Impaired executive control of emotional information in social anhedonia

Psychology Department, Harvard University, Cambridge, MA, USA.
Psychiatry Research (Impact Factor: 2.47). 03/2012; 197(1-2):29-35. DOI: 10.1016/j.psychres.2011.12.023
Source: PubMed


We examined the executive control of emotional information and its relationship to social functioning in individuals at risk for schizophrenia, defined by high social anhedonia (SA). Using the same structure as the Attentional Network Test (ANT), we developed a measure of executive control of emotional information (ANT-Emotion) in which subjects identify the direction of an arrow flanked by irrelevant angry or neutral faces. Subjects completed the ANT, ANT-Emotion, and the Social Adjustment Scale, Self-Report (SAS-SR), a measure of social functioning. While there were no group differences in the alerting, orienting, and executive control networks assessed by the ANT, high SA individuals exhibited a specific impairment in the executive control of emotional information. High SA individuals also reported poorer social functioning. However, executive control of emotional information did not mediate the relationship between SA and social functioning. These findings indicate that, in high-risk populations, the impaired ability to inhibit emotional information allows negative affective stimuli to exert inappropriate influence on cognitive processes. These results are consistent with studies indicating similar findings in schizophrenia patients, suggesting that impaired inhibition of negative emotion may be part of the liability for the disorder.

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Available from: Laura M Tully, Jun 02, 2014
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    • "However, despite evidence demonstrating attentional control deficits in SA, the impact of these deficits on social functioning is rarely considered. In our previous work, we found high SA individuals demonstrated deficits in the attentional control of emotion information on an experimental task specifically designed to assess the ability to inhibit task-incongruent irrelevant negative faces, but these deficits did not relate to social impairments (Tully et al., 2012). However, highly specific experimental tasks may be too narrow to capture the effect of attentional control on social functioning. "
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    ABSTRACT: Social anhedonia (SA), a trait-like disinterest in social contact and diminished capacity to experience pleasure from social interactions, is consistently associated with social impairments in both healthy and clinical populations. However, the mechanisms underlying the relationship between SA and social impairment are poorly understood. Attentional control, selecting and focusing on relevant information and inhibiting irrelevant, may be one such mechanism. We examined individual differences in SA, attentional control, and social impairment in 108 healthy adults. High SA related to low attentional control and high social impairment. Moreover, attentional control mediated the relationship between SA and social impairment, establishing attentional control as one mechanism underlying aberrations in the fundamental human need for social contact. Although both attentional deficits and social impairment have been separately noted in SA, the relationship between SA, attentional control and social impairment in this non-clinical sample reflects a novel contribution.
    Full-text · Article · Dec 2014 · Frontiers in Psychology
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    • "There is a growing body of evidence that anhedonia, particularly in its social form, could be related to abnormalities in emotional processing in clinical and nonclinical populations. Nonclinical individuals with high level of social anhedonia demonstrate a deficit in the executive control of socially relevant emotional information (Tully, Lincoln, & Hooker, 2012). For instance, participants with a high level of social anhedonia (who scored 2 standard deviations above the same-gender sample mean on the Chapman's Revised Social Anhedonia Scale) exhibited an increased sensitivity to affectively valenced targets as compared to controls on a word pronunciation task, whereas they did not exhibit increased semantic priming (Kerns & Berenbaum, 2000). "
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    ABSTRACT: The present study investigated the ERP correlates of the integration of emotional prosody to the emotional meaning of a spoken word. Thirty-four nonclinical participants listened to negative and positive words that were spoken with an angry or happy prosody and classified the emotional valence of the word meaning while ignoring emotional prosody. Social anhedonia was also self-rated by the subjects. Compared to congruent trials, incongruent ones elicited slower and less accurate behavioral responses, and a smaller P300 component at the brain response level. The present data suggest that vocal emotional information is salient enough to be integrated early in verbal processing. The P300 amplitude modulation by the prosody-meaning congruency positively correlated with the social anhedonia score, suggesting that the sensitivity of the electrical brain response to emotional prosody increased with social anhedonia. Interpretations of this result in terms of emotional processing in social anhedonia are discussed.
    Full-text · Article · Jan 2014 · Journal of Psychophysiology
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    ABSTRACT: Background: Genetic susceptibility to schizophrenia (SZ) has been suggested to influence the cortical systems supporting working memory (WM) and face processing. Genetic imaging studies link the SZ risk variant rs1344706 on the ZNF804A gene to psychosis via alterations in functional brain connectivity during WM, but no work has looked at the effects of ZNF804A on WM with face-processing components. Methods: We therefore investigated healthy controls that were genotyped for rs1344706 with a face WM task during functional magnetic resonance imaging. We suggested that variation at the rs1344706 locus would be associated with similar alterations as patients previously tested using the same WM task for faces. Results: The rs1344706 risk allele was indeed associated with altered activation in the right dorsolateral prefrontal (rDLPFC) cortex. We established that the rDLPFC was activated in a task-dependent manner, suggesting that the differences in activation between rs1344706 genotype groups reflected alterations in task processing. Furthermore, we demonstrated that the rDLPFC region showed significant volumetric overlap with the rDLPFC which had previously been reported to be altered during task processing for patients with SZ. Conclusions: The findings support an association between rs1344706 and alterations in DLPFC activity during WM for faces. We further suggest that WM for faces may be a useful intermediate phenotype in the investigation of genetic susceptibility to psychosis.
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