Social anhedonia is associated with neural abnormalities during face emotion processing Laura T. Germine ⁎, Lucia Garrido, Lori Bruce, Christine Hooker Department of Psychology, Harvard University, 33 Kirkland Street, Cambridge, MA 02138, USA abstract article info Article history: Received 8 November 2010 Revised 10 June 2011 Accepted 23 June 2011 Available online 30 June 2011 Keywords: Social anhedonia Emotion recognition Face processing Facial expression recognition Schizophrenia Schizotypy Human beings are social organisms with an intrinsic desire to seek and participate in social interactions. Social anhedonia is a personality trait characterized by a reduced desire for social affiliation and reduced pleasure derived from interpersonal interactions. Abnormally high levels of social anhedonia prospectively predict the development of schizophrenia and contribute to poorer outcomes for schizophrenia patients. Despite the strong association between social anhedonia and schizophrenia, the neural mechanisms that underlie individual differences in social anhedonia have not been studied and are thus poorly understood. Deficits in face emotion recognition are related to poorer social outcomes in schizophrenia, and it has been suggested that face emotion recognition deficits may be a behavioral marker for schizophrenia liability. In the current study, we used functional magnetic resonance imaging (fMRI) to see whether there are differences in the brain networks underlying basic face emotion processing in a community sample of individuals low vs. high in social anhedonia. We isolated the neural mechanisms related to face emotion processing by comparing face emotion discrimination with four other baseline conditions (identity discrimination of emotional faces, identity discrimination of neutral faces, object discrimination, and pattern discrimination). Results showed a group (high/low social anhedonia) × condition (emotion discrimination/control condition) interaction in the anterior portion of the rostral medial prefrontal cortex, right superior temporal gyrus, and left somatosensory cortex. As predicted, high (relative to low) social anhedonia participants showed less neural activity in face emotion processing regions during emotion discrimination as compared to each control condition. The findings suggest that social anhedonia is associated with abnormalities in networks responsible for basic processes associated with social cognition, and provide a starting point for understanding the neural basis of social motivation and our drive to seek social affiliation. © 2011 Elsevier Inc. All rights reserved. Introduction As fundamentally social creatures, humans are driven by the desire for meaningful and frequent social interaction (Baumeister and Leary, 1995). There are individual differences in the strength of this desire, however, and some individuals exhibit a significantly reduced drive for social affiliation known as social anhedonia (Brown et al., 2007; Kwapil, 1998; Kwapil et al., 2009). Social anhedonia (SA) has been characterized as a deficiency in the need to belong to a social group and is distinct from other constructs that might also predict abnormalities in social interaction such as social anxiety (Brown et al., 2007; Kwapil et al., 2009). Individuals high in SA exhibit a genuine preference for solitude, disengagement during social interactions (Brown et al., 2007), and reduced negative affect when alone (Kwapil et al., 2009). Higher levels of SA are related to lower levels of social support and social functioning (Blanchard et al., 2011). Reduced social support and smaller social networks are associated with differences in immune functioning and other clinically significant health outcomes (Miller et al., 2009). Furthermore, high SA has been identified as one of the single most predictive traits for future onset of schizophrenia spectrum disorders (Kwapil, 1998) and has long been recognized as a core attribute of psychosis vulnerability (Bleuler, 1950; Horan et al., 2007; Kraepelin and Gosline, 1919; Meehl, 1962; Rado, 1953; Stone et al., 2005). Altogether, existing evidence indicates that SA is a deviation in a psychologically and clinically important social and emotional process that has broad implications for our understanding of normal and abnormal functioning. Despite evidence for serious physical and mental health difficulties associated with reduced desire for social affiliation, no research to our knowledge has been done exploring the neural basis of SA in nonclinical populations. In schizophrenia, SA is considered a negative symptom that is stable (Blanchard et al., 2001) and can be reliably assessed (Horan et al., 2006). Studies of SA in schizophrenia have indicated that a number of neural systems may be involved in reduced NeuroImage 58 (2011) 935–945 ⁎ Corresponding author at: 806 William James Hall, 33 Kirkland Street, Cambridge, MA 02138, USA. E-mail addresses: lgermine@fas.harvard.edu (L.T. Germine), garridolucia@gmail.com (L. Garrido), lbruce@wjh.harvard.edu (L. Bruce), chooker@wjh.harvard.edu (C. Hooker). 1053-8119/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.neuroimage.2011.06.059 Contents lists available at ScienceDirect NeuroImage journal homepage: www.elsevier.com/locate/ynimg