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Psychopathy is characterized by extensive emotional impairments. However, the current empirical literature on empathy and alexithymia in psychopathy provides heterogeneous results. Random-effects models were performed on studies examining the association between psychopathy and the Interpersonal Reactivity Index as well as the Toronto Alexithymia Scale-20. In total, 72 articles providing 716 effect sizes and representing 15,016 participants were included in the analyses. Furthermore, differences among psychopathy factors and the role of potential moderators were assessed. We found negative relationships between psychopathy and empathy (r = −0.31), empathic concern (r = −0.29), perspective taking (r = −0.22), and personal distress (r = −0.14). In addition, our results yielded positive relationships between psychopathy and alexithymia (r = 0.21), difficulty describing feelings (r = 0.20), difficulty identifying feelings (r = 0.16), and externally-oriented thinking (r = 0.15). The results varied by psychopathy factors, and some were moderated by gender. These findings suggest that psychopathy is associated with deficits in various empathic processes as well as with an impaired perception of one's own emotions. Moreover, the results highlight the necessity to investigate these deficits not only across overall constructs, but also across their factors to further improve the understanding of aberrant emotionality in psychopathy. • Psychopathy is associated with empathy deficits as well as with alexithymia. • The strength of association varies between specific psychopathy factors. • Gender moderates the association between psychopathy and alexithymia. [ABSTRACT FROM AUTHOR]

People with Autism Spectrum Disorder (ASD) have been reported to show atypical attention and evaluative processing, in particular for social stimuli such as faces. The usual measure in these studies is an explicit, subjective judgment, which is the culmination of complex-temporally extended processes that are not typically dissected in detail. Here we addressed a neglected aspect of social decision-making in order to gain further insight into the underlying mechanisms: the temporal evolution of the choice. We investigated this issue by quantifying the alternating patterns of gaze onto faces, as well as nonsocial stimuli, while subjects had to decide which of the two stimuli they preferred. Surprisingly, the temporal profile of fixations relating to choice (the so-called “gaze cascade”) was entirely normal in ASD, as were the eventual preference choices. Despite these similarities, we found two key abnormalities: people with ASD made choices more rapidly than did control subjects across the board, and their reaction times for social preference judgments were insensitive to choice difficulty. We suggest that ASD features an altered decision-making process when basing choice on social preferences. One hypothesis motivated by these data is that a choice criterion is reached in ASD regardless of the discriminability of the options. [ABSTRACT FROM AUTHOR]

Abstract: Deficits in social cognition seem to present an intermediate phenotype for schizophrenia, and are known to be associated with an altered amygdala response to faces. However, current results are heterogeneous with respect to whether this altered amygdala response in schizophrenia is hypoactive or hyperactive in nature. The present study used functional magnetic resonance imaging to investigate emotion-specific amygdala activation in schizophrenia using a novel adaptive emotion recognition paradigm. Participants comprised 11 schizophrenia outpatients and 16 healthy controls who viewed face stimuli expressing emotions of anger, fear, happiness, and disgust, as well as neutral expressions. The adaptive emotion recognition approach allows the assessment of group differences in both emotion recognition performance and associated neuronal activity while also ensuring a comparable number of correctly recognized emotions between groups. Schizophrenia participants were slower and had a negative bias in emotion recognition. In addition, they showed reduced differential activation during recognition of emotional compared with neutral expressions. Correlation analyses revealed an association of a negative bias with amygdala activation for neutral facial expressions that was specific to the patient group. We replicated previous findings of affected emotion recognition in schizophrenia. Furthermore, we demonstrated that altered amygdala activation in the patient group was associated with the occurrence of a negative bias. These results provide further evidence for impaired social cognition in schizophrenia and point to a central role of the amygdala in negative misperceptions of facial stimuli in schizophrenia. [Copyright &y& Elsevier]

