A nation-wide twin study of social cognition in schizophrenia spectrum disorders.
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ABSTRACT:
SUBMITTER: Lemvigh CK
PROVIDER: S-EPMC8891357 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Schizophrenia and autism both feature significant impairments in social cognition and social functioning, but the specificity and mechanisms of these deficits remain unknown. Recent research suggests that social cognitive deficits in both disorders may arise from dysfunctions in the neural systems that underlie social cognition. We explored the neural activation of discrete brain regions implicated in social cognitive and face processing in schizophrenia subgroups and autism spectrum disorders during complex social judgments of faces. Twelve individuals with autism spectrum disorders (ASD), 12 paranoid individuals with schizophrenia (P-SCZ), 12 non-paranoid individuals with schizophrenia (NP-SCZ), and 12 non-clinical healthy controls participated in this cross sectional study. Neural activation, as indexed by blood oxygenation level dependent (BOLD) contrast, was measured in a priori regions of interest while individuals rated faces for trustworthiness. All groups showed significant activation of a social cognitive network including the amygdala, fusiform face area (FFA), superior temporal sulcus (STS), and ventrolateral prefrontal cortex (VLPFC) while completing a task of complex social cognition (i.e. trustworthiness judgments). ASD and P-SCZ individuals showed significantly reduced neural activation in the right amygdala, FFA, and left VLPFC as compared to controls and in the left VLPFC as compared to NP-SCZ individuals during this task. These findings lend support to models hypothesizing well-defined neural substrates of social cognition and suggest a specific neural mechanism that may underlie social cognitive impairments in both autism and paranoid schizophrenia.
| S-EPMC2740744 | biostudies-literature
Project description:Alterations in social cognition (SC) are hypothesized to underlie social communication and interaction challenges in autism spectrum disorder (ASD). The aetiological underpinnings driving this association remain unclear. We examined SC in 196 twins with ASD, other neurodevelopmental disorders or typical development using the naturalistic Movie for the Assessment of Social Cognition. Autism and its severity were assessed with the Autism Diagnostic Observation Schedule-2, and autistic traits with the Social Responsiveness Scale-2. Using within twin-pair regression models, controlling for age, sex, IQ, and unmeasured familial confounders such as genetic background and shared-environment, SC correlated with ASD diagnosis, autism severity, and autistic traits. Our findings highlight the importance of SC alterations in autism and suggest a non-shared environmental impact on the association.
| S-EPMC6606667 | biostudies-other
Project description:ContextImpaired social cognition is a cardinal feature of Autism Spectrum Disorders (ASD) and Schizophrenia (SZ). However, the functional neuroanatomy of social cognition in either disorder remains unclear due to variability in primary literature. Additionally, it is not known whether deficits in ASD and SZ arise from similar or disease-specific disruption of the social cognition network.ObjectiveTo identify regions most robustly implicated in social cognition processing in SZ and ASD.Data sourcesSystematic review of English language articles using MEDLINE (1995-2010) and reference lists.Study selectionStudies were required to use fMRI to compare ASD or SZ subjects to a matched healthy control group, provide coordinates in standard stereotactic space, and employ standardized facial emotion recognition (FER) or theory of mind (TOM) paradigms.Data extractionActivation foci from studies meeting inclusion criteria (n = 33) were subjected to a quantitative voxel-based meta-analysis using activation likelihood estimation, and encompassed 146 subjects with ASD, 336 SZ patients and 492 healthy controls.ResultsBoth SZ and ASD showed medial prefrontal hypoactivation, which was more pronounced in ASD, while ventrolateral prefrontal dysfunction was associated mostly with SZ. Amygdala hypoactivation was observed in SZ patients during FER and in ASD during more complex ToM tasks. Both disorders were associated with hypoactivation within the Superior Temporal Sulcus (STS) during ToM tasks, but activation in these regions was increased in ASD during affect processing. Disease-specific differences were noted in somatosensory engagement, which was increased in SZ and decreased in ASD. Reduced thalamic activation was uniquely seen in SZ.ConclusionsReduced frontolimbic and STS engagement emerged as a shared feature of social cognition deficits in SZ and ASD. However, there were disease- and stimulus-specific differences. These findings may aid future studies on SZ and ASD and facilitate the formulation of new hypotheses regarding their pathophysiology.
