Multimodal investigations of structural and functional brain alterations in anorexia and bulimia nervosa and their relationships to psychopathology

Biol Psychiatry. 2024 Nov 22:S0006-3223(24)01759-1. doi: 10.1016/j.biopsych.2024.11.008. Online ahead of print.

ABSTRACT

BACKGROUND: Neurobiological understanding of eating disorders (EDs) is limited. This study presents the first comparative multi-modal magnetic resonance imaging (MRI) assessments of anorexia nervosa (AN) and bulimia nervosa (BN), uncovering neurobiological differences associated with these disorders.

METHODS: This female case-control study included 57 healthy controls (HC) and 130 participants with EDs (BN and AN subtypes). Structural and functional MRI assessed gray matter volume (GMV), cortical thickness (CT), and task-based activities related to reward processing, social-emotional functioning, and response inhibition. Whole-brain group differences were correlated to ED psychopathology.

RESULTS: Significant structural differences were observed in the ED group compared to HCs, including reduced GMV in the left lateral orbitofrontal cortex and lower CT in the left rostral middle frontal gyrus and precuneus, after adjusting for BMI. Specific structural alterations were only evident in AN subgroups. GMV reductions in the orbitofrontal cortex were linked to impulsivity, while lower CT in the frontal gyrus correlated with cognitive restraint in eating, suggesting these regions may play key roles in ED psychopathology. Functional MRI also revealed notable differences. During reward anticipation, participants with EDs exhibited deactivations in the cerebellum and right superior frontal gyrus, alongside 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 underlying EDs, pointing to potential brain-based targets for developing specialized treatment.

PMID:39581292 | DOI:10.1016/j.biopsych.2024.11.008