To identify altered inter-hemispheric communication between patients with primary insomnia (PIs) and good sleepers (GSs), and their relationships with sleep and emotion-related parameters. Forty-eight PIs and 48 status-matched GSs were… Click to show full abstract
To identify altered inter-hemispheric communication between patients with primary insomnia (PIs) and good sleepers (GSs), and their relationships with sleep and emotion-related parameters. Forty-eight PIs and 48 status-matched GSs were asked to complete a number of sleep and emotion-related questionnaires. Voxel-mirrored homotopic connectivity(VMHC) and seed-based functional connectivity were used to characterize the inter-hemispheric coordination. Seven PIs were examined twice to evaluate the test-retest reliability. Support vector machine and ROC curve were applied to discriminate the two groups. Pearson correlation and mediating causality analysis were used to describe the relationships between insomnia-related brain networks and sleep/emotion-related parameters. High test-retest stability (intraclass correlation coefficient ≥ 0.8) of the VMHC maps was observed. Intra-, and inter-hemispheric coordination dysfunctions of the default mode network, visual pathways and executive control network were found. These differences received good discriminatory power to distinguish the two groups (AUC, 0.887; sensitivity, 81.3%; specificity, 87.5%). Intra-, and inter-hemispheric communication within the default mode network and visual pathways correlated with and partially mediated the insomnia-related parameters, while the executive control network correlated with post-insomnia negative emotions. Altered inter-hemispheric coordination within the default mode network and visual pathway may be identified as core predisposing or perpetuating factors in the etiology of PIs, while the executive control network may underlie the post-insomnia negative emotional symptoms. These findings may suggest that the inter-hemispheric communication might be potential neuroimaging markers to discribe underlie neurobiological mechanism of PIs and expand our understanding of the etiology of PIs.
               
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