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Temporal and topological properties of dynamic networks reflect disability in patients with neuromyelitis optica spectrum disorders

视神经脊髓炎 医学 神经科学 物理医学与康复 心理学 精神科 多发性硬化
作者
Yao Wang,Ziwei Yang,Xiumei Zheng,Xiao Liang,Jin Chen,Ting He,Yanyan Zhu,Lin Wu,Muhua Huang,Ningnannan Zhang,Fuqing Zhou
出处
期刊:Scientific Reports [Nature Portfolio]
卷期号:14 (1) 被引量:1
标识
DOI:10.1038/s41598-024-54518-7
摘要

Abstract Approximately 36% of patients with neuromyelitis optica spectrum disorders (NMOSD) suffer from severe visual and motor disability (blindness or light perception or unable to walk) with abnormalities of whole-brain functional networks. However, it remains unclear how whole-brain functional networks and their dynamic properties are related to clinical disability in patients with NMOSD. Our study recruited 30 NMOSD patients (37.70 ± 11.99 years) and 45 healthy controls (HC, 41.84 ± 11.23 years). The independent component analysis, sliding-window approach and graph theory analysis were used to explore the static strength, time-varying and topological properties of large-scale functional networks and their associations with disability in NMOSD. Compared to HC, NMOSD patients showed significant alterations in dynamic networks rather than static networks. Specifically, NMOSD patients showed increased occurrence (fractional occupancy; P < 0.001) and more dwell times of the low-connectivity state ( P < 0.001) with fewer transitions ( P = 0.028) between states than HC, and higher fractional occupancy, increased dwell times of the low-connectivity state and lower transitions were related to more severe disability. Moreover, NMOSD patients exhibited altered small-worldness, decreased degree centrality and reduced clustering coefficients of hub nodes in dynamic networks, related to clinical disability. NMOSD patients exhibited higher occurrence and more dwell time in low-connectivity states, along with fewer transitions between states and decreased topological organizations, revealing the disrupted communication and coordination among brain networks over time. Our findings could provide new perspective to help us better understand the neuropathological mechanism of the clinical disability in NMOSD.
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