Anhedonia in the psychosis risk syndrome: associations with social impairment and basal orbitofrontal cortical activity.

Victoria L Cressman,Scott A Schobel,Scott A Small,Shelly Ben-David,Holly Moore,Sara Steinfeld,Judy L Thompson,Cheryl M Corcoran

doi:10.1038/npjschz.2015.20

Abstract

Background/Objectives:Anhedonia is associated with poor social function in schizophrenia. Here, we examined this association in individuals at clinical high risk (CHR) for schizophrenia and related psychotic disorders, taking into account social anxiety. We then explored correlations between anhedonia and basal metabolic activity in selected forebrain regions implicated in reward processing.Methods:In 62 CHR individuals and 37 healthy controls, we measured social adjustment (Social Adjustment Self-Report Scale), social and physical anhedonia (Chapman Revised Anhedonia Scales), and social anxiety (Social Anxiety Scale for Adolescents) in cross-section. In a subgroup of 25 CHR individuals for whom high-spatial-resolution basal-state functional magnetic resonance imaging data were available, we also assessed correlations of these socio-affective constructs with basal cerebral blood volume in orbitofrontal cortex and related regions involved in reward processing.Results:Relative to controls, CHR individuals reported social impairment, greater social and physical anhedonia, and more social anxiety, exhibiting impairments comparable to schizophrenia. Regression analyses showed that anhedonia predicted social impairment and correlated negatively with basal cerebral blood volume within the orbitofrontal cortex (all P’s<0.05).Conclusions:Anhedonia and social anxiety are prominent in CHR individuals. Trait-like anhedonia may be a core phenotype related to orbitofrontal cortical function that, independent of symptoms, predicts social impairment. These data provide a rationale for interventions that target anhedonia and related activity in orbitofrontal cortical circuits in CHR individuals.

Highlights

Social impairment is prevalent in schizophrenia, accounting for much of its morbidity.[1]
Our second aim was to examine the hypothesis that anhedonia in clinical high-risk (CHR) individuals is related to activity in the orbitofrontal corticostriatal pathways, circuits recruited during the experience of both imagined and real rewards.[29,30,31]
No significant differences were seen between CHR individuals (n = 62) and controls (n = 37) in age, gender, ethnicity, country of birth, and intelligence quotient (IQ) (Table 1); variance was similar between the two groups

Summary

Introduction

Social impairment is prevalent in schizophrenia, accounting for much of its morbidity.[1]. Our first aim was to evaluate the contribution of anhedonia to social impairment in CHR individuals while considering social anxiety. We hypothesized that both constructs would predict social impairment, but that anhedonia would be the primary contributor. Our second aim was to examine the hypothesis that anhedonia in CHR individuals is related to activity in the orbitofrontal corticostriatal pathways, circuits recruited during the experience of both imagined and real rewards.[29,30,31] In a subset of our CHR cohort for which high-resolution basal-state functional magnetic

Methods

Results

Discussion

Conclusion