scholarly journals Social Cognition through the Lens of Cognitive and Clinical Neuroscience

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Maria Arioli ◽  
Chiara Crespi ◽  
Nicola Canessa

Social cognition refers to a set of processes, ranging from perception to decision-making, underlying the ability to decode others’ intentions and behaviors to plan actions fitting with social and moral, besides individual and economic considerations. Its centrality in everyday life reflects the neural complexity of social processing and the ubiquity of social cognitive deficits in different pathological conditions. Social cognitive processes can be clustered in three domains associated with (a) perceptual processing of social information such as faces and emotional expressions (social perception), (b) grasping others’ cognitive or affective states (social understanding), and (c) planning behaviors taking into consideration others’, in addition to one’s own, goals (social decision-making). We review these domains from the lens of cognitive neuroscience, i.e., in terms of the brain areas mediating the role of such processes in the ability to make sense of others’ behavior and plan socially appropriate actions. The increasing evidence on the “social brain” obtained from healthy young individuals nowadays constitutes the baseline for detecting changes in social cognitive skills associated with physiological aging or pathological conditions. In the latter case, impairments in one or more of the abovementioned domains represent a prominent concern, or even a core facet, of neurological (e.g., acquired brain injury or neurodegenerative diseases), psychiatric (e.g., schizophrenia), and developmental (e.g., autism) disorders. To pave the way for the other papers of this issue, addressing the social cognitive deficits associated with severe acquired brain injury, we will briefly discuss the available evidence on the status of social cognition in normal aging and its breakdown in neurodegenerative disorders. Although the assessment and treatment of such impairments is a relatively novel sector in neurorehabilitation, the evidence summarized here strongly suggests that the development of remediation procedures for social cognitive skills will represent a future field of translational research in clinical neuroscience.

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S160-S161
Author(s):  
Sara-Ann Lee ◽  
Keane Lim ◽  
Max Lam ◽  
Jimmy Lee

Abstract Background Social cognitive deficits are common, detectable across a wide range of tasks and appear to play a key role in influencing poor functioning in schizophrenia. Despite its importance as a treatment target, the factors that underlie social cognitive deficits in schizophrenia remains elusive. Schizotypy appears to be one such factor that can explain the variability in social cognitive deficits seen in schizophrenia. The study’s primary aim was to provide a more comprehensive understanding of social cognitive functioning and its relationship to schizotypy. Methods 108 patients and 70 healthy controls completed nine tasks across 4 social cognitive domains based on the SCOPE study. In addition, all participants completed the Schizotypal Personality Questionnaire. Clinical symptoms were also rated using the Brief Psychiatric Rating Scale. Results Theory of Mind, social perception, emotion processing and attribution bias were measured in patients with schizophrenia (n = 108) and healthy controls (n = 70). A social cognition composite score was calculated using principal components analysis. Cluster analysis on the derived factor scores revealed 3 clusters. Multiple univariate ANOVAS with Bonferroni correction were used to examine differences between the 3 clusters on each of the 4 social cognition domain scores, which indicated that higher social cognitive performance was related to lower schizotypy. In addition, results indicated that despite differences in the social cognitive performance among patients in the 3 clusters, they did not differ in clinical outcome measures. Discussion The primary aim of the study was to address gaps in the current literature by examining the relationship between social cognition and schizotypy. This study built upon past studies which had the tendency to focus on single, discrete domains by comparing the social cognitive performance of patients and controls using an extensive battery of tests, indexing four social cognitive domains. The significant differences on total SPQ score and the SPQ domain scores between the various clusters, coupled with the significant correlations between schizotypy and social cognition, reinforces the utility of schizotypy in refining our understanding of the variation in the degree of social cognitive deficits in schizophrenia. In conclusion, this study substantiates the importance of understanding the relationship between social cognition and schizotypy. This could support and pave the way for the development and implementation of targeted social cognitive interventions catered to the patients’ level of deficit.


