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Aberrant large- and mesoscale network segregation and integration in bulimia nervosa
Peng Zhang1, Lirong Tang2,3, Weihua Li1
1Department of Radiology, Beijing Friendship Hospital, Capital Medical University, No. 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Background:
Growing evidence indicates that bulimia nervosa (BN) is more likely driven by network-level dysfunctions rather than abnormalities in isolated brain regions. However, previous studies focusing on specific regions or connectivity features have led to a limited understanding of the complexity and integrality of network in BN. This study aimed to investigate large- and mesoscale network alterations in BN from the perspective of network segregation and integration.
Methods:
Using resting-state functional magnetic resonance imaging data from 85 BN patients and 71 healthy controls (HCs) matched for age, sex, and education, we applied a graph-theoretic framework to analyze functional network architecture in BN. Specifically, we examined group differences in within- and between-system functional connectivity (FC) as well as system segregation at both the whole-brain and system levels. Associations between network measures and clinical features were further explored.
Results:
Compared with HCs, BN patients exhibited whole-brain reduced within- and between-system FC accompanied by increased system segregation. At the system level, patients showed increased between-system FC of the default mode network (DMN), control network and ventral attention network, along with decreased DMN system segregation. The increased integration of DMN with other systems was associated with higher Beck Depression Inventory (BDI-21) scores in BN patients.
Conclusions:
The neural mechanisms of BN involve an imbalance between network segregation and integration at both global and system levels, most pronounced within the DMN, whose alterations are associated with depression and disordered eating behavior. These findings may provide potential neural substrates for some core behavioral deficits in BN.
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