Automatic processing of emotional facial expressions as a function of social anhedonia.

Anhedonia is an important feature of major depression and schizophrenia-spectrum disorders. Few neuroimaging studies have investigated neural alterations in high anhedonia, isolated from other psychopathological variables, by including only participants without clinical diagnoses. The present study examined healthy individuals scoring high (N = 18) vs. low (N = 19) in social anhedonia, who were carefully selected from a sample of N = 282 participants. To examine differences in automatic brain responses to social-affective stimuli between high vs. 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), 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. No significant group differences in brain activation emerged in other regions known to be involved in emotion and reward processing, including the amygdala and nucleus accumbens. Our results suggest that high social anhedonia in otherwise healthy individuals is associated with exaggerated automatic reactivity in the thalamus, which is a brain structure that has been implicated in the mediation of attentional processes.

The serotonin transporter availability in untreated early-onset and late-onset patients with obsessive-compulsive disorder.

The pathogenetic role of central serotonin transporters (SERT) in obsessive-compulsive disorder (OCD) has been investigated in vivo by positron emission tomography (PET) or single-photon emission computed tomography (SPECT) studies with inconsistent results. This might reflect methodological differences but possibly also the pathophysiological heterogeneity of the disorder, i.e. the age at onset of OCD. The aim of our study was to compare SERT availability in patients with OCD to healthy controls (HC) taking into account the onset type, other factors and covariates (e.g. SERT genotype, age, depression level, gender). We studied 19 drug-naive OCD patients (36±13 yr, eight females) with early onset (EO-OCD, n=6) or with late onset (LO-OCD, n=13), and 21 HC (38±8 yr, nine females) with PET and the SERT-selective radiotracer [11C]DASB. Statistical models indicated that a variety of covariates and their interaction influenced SERT availability measured by distribution volume ratios (DVR). These models revealed significant effects of onset type on DVR with lower values in LO-OCD (starting at age 18 yr) compared to EO-OCD and HC in limbic (e.g. the amygdala), paralimbic brain areas (the anterior cingulate cortex), the nucleus accumbens and striatal regions, as well as borderline significance in the thalamus and the hypothalamus. The putamen, nucleus accumbens and hypothalamus were found with significant interaction between two SERT gene polymorphisms (SERT-LPR and VNTR). These findings suggest that late but not early onset of OCD is associated with abnormally low SERT availability. In part, functional polymorphisms of the SERT gene might determine the differences.