Background Addicts to specific internet applications involving communication features showed increased social anxiety, emotional competence deficits and impaired prefrontal-related inhibitory control. The dorsal Anterior Cingulate Cortex (dACC) likely plays an important role in cognitive control and negative affect (such as social exclusion, pain or anxiety). Aim To assess (social) anxiety-related inhibitory control in specific internet addiction (addicted use of games and social networks) and its relation to altered dACC activation. Methods N = 44 controls and n = 51 specific internet addicts completed an anxious words-based Affective Go/No-Go task (AGN). A subsample of n = 23 healthy controls and n = 25 specific internet addicts underwent functional Magnetic Resonance Imaging (fMRI) while completing an Emotional Stroop Task (EST) with socially anxious, positive, negative and neutral words. Subgroups of internet gaming and social network addicts were exploratively assessed. Psychometric measures of social anxiety, emotional competence and impulsivity were additionally explored. Results Specific internet addicts showed higher impulsivity, social anxiety and reduced emotional competence. Between-group differences in AGN and EST behavioral measures were not detected. No group differences were found in the dACC, but explorative analyses revealed decreased left middle and superior temporal gyrus activation during interference of socially anxious words in internet gaming and relative to social network addicts. Conclusion Given the function of the left middle temporal gyrus in the retrieval of words or expressions during communication, our findings give a first hint that social words might be less retrievable in the semantic storage of internet gaming addicts, possibly indicating deficiencies in handling speech in social situations. [ABSTRACT FROM AUTHOR]

Detecting and evaluating emotional information from facial expressions as a basis for behavioural adaption belong to the core social-cognitive abilities of mankind. Dysfunctions in emotional face processing are observed in several major psychiatric disorders like depression and schizophrenia. In search for psychiatric disease biomarkers using the imaging genetics approach, serotonergic gene polymorphisms have been associated with altered brain circuit activation during emotional face processing. Especially the 5-HTTLPR gene polymorphism has been extensively investigated in association with emotion regulation processes. In this article, imaging genetics literature on emotional face processing, reporting genetic effects of 5-HTTLPR in healthy volunteers is reviewed. Additionally, these results are regarded in relation to pharmacologic challenge (antidepressants, acute tryptophan depletion) imaging studies and discussed in light of recent neurobiological evidence with a focus on serotonin (5-HT 1A , 5-HT 2C , 5-HT 2A ) receptor findings. [ABSTRACT FROM AUTHOR]

Abstract: Dopamine is known as the main neurotransmitter modulating the activation of the reward system of the brain. The DRD2 TaqIA polymorphism is associated with dopamine D2 receptor density which plays an important role in the context of reward. Persons carrying an A1 allele have a lower D2 receptor density and a higher risk to show substance abuse. The present study was designed to investigate the influence of the DRD2 TaqIA polymorphism and the selective D2 receptor agonist bromociptine on the activation of the reward system by means of functional magnetic resonance imaging (fMRI). In a double-blind crossover study with 24 participants we found an increase of reward system activation from placebo to bromocriptine only in subjects carrying the A1 allele. Furthermore, only A1 carrier showed an increase of performance under bromocriptine. The results are interpreted as reflecting a specific sensitivity for dopamine agonists in persons carrying an A1 allele and may complement actual data and theories of the development of addiction disorders postulating a higher genetic risk for substance abuse in carrier of the A1 allele. [Copyright &y& Elsevier]

Prior studies with schizophrenia patients described a reduced ability to discriminate between correct and false memories in terms of confidence compared to control groups. This metamemory bias has been associated with the emergence and maintenance of delusions. The relation to neuropsychological performance and other clinical dimensions is incompletely understood. In a cross-sectional study, metamemory functioning was explored in 32 schizophrenia patients and 25 healthy controls. Metamemory was assessed using a verbal recognition task combined with retrospective confidence level ratings. Associations of metamemory performance with six neuropsychological domains (executive functioning/problem solving, speed of processing, working memory, verbal and visual learning, and attention/vigilance) and psychopathological measures were analyzed. Results revealed a significantly smaller discrepancy between confidence ratings for correct and incorrect recognitions in the patient group. Furthermore, patients showed significantly lower recognition accuracy in the metamemory task and marked deficits in all neuropsychological domains. Across all participants, metamemory performance significantly correlated with executive functioning and working memory. No associations with delusions were found. This data confirms prior findings of metamemory biases in schizophrenia. Selective neuropsychological abilities seem to be modulating factors of metamemory functioning. Longitudinal studies in at risk mental state and first-episode patients are needed to reveal causal interrelations. [ABSTRACT FROM AUTHOR]

