Disturbances In Social Cognition Research Articles

The association between cannabis use and facial emotion recognition in schizophrenia, siblings, and healthy controls: Results from the EUGEI study

Schizophrenia is frequently accompanied with social cognitive disturbances. Cannabis represents one established environmental factor associated with the onset and progression of schizophrenia. The present cross-sectional study aimed to investigate the association of facial emotion recognition (FER) performance with cannabis use in 2039 patients with schizophrenia, 2141 siblings, and 2049 healthy controls (HC). FER performance was measured using the Degraded Facial Affect Recognition Task (DFAR). Better FER performance as indicated by higher DFAR-total scores was associated with lifetime regular cannabis use in schizophrenia (B = 1.36, 95% CI 0.02 to 2.69), siblings (B = 2.17, 95% CI 0.79 to 3.56), and HC (B = 3.10, 95% CI 1.14 to 5.06). No associations were found between DFAR-total and current cannabis use. Patients with schizophrenia who started to use cannabis after the age of 16 showed better FER performance than patients who started earlier (B = 2.50, 95% CI 0.15 to 4.84) and non-users (B = 3.72, 95 CI 1.96 to 5.49). Better FER performance was found also in siblings who started to use cannabis after 16 compared to non-users (B = 2.37, 95% CI 0.58 to 4.16), while HC using cannabis performed better than non-users at DFAR-total regardless of the age at onset. Our findings suggest that lifetime regular cannabis use may be associated with better FER regardless of the psychosis risk, but that FER might be moderated by age at first use in people with higher genetic risk. Longitudinal studies may clarify whether there is a cause-and-effect relationship between cannabis use and FER performance in psychotic and non-psychotic samples.

Pharmacological interventions for social cognitive impairments in schizophrenia: A protocol for a systematic review and network meta-analysis.

BackgroundSocial cognitive impairments adversely affect social functioning (e.g., employment status) in patients with schizophrenia. Although pharmacological interventions have been suggested to provide some benefits on social cognition, little information is available on the comparative efficacy of pharmacotherapy. Thus, the aim of this planned systematic review and network meta-analysis is to perform a quantitative comparison of the effects of various psychotropic drugs, including supplements, on social cognition disturbances of schizophrenia.MethodsThe literature search will be carried out using the PubMed, Embase, Cochrane Central Register of Controlled Trials, PsycINFO, ClinicalTrials.gov, and International Clinical Trials Registry Platform databases from inception onward. Randomized controlled trials that examined the efficacy of drugs in social cognitive disturbances will be included, based on the most recent studies and the broader literature than previously searched. This protocol defines a priori the methods that will be used for study selection, data collection, quality assessment, and statistical syntheses.DiscussionThe findings this work are expected to help promote the development of better therapeutics of social cognitive impairments in schizophrenia and related psychiatric conditions.Systematic Review Registration[www.crd.york.ac.uk/prospero], identifier [CRD42021293224].

Social Perception Deficit as a Factor of Vulnerability to Psychosis: A Brief Proposal for a Definition.

Disturbances in social cognition are a core feature of schizophrenia. While most research in the field has focused on emotion perception, social knowledge, theory of mind, and attribution styles, the domain of social perception has received little specific attention. In this paper, we suggest that this issue can be explained by the lack of a precise and unitary definition of the concept, this leads to the existence of different competing uses of the concept and their conflation with other domains of social cognition. Relying on resources coming from the ecological approach to psychology and the phenomenological tradition in psychiatry, we propose that the concept of Social Perception should be used to refer to low-level pre-reflective processes underlying the awareness of interpersonal interactions with and between others. Clinical data suggests that people with schizophrenia have problems perceiving social situations as opportunities for social engagement, so, in order to fulfil this explanatory need, we propose that the term should be used to capture this important—yet neglected—domain of social cognition. We conclude with the discussion of some future directions for research derived from our proposal.

Disturbed Social Information Processing as a Mechanism in the Development of Social Anxiety Disorder

AbstractSocial anxiety disorder (SAD) is one of the most common mental disorders and becomes chronic if left untreated. Even when it is treated, outcomes are less promising than for other anxiety disorders. Thus, many are interested in preventing SAD and in the mechanisms involved in the development of SAD. In this article, I propose in a new model that disturbances in social cognition (cognitive biases, emotion recognition and understanding, negative expectations) and dysregulated social emotions (social fear and self‐conscious emotional arousal) in toddlerhood and early childhood lead to avoidance and high levels of anxiety in social situations. When repeated over time, these impair daily functioning and result in a disorder. Biological factors (e.g., fearful temperament), environmental factors (e.g., parental mentalizing), and past experiences may be distal factors that contribute to the development of SAD via disturbed sociocognitive processing and dysregulated emotions. Based on this model, I conclude by describing clinical implications and recommendations for research.

