Deficits in brain default mode network connectivity mediate the relationship between poor sleep quality and anxiety severity

楔前 默认模式网络 焦虑 心理学 调解 静息状态功能磁共振成像 功能磁共振成像 神经科学 临床心理学 前额叶皮质 失眠症 精神科 认知 政治学 法学
作者
Zhifu Shen,Xue Yang,Tianwei She,Guangli Zhao,Zeyang Dou,Yucai Luo,Wenting Lin,Wantai Dang,Siyi Yu
出处
期刊:Sleep [Oxford University Press]
卷期号:47 (3) 被引量:21
标识
DOI:10.1093/sleep/zsad296
摘要

Abstract Study Objectives Chronic insomnia disorder (CID) is a prevalent sleep disorder that frequently cooccurs with anxiety. The association between insomnia and anxiety has been established; however, the neurobiological basis of this relationship remains unclear. This study aimed to investigate the neural markers of CID patients with and without anxiety and to determine whether specific neural connectivity mediates the relationship between insomnia and anxiety. Methods This study included 180 participants, comprising CID patients with anxiety (CID-A), CID patients without anxiety (CID-NA), and good sleep controls. All participants completed self-reported measures of sleep quality and anxiety severity and underwent functional magnetic resonance imaging. Brain functional integration was measured using functional connectivity density (FCD) and resting-state functional connectivity (rsFC). Correlation and mediation analyses were used to examine the relationships among brain connectivity, sleep quality, and anxiety severity. Results The CID-NA and CID-A groups showed decreased local FCD in the medial prefrontal cortex (mPFC) and disrupted rsFC between the precuneus and other brain regions. Only the CID-A group exhibited altered long-range FCD in the precuneus and the rsFC between the anterior default mode network (DMN, e.g. mPFC) and posterior DMN (e.g. precuneus). Mediation analysis revealed DMN dysconnectivity underlying the association between poor sleep quality and anxiety symptoms. Conclusions This study identified shared and distinct brain circuit disruptions in the CID-NA and CID-A groups, with deficits in DMN connectivity as a potential neural mechanism through which disrupted sleep augments anxiety. These findings may facilitate the development of personalized therapies for insomnia and associated anxiety problems.
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