Objective Previous studies demonstrated that a history of childhood trauma is linked to mental disorders in adulthood, particularly to depression. Adverse childhood experiences are also considered to contribute to the risk of hypochondriasis, but the results of previous studies have not been conclusive with respect to the strength and specificity of this association. Therefore, we compared the association of adverse childhood experiences with both hypochondriasis and depression. Methods Fifty-eight patients with hypochondriasis, 52 patients with depression, and 52 healthy control participants completed the Childhood Trauma Questionnaire (CTQ) which assesses 5 varieties of abuse and neglect. A clinical interview (SCID-I) was used to establish DSM-IV diagnoses. Associations between childhood maltreatment, hypochondriasis and depression were estimated by means of analyses of variance and multiple linear regression analyses. Results In comparison to hypochondriacal and healthy participants, patients with a current depressive disorder reported more emotional abuse as well as more emotional and physical neglect during childhood. Patients with hypochondriasis reported more emotional neglect than healthy individuals. However, when predicting the CTQ trauma types by diagnostic category adjusting for sex and comorbid DSM-IV diagnoses, emotional abuse, emotional neglect, physical abuse, physical neglect, as well as the CTQ total score were significantly associated with depression, but none of the CTQ scores was significantly related to hypochondriasis. Conclusions The findings suggest a robust association of childhood maltreatment with depression but not with hypochondriasis. This result does not support etiological models of hypochondriasis which rely on childhood maltreatment as a risk factor for the development of this disorder. [ABSTRACT FROM AUTHOR]

Abstract: To gain further insight into interpersonal dysfunction in Borderline Personality Disorder (BPD) we investigated the effects of emotional cues and the fairness of a social partner on the ability to infer other peoples'' intentions in a virtual social exchange. 30 BPD patients and 30 nonpatients were asked to play a multiround trust game with four virtual trustees. The trustees varied in regard to fairness and presence of emotional facial cues which were both linked to repayment ratio. BPD patients adjusted their investment to the fairness of their partner. In contrast, nonpatients disregarded the trustees'' fairness in the presence of emotional facial expressions. Both groups performed equally in an emotion recognition task and assessed the trustees'' fairness comparably. When the unfair trustee provided emotional cues, BPD patients assessed their own behavior as more fair, while the lack of cues led patients to assess their own behavior as unfair. BPD patients are superior in the attribution of mental states to interaction partners when emotional cues are present. While the emotional expressions of a partner dominated the exchange behavior in nonpatients, BPD patients used the objective fairness of their social counterparts to guide their own behavior despite the existence of emotional cues. [Copyright &y& Elsevier]

Background: Genome-wide association studies are a powerful tool for unravelling the genetic background of complex disorders such as major depression. Methods: We conducted a genome-wide association study of 604 patients with major depression and 1364 population based control subjects. The top hundred findings were followed up in a replication sample of 409 patients and 541 control subjects. Results: Two SNPs showed nominally significant association in both the genome-wide association study and the replication samples: 1) rs9943849 (p combined = 3.24E-6) located upstream of the carboxypeptidase M (CPM) gene and 2) rs7713917 (p combined = 1.48E-6), located in a putative regulatory region of HOMER1. Further evidence for HOMER1 was obtained through gene-wide analysis while conditioning on the genotypes of rs7713917 (p combined = 4.12E-3). Homer1 knockout mice display behavioral traits that are paradigmatic of depression, and transcriptional variants of Homer1 result in the dysregulation of cortical-limbic circuitry. This is consistent with the findings of our subsequent human imaging genetics study, which revealed that variation in single nucleotide polymorphism rs7713917 had a significant influence on prefrontal activity during executive cognition and anticipation of reward. Conclusion: Our findings, combined with evidence from preclinical and animal studies, suggest that HOMER1 plays a role in the etiology of major depression and that the genetic variation affects depression via the dysregulation of cognitive and motivational processes. [ABSTRACT FROM AUTHOR]