Dissociating Profiles of Social Cognitive Disturbances Between Mixed Personality and Anxiety Disorder.

BackgroundAn emerging body of research has begun to elucidate disturbances to social cognition in specific personality disorders (PDs). No research has been conducted on patients with Mixed Personality Disorder (MPD), however, who meet multiple diagnostic criteria. Further, very few studies have compared social cognition between patients with PD and those presenting with symptomatic diagnoses that co-occur with personality pathologies, such as anxiety disorder (AD). The aim of this study was to provide a detailed characterization of deficits to various aspects of social cognition in MPD and dissociate impairments specific to MPD from those exhibited by patients with AD who differ in the severity of personality pathology.MethodBuilding on our previous research, we administered a large battery of self-report and performance-based measures of social cognition to age-, sex- and education-matched groups of patients with MPD or AD, and healthy control participants (HCs; n = 29, 23, and 54, respectively). This permitted a detailed profiling of these clinical groups according to impairments in emotion recognition and regulation, imitative control, low-level visual perspective taking, and empathic awareness and expression.ResultsThe MPD group demonstrated poorer emotion recognition for negative facial expressions relative to both HCs and AD. Compared with HCs, both clinical groups also performed significantly worse in visual perspective taking and interference resolution, and reported higher personal distress when empathizing and more state-oriented emotion regulation.ConclusionWe interpret our results to reflect dysfunctional cognitive control that is common to patients with both MPD and AD. Given the patterns of affective dispositions that characterize these two diagnostic groups, we suggest that prolonged negative affectivity is associated with inflexible styles of emotion regulation and attribution. This might potentiate the interpersonal dysfunction exhibited in MPD, particularly in negatively valenced and challenging social situations.

Social Cognition and Obsessive-Compulsive Disorder: A Review of Subdomains of Social Functioning.

Disturbances in social cognitive processes such as the ability to infer others' mental states importantly contribute to social and functional impairments in psychiatric disorders. Yet, despite established social, emotional, and cognitive problems, the role of social cognition in obsessive-compulsive disorder is largely overlooked. The current review provides a first comprehensive overview of social (neuro)cognitive disturbances in adult patients with obsessive-compulsive disorder. Results of our review indicate various social cognitive alterations. Patients with obsessive-compulsive disorder show deficits in the recognition of affective social cues, specifically facial expressions of disgust, and more general deficits in theory of mind/mentalizing. Additionally, patients show heightened affective reactions and altered neural responding to emotions of self and others, as well as poor emotion regulation skills, which may contribute to poor social functioning of patients. However, the discrepancies in findings and scarcity of studies make it difficult to draw firm conclusions with regard to the specificity of social cognitive disturbances. The review offers directions for future research and highlights the need to investigate obsessive-compulsive disorder from an interactive social neurocognitive perspective in addition to the prevalent passive spectator perspective to advance our understanding of this intricate and burdensome disorder.

Disease trajectories in behavioural variant frontotemporal dementia, primary psychiatric and other neurodegenerative disorders presenting with behavioural change

Behavioural variant frontotemporal dementia (bvFTD) is characterized by behavioural and social cognitive disturbances, while various psychiatric and neurodegenerative disorders may have similar clinical symptoms. Since neurodegenerative disorders are eventually progressive, whereas primary psychiatric disorders are not, this study aimed to investigate whether the change in clinical symptoms over time differed between groups and which biomarkers predicted rate of decline.Disease trajectories (median follow-up = 3 years) of frontal and stereotyped behaviour, general and frontal cognitive functioning, and social cognition were examined in bvFTD (n = 34), other neurodegenerative (n = 28) and primary psychiatric disorders (n = 43), all presenting with late-onset frontal lobe syndrome (45–75 years), using linear mixed models. To gain more insight in underlying pathological processes driving disease progression, we studied the association of baseline cerebrospinal fluid (CSF) (neurofilament light (NfL) and YKL-40 levels, phosphotau181 to total tau ratio) and neuroimaging markers with disease trajectories.Frontal behavioural symptoms (e.g., disinhibition, apathy) worsened over time in bvFTD, whereas they improved in psychiatric disorders and remained stable in other neurodegenerative disorders. General and frontal cognitive decline was observed in bvFTD and other neurodegenerative disorders, but not in psychiatric disorders. None of the groups showed change in stereotypy and social cognition. For all diagnostic groups, higher CSF NfL levels were associated with faster frontal cognitive decline. A modest association was observed between caudate volume and stereotyped behaviour.Tracking frontal behavioural symptoms and cognition has potential to distinguish bvFTD from other disorders. CSF NfL levels seem to be associated with decline in frontal cognitive functioning.

