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Altered Individualized Structural Covariance Networks Underlie Depressive and Anxiety Symptoms in Chronic Insomnia
Liang Gong1, Duan Liu1, Bei Zhang1
1Department of Neurology, West China School of Medicine, Sichuan University, Sichuan University affiliated Chengdu Second People's Hospital, Chengdu, China.
Purpose:
Chronic insomnia disorder (CID) is highly comorbid with depression and anxiety, yet the neurostructural basis of this affective comorbidity remains unclear. This study aimed to investigate individualized structural covariance network (iSCN) alterations in CID and their associations with depressive and anxiety symptoms using a novel dynamic time warping (DTW) approach.
Methods:
A total of 257 CID patients and 247 good sleep controls (GSCs) underwent T1-weighted structural magnetic resonance imaging. Individualized SCNs were constructed based on gray matter volume using the DTW algorithm to quantify interregional morphological similarity. Graph theory analysis was applied to assess global and nodal network topological properties. Clinical symptoms were evaluated using standardized scales (PSQI, SDS, SAS). FINDINGS: Compared with GSCs, patients with CID exhibited significant disruptions in global network topology, including reduced local efficiency, global efficiency, and small-world properties (Gamma and Sigma). At the nodal level, both increased and decreased nodal degree and betweenness centrality were observed in regions involved in emotion regulation, arousal, and sensory processing, including the orbitofrontal cortex, amygdala, thalamus, and caudate nucleus. These nodal metrics were significantly associated with depressive and anxiety symptom severity after correction for multiple comparisons.
Conclusion:
Our findings demonstrate that CID is characterized by disrupted iSCN organization, and that nodal alterations within emotion-, arousal-, and sensory-related regions are associated with the severity of depressive and anxiety symptoms. These findings identify altered large-scale structural coordination as a neural correlate of affective symptom burden in CID.
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