Abstract

Patients with anorexia nervosa (AN) display impaired social interactions, implicated in the development and prognosis of the disorder. Importantly, social behavior is modulated by reward-based processes, and dysfunctional at-brain-level reward responses have been involved in AN neurobiological models. However, no prior evidence exists of whether these neural alterations would be equally present in social contexts. In this study, we conducted a cross-sectional social-judgment functional magnetic resonance imaging (fMRI) study of 20 restrictive-subtype AN patients and 20 matched healthy controls. Brain activity during acceptance and rejection was investigated and correlated with severity measures (Eating Disorder Inventory -EDI-2) and with personality traits of interest known to modulate social behavior (The Sensitivity to Punishment and Sensitivity to Reward Questionnaire). Patients showed hypoactivation of the dorsomedial prefrontal cortex (DMPFC) during social acceptance and hyperactivation of visual areas during social rejection. Ventral striatum activation during rejection was positively correlated in patients with clinical severity scores. During acceptance, activation of the frontal opercula-anterior insula and dorsomedial/dorsolateral prefrontal cortices was differentially associated with reward sensitivity between groups. These results suggest an abnormal motivational drive for social stimuli, and involve overlapping social cognition and reward systems leading to a disruption of adaptive responses in the processing of social reward. The specific association of reward-related regions with clinical and psychometric measures suggests the putative involvement of reward structures in the maintenance of pathological behaviors in AN.

Highlights

  • Anorexia nervosa (AN) is a severe and disabling psychiatric disorder

  • Depressive and anxiety symptoms were higher in patients compared to controls, but Bonferroni-corrected statistical significance was only observed for depressive symptoms (Table 1)

  • Our results suggest a possible link between altered patterns of social relationships in AN and dysfunctional reward-related brain responses

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Summary

Introduction

With limited evidencebased treatments available, at least 25% of patients show poor clinical outcome and high levels of functional and social impairment [1,2,3,4,5]. These data highlight the need for a better understanding of the underlying pathophysiological bases of AN, including the identification and precise delineation of the complex neural systems involved [6]. Little is known about the neural substrates responsible of these abnormal responses to social stimuli or their relevance in the disorder

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