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

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

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.

Conflict of interest statement

Dr SASc is a full-time employee of F Hoffmann-La Roche Ltd, in the role of translational medicine leader. Dr SASc’s work on the projects reported herein occurred prior to his assuming employment at Roche. The remaining authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mean scores for healthy controls (black bars) and clinical high-risk patients (CHR; gray bars) for measures of social adjustment impairment, anhedonia and social anxiety. Error bars represent the s.e.m. (a) SAS-SR (b) total scores for the Chapman Revised Anhedonia Scales (c) Chapman Social and Physical Anhedonia Scales. (d) SAS-A. (e) SAS-A subscales: FNE, social avoidance specific to new situations or unfamiliar peers (new situations), and social avoidance and distress in general (generalized). Higher scores indicate greater impairment on all scales. *Student’s t-test for group comparisons of CHR patients and healthy controls, P<0.01 (two tailed). CHR, clinical high risk; FNE, fear of negative evaluation; SAS-A, Social Anxiety Scale for Adolescents; SAS-SR, Social Adjustment Scale Self-Report.
Figure 2
Figure 2
Scatterplots and correlations in clinical high-risk patients of social impairment with (a) total anhedonia and (b) total social anxiety. Pearson’s correlations; **P<0.001; Pearson’s correlation (trend) &P=0.05.
Figure 3
Figure 3
Correlation between anhedonia and basal cerebral blook volume in the orbitofrontal cortex. (a) Region of interest contours for the orbitofrontal cortex (in violet). (b) Correlation of resting CBV with total anhedonia. Pearson’s correlation; *P<0.05. CBV, cerebral blood volume.

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Source: PubMed

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