Abstract
BACKGROUND: Anorexia nervosa (AN) and bulimia nervosa (BN) are two primary subtypes of eating disorders (ED), often presenting with overlapping clinical features that complicate diagnosis. Despite shared symptoms, the underlying neural mechanisms of two subtypes remain incompletely understood. Delineating both shared and unique neural alterations may support biomarker discovery and inform targeted interventions. METHODS: We recruited 28 patients with AN, 26 with BN, and 31 matched healthy controls (HC), aged from 14 to 40 years old. Resting-state functional magnetic resonance image (Rs-fMRI) data were acquired to investigate alterations in spontaneous brain activity. Four voxel-wise metrics were analyzed: amplitude of low-frequency fluctuation (ALFF), fractional amplitude of low-frequency fluctuation (fALFF), regional homogeneity (ReHo), and degree centrality (DC). Symptom severity was assessed using the Eating Disorder Examination-Questionnaire (EDEQ), which includes four subscales: Eating concern (EDEQ_E), Shape concern (EDEQ_S), Weight concern (EDEQ_W), and Restraint (EDEQ_R). Pearson correlation analysis was used to examine associations between altered imaging metrics and clinical variables. RESULTS: Both AN and BN exhibited convergent alterations, including reduced activity in the bilateral middle frontal gyrus (MFG), insular cortex (INS), superior temporal gyrus (STG), and left parahippocampal gyrus (PHG), alongside increased activity in the bilateral striatum, middle occipital gyrus (MOG), and cerebellum. Disorder-specific alterations in AN included increased activity in the right striatum and right precuneus, increased DC in the right superior frontal gyrus (SFG), and decreased fALFF and DC in the left calcarine. In contrast, patients with BN exhibited elevated fALFF in the right precentral gyrus (PCG_R) and increased DC in the right calcarine. Correlation analyses revealed negative association between the ReHo value of the MOG_L and EDEQ, and positive associations between the DC value of the PCG_R and EDEQ and EDEQ_E in patients with BN. CONCLUSION: Our findings revealed both shared and diagnosis-specific alterations in intrinsic brain activity within the cortico- striatal-limbic circuit, underscoring its role in the pathophysiology of ED.