Bulimia nervosa (BN) is characterized by episodic binge eating and purging behaviors. Disrupted neural processes of self-regulation, taste-rewarding, and body image has been associated with the pathogenesis of BN. However, the structural basis for these behavioral and functional deficits remains largely unknown. We employed diffusion tensor imaging and graph theory approaches (including the nodal properties and network-based statistics (NBS)) to characterize the whole-brain structural network of 48 BN and 44 healthy women. For nodal measures of strength, local efficiency, and betweenness centrality, BN patients displayed abnormal increases in multiple left-lateralized nodes within the mesocorticolimbic reward circuitry (including the orbitofrontal cortex, anterior cingulate, insular, medial temporal, and subcortical areas), lateral temporal-occipital cortex, and precuneus, while reduced global efficiency was observed in the right-lateralized nodes within the dorsolateral prefrontal cortex, mesocorticolimbic circuitry, somatosensory and visuospatial system. Several mesocorticolimbic nodes significantly correlated with BN symptoms. At a network level, we found increased left-lateralized connections primarily within the orbitofrontal cortex and its connections to mesocorticolimbic and lateral temporal-occipital areas, but reduced right-lateralized connections across the inferior frontal gyrus and insula, as well as their connections to the lateral temporal cortex. This study revealed BN-related changes in white-matter connections across the prefrontal control, mesocorticolimbic reward, somatosensory and visuospatial systems. The hemispheric-specific change could be an important aspect of the pathophysiology of BN. By characterizing whole-brain structural network changes of BN, our study provides novel evidence for understanding the behavioral and functional deficits of the disorder.
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