Multimodal Investigations of Structural and Functional Brain Alterations in Anorexia and Bulimia Nervosa and Their Relationships to Psychopathology.
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Yu Xinyang, Robinson Lauren, Bobou Marina, Zhang Zuo, Banaschewski Tobias, Barker Gareth J, Bokde Arun L W, Flor Herta, Grigis Antoine, Garavan Hugh, Gowland Penny, Heinz Andreas, Brühl Rüdiger, Martinot Jean-Luc, Paillère Martinot Marie-Laure, Artiges Eric, Nees Frauke, Orfanos Dimitri Papadopoulos, Lemaître Hervé, Poustka Luise, Hohmann Sarah, Holz Nathalie, Bäuchl Christian, Smolka Michael N, Stringaris Argyris, Walter Henrik, Whelan Robert, Sinclair Julia, Schumann Gunter, Schmidt Ulrike, Desrivières Sylvane, IMAGEN, STRATIFY, and ESTRA Consortia
Аннотация
METHODS: This case-control study included 57 healthy female control participants and 130 female participants with EDs (bulimia nervosa and anorexia nervosa subtypes). Structural and functional magnetic resonance imaging assessed gray matter volume (GMV), cortical thickness, and task-based activities related to reward processing, socioemotional functioning, and response inhibition. Whole-brain group differences were correlated with ED psychopathology.
RESULTS: Significant structural differences were observed in the ED group compared with healthy control participants, including reduced GMV in the left lateral orbitofrontal cortex and lower cortical thickness in the left rostral middle frontal gyrus and precuneus after adjusting for body mass index. Specific structural alterations were only evident in anorexia nervosa subgroups. GMV reductions in the orbitofrontal cortex were linked to impulsivity, while lower cortical thickness in the frontal gyrus correlated with cognitive restraint in eating, suggesting that these regions may play key roles in ED psychopathology. Functional magnetic resonance imaging also revealed notable differences. During reward anticipation, participants with EDs exhibited deactivations in the cerebellum and right superior frontal gyrus together with reduced activation in the left lingual gyrus. These functional changes were associated with heightened neuroticism. Mediation analyses suggested that starvation-related GMV reductions in EDs disrupt reward-related brain function, increase neuroticism, and reinforce cognitive restraint, likely contributing to the persistence of ED symptoms.
CONCLUSIONS: These findings illuminate key neurobehavioral mechanisms that underlie EDs and point to potential brain-based targets for developing specialized treatment.