S59. CHILDHOOD TRAUMA IS ASSOCIATED WITH SOCIAL COGNITION AND SCHIZOTYPAL PERSONALITY TRAITS IN PSYCHOTIC AND HEALTHY POPULATIONS

BackgroundChildhood trauma is a transdiagnostic risk factor for adult psychiatric disorders, including schizophrenia and bipolar-I disorder. Recent meta-analytic and epidemiological studies suggest a 3-fold increase in risk for psychotic symptoms in adulthood, following childhood trauma exposure. However, associations between trauma exposure and schizotypal personality traits, as well as cognitive and social cognitive abilities, have been less well studied in clinical populations spanning the psychotic-mood spectrum.MethodsParticipants were 79 schizophrenia cases, 84 bipolar disorder cases, and 75 healthy control participants who completed the Childhood Trauma Questionnaire (CTQ), the Schizotypal Personality Questionnaire (SPQ), and a standard battery of cognitive tests (to measure executive functions, working memory, attention, immediate and delayed memory), as well as social cognitive tests of facial emotion processing (the Ekman 60 faces task) and Theory-of-Mind (The Awareness of Social Inference Test; TASIT). The CTQ measures childhood trauma exposure on 5 domains (physical abuse, emotional abuse, sexual abuse, physical neglect, emotional neglect); clinically significant levels of childhood trauma exposure on at least one domain (according to specified thresholds for each domain) were evident in 54 schizophrenia cases, 55 bipolar disorder cases, and 26 healthy individuals. Trauma-exposed and non-exposed groups were compared on schizotypal personality features (referred to as ‘schizotypy’), cognitive and social cognitive abilities.ResultsIn both the clinical groups and healthy controls, trauma-exposed participants reported higher levels of schizotypy, especially suspiciousness, relative to non-exposed individuals; this was revealed in the context of higher overall schizotypy levels in both schizophrenia and bipolar disorder, relative to healthy controls. Similarly, while the schizophrenia group showed lower social cognitive and cognitive performances relative to both the bipolar disorder and healthy control groups, trauma-exposed individuals showed deficits in social cognitive, but not general cognitive abilities, regardless of case versus control status.DiscussionThese findings suggest that childhood trauma exposure has long-term effects on schizotypy, especially suspiciousness, and complex social cognitive abilities in both healthy and psychotic populations. However, there was no interaction of clinical group with trauma exposure in relation to schizotypal personality dimensions, and the influence of early life trauma on cognitive functions was not distinguishable from the effects of psychotic illness in adulthood. It is possible that traumagenic processes contribute to paranoid ideation and social cognitive disturbances that contribute to psychosis-proneness in the general population, consistent with historical models of schizotypy as latent liability for schizophrenia and related psychotic disorders.

A systematic review of the neurobiological underpinnings of borderline personality disorder (BPD) in childhood and adolescence.

Contemporary theories for the aetiology of borderline personality disorder (BPD) take a lifespan approach asserting that inborn biological predisposition is potentiated across development by environmental risk factors. In this review, we present and critically evaluate evidence on the neurobiology of BPD in childhood and adolescence, compare this evidence to the adult literature, and contextualise within a neurodevelopmental framework. A systematic review was conducted to identify studies examining the neurobiological (i.e. genetic, structural neuroimaging, neurophysiological, and neuropsychological) correlates of BPD symptoms in children and adolescents aged 19 years or under. We identified, quality assessed, and narratively summarised 34 studies published between 1980 and June 2016. Similar to findings in adult populations, twin studies indicated moderate to high levels of heritability of BPD, and there was some evidence for gene-environment interactions. Also consistent with adult reports is that some adolescents with BPD demonstrated structural (grey and white matter) alterations in frontolimbic regions and neuropsychological abnormalities (i.e. reduced executive function and disturbances in social cognition). These findings suggest that neurobiological abnormalities observed in adult BPD may not solely be the consequence of chronic morbidity or prolonged medication use. They also provide tentative support for neurodevelopmental theories of BPD by demonstrating that neurobiological markers may be observed from childhood onwards and interact with environmental factors to increase risk of BPD in young populations. Prospective studies with a range of repeated measures are now required to elucidate the temporal unfurling of neurobiological features and further delineate the complex pathways to BPD.

