P 10 Automatic processing of masked facial emotions in social anhedonia

• Published in: Clinical neurophysiology 2017-10, Vol.128 (10), p.e331-e331
• Main Authors: Günther, V., Zimmer, J., Lobsien, D., Suslow, T.
• Format: Article
• Language: English
• ISSN: 1388-2457; 1872-8952
• DOI: 10.1016/j.clinph.2017.06.089

Anhedonia, the reduced ability to experience pleasure, is a prominent feature of major depression and schizophrenia-spectrum disorders. Anhedonia is not only a state accompanying psychiatric disorders but is also considered as a personality trait, which might increase the susceptibility to psychiatric disorders. Only few neuroimaging studies investigated neural alterations in high anhedonia, isolated from other psychopathological variables, by including only participants without clinical diagnoses. Although findings from previous studies in healthy populations are rather heterogeneous, prior research suggests neurobiological alterations in the perception of emotional and rewarding stimuli as underlying mechanisms in the manifestation of anhedonia. The present study examined healthy individuals scoring high vs. low in social anhedonia, thoroughly selected from a sample of N=282 participants. As a subtype of reduced hedonic capacity in general, social anhedonia refers to a diminished hedonic experience in interpersonal contacts. In order to reveal differences in automatic brain responses to social-affective stimuli between high compared to low social anhedonia participants, we used functional magnetic resonance imaging. To assess early, automatic stages of emotion processing, we administered a paradigm presenting brief (33ms) and backward-masked happy, sad, and neutral facial expressions. Individuals high in social anhedonia demonstrated increased activation in the bilateral thalamus and left red nucleus in response to masked sad faces relative to individuals low in social anhedonia. Regardless of stimulus valence, no significant group differences in brain activation emerged in other regions known to be involved in emotion and reward processing, including amygdala and nucleus accumbens. Our results suggest that high social anhedonia in otherwise healthy individuals is associated with exaggerated automatic reactivity in the thalamus, a brain structure that has been implicated in the pathophysiology of major depression. Heightened processing of depression-related stimuli in the thalamus might be a mechanism through which social anhedonia increases the vulnerability to major depression.