BJPsych Open ◽  
2021 ◽  
Vol 7 (S1) ◽  
pp. S300-S300
Author(s):  
Michael Weightman ◽  
Bernhard Baune

AimsThis poster aims to examine the impact of social cognitive deficits on psychosocial functioning in depressed patients, as well as summarise the utility of various evidence-based therapeutic interventions employed to target these deficits. The stated hypotheses were twofold: (1) that social cognitive impairment in major depressive disorder will correlate with poorer psychosocial functioning; and (2) that these deficits will respond to existing anti-depressant therapies.BackgroundSocial cognition is an important adaptive trait that incorporates the identification, perception and interpretation of socially relevant information from the external world. It is frequently affected in major depressive disorder such that depressed patienMethodA review of the existing literature was performed in order to test the stated hypotheses. Pertinent sources were identified via the MEDLINE, EMBASE, PsycINFO, PubMed, Scopus and Google Scholar databases. A total of 107 studies met inclusion criteria for review.ResultImpaired social cognitive performance in depressed patients correlated with poorer psychosocial functioning across the key domains of general cognitive functioning and quality of life. Many current anti-depressant therapies were found to have a normalising effect on the social cognitive abilities of depressed subjects, both at a neural and functional level. Anti-depressant medications, in particular citalopram and reboxetine, appeared to correct facial affect recognition deficits, while a psychotherapeutic approach demonstrated improvements in theory of mind and negative interpretive bias. Data relating to other common treatments, such as electroconvulsive therapy, are limited.ConclusionThe impact and treatment of social cognitive deficits in major depressive disorder is an important emerging field. The social cognitive deficits evident in depressed patients are sometimes subtle, but afford a significant functional impact. Additionally, it appears these impairments are at least partially reversible using anti-depressants or psychotherapy.


Author(s):  
Manju Kumari ◽  
Ankita Sharma

<p><strong>Orndorff and his colleagues [1]</strong> suggested that if a neural activity is considered a treatment variable instead of outcome, it widens the scope of research and has a specific implication for social neuroscience. Given this, the empirical evidence is collected and analyzed where neural activity as self-manipulation design through neurofeedback training specifically for social cognition deficit is done. The objective of the present article is to provide a systematic review of 1) how NFT is utilized to treat social cognitive deficits, 2) how NFT is utilized to target Social Cognition Deficit in ASD, 3) examining the directions, strengths, and quality of evidence to support the use of NFT for ASD. The databases for studies were searched in PubMed, MEDLINE, EMBASE, Springer, Science Direct, Psychinfo, and Google Scholar, using combinations of the following keywords: ‘Neurofeedback,’ ‘Autism Spectrum Disorder,’ ‘Mu Rhythm’ and ‘Social Cognition.’ Studies were eligible for inclusion if they were specific to 1) autistic and typically developed population, 2) intervention study, 3) Delivered by NFT, 4) participants showed social cognitive deficit and/or improvement. Total one eighty-seven studies were found of key interest; out of which 17 studies were eligible for inclusion in this review. All studies reported the improvement in different domains of social cognition and were moderately methodologically sound. Eleven out of seventeen studies satisfied the trainability and interpretability criteria suggested by <strong>Zoefel and his colleagues [2].</strong> The conclusion from the present review is in line with comments of <strong>Marzbani and colleagues [3]</strong> that, ‘current research does not provide sufficient conclusive results about its efficacy.’ The patterns and directions concluded from studies related to protocol, methodology and results are discussed in detail in the present review.</p>


2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S152-S153
Author(s):  
Lindsay Oliver ◽  
Iska Moxon-Emre ◽  
Aristotle Voineskos ◽  
Stephanie Ameis