Sex and Diagnosis-Specific Associations Between DNA Methylation of the Oxytocin Receptor Gene With Emotion Processing and Temporal-Limbic and Prefrontal Brain Volumes in Psychotic Disorders

BackgroundThe oxytocin (OT) system, including receptor epigenetic mechanisms, has been shown to influence emotion processing, especially in females. Whether OT receptor (OXTR) epigenetic alterations occur across psychotic disorders in relation to illness-related disturbances in social cognition and brain anatomy is unknown. MethodsParticipants with affective and nonaffective psychotic disorders (92 women, 75 men) and healthy controls (38 women, 37 men) from the Chicago site of the Bipolar and Schizophrenia Network on Intermediate Phenotypes study completed the Penn Emotion Recognition Test, a facial emotion recognition task. We measured cytosine methylation at site −934 upstream of the OXTR start codon in DNA from whole blood and for the first time their relationship with plasma OT levels assessed by enzyme-immunoassay. Volumes of brain regions supporting social cognition were measured from magnetic resonance imaging scans using FreeSurfer. ResultsPatients with prototypic schizophrenia features showed higher levels of DNA methylation than those with prototypic bipolar features. Methylation was higher in women than men and was associated with poorer emotion recognition only in female patients and controls. Greater methylation was associated with smaller volumes in temporal-limbic and prefrontal regions associated previously with social cognition but only in healthy women and females with schizophrenia. ConclusionsDNA methylation of the OXTR site −934 was higher in schizophrenia spectrum than bipolar patients. Among patients, it was linked to behavioral deficits in social cognition and neuroanatomic structures known to support emotion processing only in schizophrenia spectrum individuals.

The relationship between alexithymia, empathy and moral judgment in patients with multiple sclerosis.

Converging research in patients with multiple sclerosis (MS) has shown increased rates of alexithymia and disturbances in social cognition, including empathy and theory of mind. Moral judgment is one of the most complex spheres of human cognition, relying on intricate neural circuits related to many other affective, social, cognitive and behavioral processes. Relapsing-remitting MS patients (n = 38) and age-, gender- and education-matched controls (n = 38) completed a measure of alexithymia (Toronto Alexithymia Scale), a measure of empathy (Interpersonal Reactivity Index) and a series of moral dilemmas, for which measures of moral permissibility, emotional reactivity and moral relativity (the perception of how one's moral attitudes compare to the attitudes of the rest of the people) were derived. Relative to controls, patients exhibited decreased levels of other-oriented empathy [empathic concern (P < 0.01) and fantasy (P < 0.01)], increased levels of self-oriented personal distress (P < 0.01), as well as higher rates of alexithymia (P < 0.001). Moral permissibility was significantly reduced in patients with MS (P = 0.038), who also showed higher levels of emotional reactivity (P < 0.01). Additionally, a significantly higher number of patients than controls considered that respondents would deliver similar judgments to the same moral scenarios (P < 0.001). Understanding such complex interactions between individual dispositions and moral cognition has the potential to contribute to the development of better assessment and intervention strategies for MS patients, enhancing quality of life by achieving better social participation.

Social Perspective Coordination in Youth with Borderline Personality Pathology

This study investigated social perspective coordination (SPC) in youth (15-24-year-olds) with first-presentation borderline personality disorder (BPD). SPC is defined as the capacity to differentiate and integrate the perspective of the self with the perspectives of others (Selman, Beardslee, Schultz, Krupa, & Podorefsky, 1986). Two groups: patients with full or sub-syndromal BPD (n = 30) and patients with major depressive disorder (MDD; n = 30) completed measures of SPC derived from the interpersonal negotiation strategies (INS) model (Selman et al., 1986). Compared with the MDD group, the BPD group responded to all vignettes with significantly lower SPC scores and SPC was a significant predictor of BPD status over and above self-reported, personality factors (Neuroticism and Agreeableness), attachment disturbance and functional impairment. These findings suggest that disturbances in social cognition are an important characteristic of individuals with BPD pathology. These difficulties extended beyond attachment contexts and were not limited to situations involving BPD-related themes of abandonment, deprivations or mistrust/abuse.

