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Altered brain network topological properties in insomniacs with prolonged sleep onset latency: a graph-based
Xuejiao Yin1, Rui Yin2, Yupei Hao1
1Beijing Key Laboratory of Acupuncture Neuromodulation, Department of Acupuncture and Moxibustion, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, 100010, China.
Background:
Chronic insomnia disorder (CID) is one of the most common but heterogeneous sleep disturbances with varied clinical manifestations. A more in-depth understanding of the brain functional deviations associated with symptom subtypes will help elucidate the mechanisms involved in CID. The present study examined the topological properties of the brain networks associated with the CID subtype, focusing particularly on prolonged sleep onset latency (SOL), to ascertain whether these properties mediate the diverse clinical subtypes of CID.
Methods:
Ninety-two participants were included in the study, comprising 42 CID patients with prolonged SOL (PSOL group), 24 CID patients with non-prolonged SOL (NPSOL group), and 26 sex- and age-matched good sleepers (GS group). Graph theoretical analysis was used to assess the brain network's global and nodal topological property deviations among these groups. Spearman's correlation analyses were performed to explore the relationship between topological properties and clinical measures.
Results:
Although the PSOL and NPSOL groups showed similar alterations in network topological properties compared with good sleepers, the PSOL group exhibited specific deviations from the NPSOL group, including reduced nodal efficiency (Ne) of the left ventral prefrontal cortex (vPFC) and increased global shortest path length (Lp). Notably, the decreased Ne in the vPFC and increased Lp both correlated with higher Sleep Latency Score (SLS) (r = -0.397, p < 0.001; r = 0.336, p = 0.001).
Conclusion:
Clinical subtypes of CID have shared and unique alterations in brain network topological properties. Prolonged SOL is particularly associated with disruptions in global information integration and impaired nodal transmission efficiency of vPFC. These findings shed new light on the neural mechanisms underlying CID heterogeneity.
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