| S-EPMC3187762 | biostudies-literature
Project description:BackgroundResearch has shown that patients with schizophrenia spectrum disorders (SSD) can be distinguished from controls on the basis of their non-verbal expression. For example, patients with SSD use facial expressions less than normals to invite and sustain social interaction. Here, we sought to examine whether non-verbal expressivity in patients corresponds with their impoverished social competence and neurocognition.MethodFifty patients with SSD were videotaped during interviews. Non-verbal expressivity was evaluated using the Ethological Coding System for Interviews (ECSI). Social competence was measured using the Social Behaviour Scale and psychopathology was rated using the Positive and Negative Symptom Scale. Neurocognitive variables included measures of IQ, executive functioning, and two mentalising tasks, which tapped into the ability to appreciate mental states of story characters.ResultsNon-verbal expressivity was reduced in patients relative to controls. Lack of "prosocial" nonverbal signals was associated with poor social competence and, partially, with impaired understanding of others' minds, but not with non-social cognition or medication.ConclusionThis is the first study to link deficits in non-verbal expressivity to levels of social skills and awareness of others' thoughts and intentions in patients with SSD.
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Project description:Social anhedonia (SA) is a trait-like phenomenon observed across schizophrenia-spectrum disorders (SSDs). While in-the-moment social pleasure experiences are intact in SSDs, anticipatory pleasure experiences may be disrupted. Thus, the prediction of future emotions in social situations, or social affective forecasting (SAF), may play a role in SA. Therefore, we utilized daily diary methods to examine SAF in SSD and the association between SAF and SA in 34 SSD and 43 non-SSD individuals. SAF was calculated as the absolute difference between anticipatory and consummatory ratings of 13 positive and negative emotions for daily social interactions reported across eight days. Results suggest that individuals with SSDs are less accurate in forecasting negative, but not positive emotions, for future social interactions. Further, poorer forecasting accuracy of negative emotions were associated with elevated levels of SA and lower social pleasure. Together, these data suggest that inaccuracies in forecasting negative emotions may be a worthwhile intervention target for reducing SA in SSDs.
| S-EPMC9663197 | biostudies-literature
Project description:The purpose of this pilot study was to assess the efficacy of a new social cognition (SC) remediation intervention, the Social Cognition Individualized Activities Lab (SoCIAL), for subjects with schizophrenia. The training includes a module for emotion recognition and one for theory of mind. A comparison with a validated cognitive remediation intervention, the Social Skills And Neurocognitive Individualized Training (SSANIT), was conducted to verify the efficacy of the SoCIAL in improving SC. Ten stabilized patients with schizophrenia accepted to participate. Five patients were randomized to SoCIAL and five to SSANIT. The SoCIAL intervention includes individual sessions of neurocognitive individualized training (NIT) and group sessions of SC training. SSANIT includes individual sessions of NIT and group sessions of social skills individualized training. The interventions were matched for the overall treatment duration (20 weeks) and for the frequency of the sessions (two times a week, one for SoCIAL or social skills individualized training and one for NIT, with a duration of 80 minutes for each session). Results showed a significant treatment effect (effect size: Cohen's d 0.32) on the primary outcome; in fact, only the SoCIAL intervention improved theory of mind. Patients receiving the SoCIAL intervention also showed an improvement of avolition. These preliminary findings support further development of the SoCIAL and suggest that cognitive remediation should include an SC module.
| S-EPMC5530058 | biostudies-other
Project description:ObjectiveNeurocognitive impairment has been extensively studied in people with schizophrenia spectrum disorders and seems to be one of the major determinants of functional outcome in this clinical population. Data exploring the link between neuropsychological deficits and the risk of violence in schizophrenia has been more inconsistent. In this study, we analyse the differential predictive potential of neurocognition and social cognition to discriminate patients with schizophrenia spectrum disorders with and without a history of severe violence.MethodsOverall, 398 (221 cases and 177 controls) patients were recruited in forensic and general psychiatric settings across five European countries and assessed using a standardized battery.ResultsEducation and processing speed were the strongest discriminators between forensic and non-forensic patients, followed by emotion recognition. In particular, increased accuracy for anger recognition was the most distinctive feature of the forensic group.ConclusionsThese results may have important clinical implications, suggesting potential enhancements of the assessment and treatment of patients with schizophrenia spectrum disorders with a history of violence, who may benefit from consideration of socio-cognitive skills commonly neglected in ordinary clinical practice.
