目的:冻结步态(FOG),特定的威胁生存的步态障碍,多系统萎缩(MSA)患者需要紧急探索,其特征是在症状发作后10年内迅速进展和死亡。这项研究的目的是探索MAS和FOG患者的低阶和高阶功能网络的拓扑组织。
方法:使用图论方法对24例无FOG的MSA患者计算并进一步分析了低阶功能连通性(LOFC)和高阶功能连通性FC(HOFC)网络,20名FOG患者,和25个健康对照。研究了FOG患者脑活动与冻结症状严重程度之间的关系。
结果:关于全局拓扑属性,患有FOG的患者表现出全脑网络的改变,背侧注意网络(DAN),额顶叶网络(FPN),和默认网络(DMN),与没有FOG的患者相比。在节点级别,FOG患者在感觉运动网络(SMN)中表现出降低的淋巴结中心性,丹,腹侧注意力网络(VAN),FPN,边缘区域,海马网络和基底神经节网络(BG),增加了FPN中的节点中心性,DMN,视觉网络(VIN)和,小脑网络。右下额沟的结节中心,左杏仁核和左伏核(NAC)与FOG严重程度呈负相关。
结论:这项研究确定了患有FOG的MSA患者在低水平和高水平上功能相互作用的拓扑结构被破坏,拓扑结构发生了广泛的改变,尤其是那些与FPN损坏有关的。这些发现为复杂网络的功能失调机制提供了新的见解,并为MSA患者的FOG提供了潜在的神经影像学生物标志物。
Freezing of gait (FOG), a specific survival-threatening gait impairment, needs to be urgently explored in patients with multiple system atrophy (MSA), which is characterized by rapid progression and death within 10 years of symptom onset. The objective of this
study was to explore the topological organisation of both low- and high-order functional networks in patients with MAS and FOG.
Low-order functional connectivity (LOFC) and high-order functional connectivity FC (HOFC) networks were calculated and further analysed using the graph theory approach in 24 patients with MSA without FOG, 20 patients with FOG, and 25 healthy controls. The relationship between brain activity and the severity of freezing symptoms was investigated in patients with FOG.
Regarding global topological properties, patients with FOG exhibited alterations in the whole-brain network, dorsal attention network (DAN), frontoparietal network (FPN), and default network (DMN), compared with patients without FOG. At the node level, patients with FOG showed decreased nodal centralities in sensorimotor network (SMN), DAN, ventral attention network (VAN), FPN, limbic regions, hippocampal network and basal ganglia network (BG), and increased nodal centralities in the FPN, DMN, visual network (VIN) and, cerebellar network. The nodal centralities of the right inferior frontal sulcus, left lateral amygdala and left nucleus accumbens (NAC) were negatively correlated with the FOG severity.
This
study identified a disrupted topology of functional interactions at both low and high levels with extensive alterations in topological properties in MSA patients with FOG, especially those associated with damage to the FPN. These findings offer new insights into the dysfunctional mechanisms of complex networks and suggest potential neuroimaging biomarkers for FOG in patients with MSA.