S61-03 Social cognition and psychosocial functioning in schizophrenia

Ability for empathy and theory of mind are diminshed in patients with schizophrenia. These kinds of social cognition are, however, necessary to interact with other people and obtain a well-balanced psychosocial functioning level, i.e. to have friends, to go for work, to be in partnership and so on. Own studies revealed that disturbances in social cognition are accompanied by fMRI activation deficits in distinct regions of the underlying neuronanatomical loop in schizophrenia. The most significant difference compared to healthy controls was found in the region of the anterior cingulate cortex (ACC) and medial prefrontal cortex (mPFC). We think that training of social cognition would improve both the neurobiological hypoactivation and the ability for empathy and theory of mind. As consequence, psychosocial functioning of the patients should be become better as measured e.g. by the personal and social performance scale (PSP). To emphazise the close relationship between social cognition, ist underlying neuobiology and psychosocial functioning is the main purpose of this lecture.

X Chromosomal effects on social cognitive processing and emotion regulation: A study with Klinefelter men (47,XXY)

Studying Klinefelter syndrome (47,XXY), a genetically defined disorder characterized by the presence of an additional X chromosome, can reveal insights into genotype–phenotype associations. Increased vulnerability to psychiatric disorders characterized by difficulties in social interactions, such as schizophrenia and autism, has been reported for this population. The reported social difficulties in 47,XXY men may arise as a consequence of impairments in the processing of social and emotional information. The present study is the first investigation of social–emotional information processing in this X chromosomal disorder. 32 Klinefelter men and 26 men from the general population, with the groups matched for age, educational level and I.Q., participated in the study. Several tasks were included, reflecting aspects of social–emotional information processing on levels of perception, experience and expression: labeling of facial expressions of emotion, emotion–cognition interactions in decision making and emotion regulation, that refers to subjective experience and identification of emotional arousal as well as verbal expression of emotions. A discrepancy between cognitive appraisal of emotions and emotional arousal was observed in Klinefelter syndrome. Taken together, Klinefelter men seem less accurate in perception of socio-emotional cues such as angry facial expressions, they are less able to identify and verbalize their emotions, but experience increased levels of emotional arousal, in comparison to the general population. Besides describing the social–emotional phenotype of this X chromosomal disorder, the present data may prove to be an important contribution to the development of more general models describing pathways to neuropsychiatric disorders characterized by social cognitive disturbances.

Social cognition, brain networks and schizophrenia

A better understanding of the neural basis of social cognition including mindreading (or theory of mind) and empathy might help to explain some deficits in social functioning in people with schizophrenia. Our aim was to review neuroimaging and neuropsychological studies on social cognition, as they may shed light on the neural mechanisms of social cognition and its dysfunction in patients with schizophrenia. A selective literature review was undertaken. Neuroimaging and neuropsychological studies suggest convergence upon specific networks for mindreading and empathy (the temporal cortex, amygdala and the prefrontal cortex). The frontal lobe is likely to play a central role in enabling social cognition, but mindreading and empathic abilities may require relatively different weighting of subcomponents within the same frontal-temporal social cognition network. Disturbances in social cognition may represent an abnormal interaction between frontal lobe and its functionally connected cortical and subcortical areas. Future studies should seek to explore the heterogeneity of social dysfunction within schizophrenia.

Visual scanpath dysfunction in first-degree relatives of schizophrenia probands: evidence for a vulnerability marker?

Previous research demonstrates that people with schizophrenia have abnormally ‘restricted’ visual scanpaths to face and facial expression stimuli, which appear to be diagnostically specific to schizophrenia [Schizophr. Res. 55 (2002) 159; Biol. Psychiatry 52 (2002) 338]. This study examined the familial transmission of ‘restricted’ scanpaths in first-degree relatives of schizophrenia subjects. We recorded visual scanpaths for 65 schizophrenia subjects, 37 biological first-degree relatives and 61 nonrelated ‘healthy’ control subjects in two experiments: ‘face recognition’ and ‘facial affect recognition’. Concurrent behavioral tasks were face matching and expression matching, each under two multiple-choice conditions (seven or three options). As predicted, first-degree relatives generally showed an attenuated form of the markedly ‘restricted’ scanpaths of schizophrenia subjects across all face stimuli. The notable exception to this pattern was the relatives' extreme avoidance of facial features (compared to both schizophrenia and healthy control groups). Our results offer the first evidence that some components of visual scanpath dysfunction may represent a trait marker in the familial transmission of schizophrenia, but that first-degree relatives may have additional disturbances in social cognition associated with the perception of facial features.