Brain research · 2026
Altered default mode network homogeneity in chronic insomnia disorder: modulation by modified suanzaoren decoction and estazolam, and machine learning classification.
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Wei Shubao, Zhang Leyi, Chen Xiuqiong, Han Yiding, Lv Dongsheng, Yao Ping, Chen Lixia, Yuan Yonggui, Zhao Jingping, Ou Yangpan, Guo Zhiguo, Guo Wenbin
Аннотация
OBJECTIVE: Chronic Insomnia Disorder (CID) is characterized by maladaptive self-referential thinking linked to default mode network (DMN) dysfunction. Network Homogeneity (NH), a measure of local functional integration within networks, may capture this dysregulation but remains underexplored in CID and its response to treatment, particularly herbal medicine.
METHODS: This study employed resting-state functional magnetic resonance imaging (fMRI) to investigate DMN NH in 82 patients with CID (52 treated with Modified Suanzaoren Decoction [MSZRD], 30 with Estazolam) and 65 matched healthy controls (HCs). NH was calculated for the DMN. Baseline differences, longitudinal treatment effects (mixed-effects model), and correlations with clinical scores were examined. A support vector machine (SVM) classifier used baseline NH features for diagnostic discrimination.
RESULTS: At baseline, CID patients exhibited widespread abnormal NH in DMN nodes, including the temporal lobes, precuneus, and orbitofrontal cortex (OFC), compared to HCs. Post-treatment, a significant time effect (increased NH) was found in the right inferior frontal orbital gyrus (IFOG) and right superior temporal gyrus (STG) across both groups. Crucially, a group-by-time interaction was identified in the right medial frontal orbital gyrus (MFOG), where NH increased after MSZRD but decreased after Estazolam. Baseline NH in temporal regions correlated positively with insomnia and anxiety severity. The SVM classifier achieved significant accuracy in distinguishing patients from HCs.
CONCLUSIONS: CID is characterized by dysfunctional integration within the DMN. MSZRD and Estazolam demonstrate both convergent and divergent neuromodulatory effects, with MSZRD uniquely altering NH in a key prefrontal regulatory hub.
METHODS: This study employed resting-state functional magnetic resonance imaging (fMRI) to investigate DMN NH in 82 patients with CID (52 treated with Modified Suanzaoren Decoction [MSZRD], 30 with Estazolam) and 65 matched healthy controls (HCs). NH was calculated for the DMN. Baseline differences, longitudinal treatment effects (mixed-effects model), and correlations with clinical scores were examined. A support vector machine (SVM) classifier used baseline NH features for diagnostic discrimination.
RESULTS: At baseline, CID patients exhibited widespread abnormal NH in DMN nodes, including the temporal lobes, precuneus, and orbitofrontal cortex (OFC), compared to HCs. Post-treatment, a significant time effect (increased NH) was found in the right inferior frontal orbital gyrus (IFOG) and right superior temporal gyrus (STG) across both groups. Crucially, a group-by-time interaction was identified in the right medial frontal orbital gyrus (MFOG), where NH increased after MSZRD but decreased after Estazolam. Baseline NH in temporal regions correlated positively with insomnia and anxiety severity. The SVM classifier achieved significant accuracy in distinguishing patients from HCs.
CONCLUSIONS: CID is characterized by dysfunctional integration within the DMN. MSZRD and Estazolam demonstrate both convergent and divergent neuromodulatory effects, with MSZRD uniquely altering NH in a key prefrontal regulatory hub.