Network analysis reveals disrupted functional brain circuitry in drug-naive social anxiety disorder
Network analysis reveals disrupted functional brain circuitry in drug-naive social anxiety disorder
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网络分析揭示未用药社交焦虑症中大脑功能回路的破坏
DOI：
10.1016/j.neuroimage.2017.12.011
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发表时间：
2017
期刊：
影响因子：
5.7
通讯作者：
et al.
中科院分区：
文献类型：
--
作者：
Xun Yan;Jin Liu;Yajing Meng;et al.
社交焦虑症（SAD）是一种常见的致残性疾病，其特征是过度恐惧和逃避公众监督。心理放射学研究表明，SAD患者的情绪和行为缺陷与局部脑功能和功能连接异常有关。然而，很少有人知道是否与SAD患者的内在功能性脑网络拓扑破坏。在这里，我们收集了来自33名药物初治SAD患者和32名健康对照（HC）的静息状态fMRI数据，构建了功能网络与34个预定义区域的基础上，以前的元分析研究与基于任务的功能磁共振成像SAD，并进行基于网络的统计和图论分析。基于网络的统计分析揭示了一个单一的连接异常的电路，包括额叶边缘回路（称为“恐惧回路”，包括背外侧前额叶皮层，腹内侧前额叶皮层和背外侧前额叶皮层）和后扣带/枕区支持知觉加工。在这个单一改变的网络中，SAD患者的功能连接性高于HC。在全球层面上，图论分析显示，患者表现出较低的归一化特征路径长度比HC，这表明一个障碍相关的网络拓扑结构向随机配置的转变。在海马旁回、后扣带回、背外侧前额叶、小脑和距状沟检测到SAD相关的节点度、效率和参与系数缺陷。异常连接的方面与焦虑症状有关。这些发现突出了SAD中功能性脑网络组织的异常拓扑组织，这为社交焦虑患者过度恐惧和避免社交互动的神经机制提供了见解。
Social anxiety disorder (SAD) is a common and disabling condition characterized by excessive fear and avoidance of public scrutiny. Psychoradiology studies have suggested that the emotional and behavior deficits in SAD are associated with abnormalities in regional brain function and functional connectivity. However, little is known about whether intrinsic functional brain networks in patients with SAD are topologically disrupted. Here, we collected resting-state fMRI data from 33 drug-naive patients with SAD and 32 healthy controls (HC), constructed functional networks with 34 predefined regions based on previous meta-analytic research with task-based fMRI in SAD, and performed network-based statistic and graph-theory analyses. The network-based statistic analysis revealed a single connected abnormal circuitry including the frontolimbic circuit (termed the “fear circuit”, including the dorsolateral prefrontal cortex, ventral medial prefrontal cortex and insula) and posterior cingulate/occipital areas supporting perceptual processing. In this single altered network, patients with SAD had higher functional connectivity than HC. At the global level, graph-theory analysis revealed that the patients exhibited a lower normalized characteristic path length than HC, which suggests a disorder-related shift of network topology toward randomized configurations. SAD-related deficits in nodal degree, efficiency and participation coefficient were detected in the parahippocampal gyrus, posterior cingulate cortex, dorsolateral prefrontal cortex, insula and the calcarine sulcus. Aspects of abnormal connectivity were associated with anxiety symptoms. These findings highlight the aberrant topological organization of functional brain network organization in SAD, which provides insights into the neural mechanisms underlying excessive fear and avoidance of social interactions in patients with debilitating social anxiety.