| S-EPMC8651972 | biostudies-literature
Project description:First-episode schizophrenia (FES) spectrum disorders are associated with pronounced cognitive dysfunction across all domains. However, less is known about the course of cognitive functioning, following the first presentation of psychosis, and the relationship of cognition to clinical course during initial treatment. The present longitudinal study examined the magnitude of neurocognitive impairment, using the MATRICS Consensus Cognitive Battery, in patients experiencing their first episode of psychosis at baseline and after 12 weeks of randomized antipsychotic treatment with either aripiprazole or risperidone. At baseline, FES patients evidenced marked impairments in cognitive functioning. Notably, performance on the mazes task of planning and reasoning significantly predicted the likelihood of meeting stringent criteria for positive symptom remission during the first 12 weeks of the trial. Performance on indices of general cognitive function, working memory, and verbal learning improved over time, but these improvements were mediated by improvements in both positive and negative symptoms. We did not detect any differential effects of antipsychotic medication assignment (aripiprazole vs risperidone) on cognitive functioning. Our results suggest that a brief paper-and-pencil measure reflecting planning/reasoning abilities may index responsivity to antipsychotic medication. However, improvements in cognitive functioning over time were related to clinical symptom improvement, reflecting "pseudospecificity."
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Project description:People with schizophrenia-spectrum disorders (SSD) often experience impairments in non-social motivation. In this study, we extended this line of investigation by examining specific components of social motivation and the extent to which these components work together in people with and without a recent-onset SSD. Sixty-four people with a recent-onset SSD and 26 controls completed a task that allowed us to examine changes in anticipated pleasure, decisions to trust, and effort expenditure over the course of repeated interactions with positive or negative outcomes. Compared to controls, we found that people in the SSD group placed less trust, tended to anticipate less pleasure, and expended less effort to increase the likelihood of future interactions with positive outcomes. Further, in the SSD group, effort expenditure was not associated with either anticipated pleasure or decisions to trust. While there were no group differences in anticipated pleasure or trust placed during interactions with negative outcomes, people in the SSD group expended less effort to decrease to the likelihood of future interactions. Taken together, our findings suggest that people with a recent-onset SSD may experience both impairment and disconnection between various components of social motivation for interactions with positive outcomes. Implications for interventions for social engagement in people with SSD are discussed.
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Project description:Whether aberrant cerebral blood flow (CBF) in schizophrenia is affected by genetic influences, and consequently a potential marker for genetic susceptibility, is unknown. Our aims were to determine the heritability of CBF in thalamic, frontal, and striatal areas, and to ascertain if associations with disease were under genetic influence. Monozygotic (MZ) twin pairs concordant (n = 2) or discordant (n = 20) for schizophrenia spectrum disorders (ICD-10 F2x.x), matched on sex and age with dizygotic (DZ; n = 20) and healthy control pairs (MZ: n = 27; DZ: n = 18; total: n = 181 individuals), were recruited via the National Danish Twin Register. CBF in thalamus, frontal lobes, and putamen was measured with pseudo-continuous arterial spin labeling on a 3 T magnetic resonance scanner. Twin statistics were performed with structural equation modeling. CBF in the frontal lobes was heritable (h2 = 0.44, 95% CI [0.22-0.60]) but not correlated to disease. CBF correlated to schizophrenia spectrum disorders in the left thalamus (r = 0.17, [0.03-0.31]; P = 0.02), as well as in the left putamen (r = 0.19, [0.05-0.32]; P = 0.007) and the right putamen (r = 0.18, [0.03-0.32]; P = 0.02). When restricting the sample to schizophrenia (F20.x) only, shared genetic influences between CBF in the left putamen and schizophrenia liability (phenotypic correlation = 0.44, [0.28-0.58], P < 0.001) were found. Our results provide heritability estimates of CBF in the frontal lobes, and we find CBF in thalamus and putamen to be altered in schizophrenia spectrum disorders. Furthermore, shared genetic factors influence schizophrenia liability and striatal perfusion. Specifically, higher perfusion in the left putamen may constitute a marker of genetic susceptibility for schizophrenia.
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