之间发现正相关。
结论：CTN患者的SN可能更脆弱。伴随着富人俱乐部的重组，网络沟通效率较低和功能动力学受损主要归因于非枢纽区域的功能障碍.作为补偿,涉及疼痛处理和情绪调节的馈线连接的疼痛传递途径可能会加强。本地和饲养子网络可以用作诊断或预后的潜在生物标志物。
方法：我们同时收集了29例CTN患者（9例男性，平均年龄=54.59岁)和34个匹配的健康对照(HCs)(12名男性，平均年龄=54.97岁)来构建结构网络(SNs)和功能网络(FNs)。根据每个组的SN和不同的连接类型，分别确定了丰富的俱乐部组织。对于这两种网络类型，我们计算了基本连通性属性（网络密度和强度）和拓扑属性（全局/局部/节点效率和小世界性）。此外，获得SN-FN偶联。评估了所有这些特性与临床措施之间的关系。
结果：与其FN相比，CTN患者的SN受到更严重的干扰，包括其拓扑属性(降低的网络效率和小世界)，并且观察到网络密度和强度的降低。患者表现出富人俱乐部建筑的重组，其中SN中节点效率降低的节点主要是非集线器区域，局部连接与改变的整体效率和全脑耦合密切相关。虽然发现饲养者的皮质-皮质下连接在患者的SN中得到加强，在所有类型的连接中，网络之间的耦合都增加了。最后,疾病严重程度(持续时间，疼痛强度，和情感改变)与耦合(丰富的俱乐部，馈线,和整个大脑）和网络强度（SN的丰富俱乐部和FN的本地连接）。仅在疼痛强度与局部连接的耦合之间发现正相关。
结论：CTN患者的SN可能更脆弱。伴随着富人俱乐部的重组，网络沟通效率较低和功能动力学受损主要归因于非枢纽区域的功能障碍.作为补偿,涉及疼痛处理和情绪调节的馈线连接的疼痛传递途径可能会加强。本地和饲养子网络可以用作诊断或预后的潜在生物标志物。