Abstract Background Schizophrenia spectrum disorders (SSDs) and autism spectrum disorder (ASD) both feature social cognitive deficits, which are highly debilitating. These include lower-level processes (e.g. emotion recognition), thought to be subserved by a frontoparietal mirroring network, and higher-level mentalizing processes (e.g. theory of mind), involving cortical midline and lateral temporal brain regions. Across both disorders, impairments in social cognition persist over time, drive disability, and predict functional outcome. Overlapping symptoms in SSDs and ASD have long been recognized, particularly in the realm of social deficits. However, despite some studies including both individuals with SSDs and ASD showing similar levels of social cognitive impairment, including lower-level and higher-level deficits, results are mixed. Thus, our objective was to determine based on the extant literature how deficits in social cognition diverge or overlap between individuals with SSDs and ASD by conducting a systematic review and meta-analysis of studies directly comparing these groups on behavioural social cognitive measures. Methods Literature searches were conducted in MEDLINE, Embase, PsycINFO, and Web of Science to identify articles that utilized behavioural measures to assess social cognition in both SSD and ASD samples. Of 3682 articles identified, 28 met all inclusion criteria. Across the accepted articles, lower-level (e.g. facial and/or context-embedded emotion recognition) and higher-level (e.g. intention understanding, perspective taking) social cognitive measures were identified, and random-effects meta-analyses were conducted for each category. A separate meta-analysis was also conducted for the Reading the Mind in the Eyes test given that it was the most commonly used social cognitive metric. Effect sizes were estimated using Hedges’ g. Homogeneity of effects and publication bias were also assessed for each meta-analysis. Results A significant difference in lower-level social cognitive performance was found between individuals with SSDs and ASD, with the SSD group performing better than the ASD group (Hedges’ g = 0.30, 95% CI [0.05, 0.56], p = .018). In contrast, there was no significant difference in higher-level social cognitive performance between SSD and ASD groups (Hedges’ g = -0.14, 95% CI [-0.52, 0.24], p = .46). Similarly, the Reading the Mind in the Eyes test meta-analysis revealed no significant difference in effect sizes between disorders (Hedges’ g = 0.24, 95% CI [-0.07, 0.55], p = .14). Effect size distributions were significantly heterogeneous in all three cases (all p &lt; .001). Discussion Based on meta-analyses of the extant literature, both shared and differential social cognitive deficits may be present between individuals with SSDs and ASD. Though no differences were detected between SSD and ASD groups on higher-level social cognitive tasks or the Reading the Mind in the Eyes test, lower-level social cognitive deficits were found to be more severe in individuals with ASD than SSDs. Notably, the majority of studies included in the meta-analyses had small sample sizes, and heterogeneity of effect sizes was apparent. Thus, studies including larger sample sizes and validated measures of social cognition in conjunction with other methodologies are needed to substantiate these results, and better understand the shared and unique behavioural underpinnings and associated neural circuit abnormalities underlying social cognitive deficits in SSDs and ASD.


2015 ◽  
Vol 46 (4) ◽  
pp. 699-716 ◽  
Author(s):  
E. Bora ◽  
C. Pantelis

BackgroundImpairment in social cognition is an established finding in autism spectrum disorders (ASD). Emerging evidence suggests that attention-deficit/hyperactivity disorder (ADHD) might be also associated with deficits in theory of mind (ToM) and emotion recognition. However, there are inconsistent findings, and it has been debatable whether such deficits persist beyond childhood and how similar social cognitive deficits are in ADHD v. ASD.MethodWe conducted a meta-analysis of social cognition, including emotion recognition and ToM, studies in ADHD compared with healthy controls and ASD. The current meta-analysis involved 44 studies comparing ADHD (n = 1999) with healthy controls (n = 1725) and 17 studies comparing ADHD (n = 772) with ASD (n = 710).ResultsFacial and vocal emotion recognition (d = 0.40–0.44) and ToM (d = 0.43) abilities were significantly impaired in ADHD. The most robust facial emotion recognition deficits were evident in anger and fear. Social cognitive deficits were either very subtle (emotion recognition) or non-significant (ToM) in adults with ADHD. Deficits in social cognition, especially ToM, were significantly more pronounced in ASD compared with ADHD. General cognitive impairment has contributed to social cognitive deficits in ADHD.ConclusionsPerformance of individuals with ADHD on social cognition lies intermediate between ASD and healthy controls. However, developmental trajectories of social cognition probably differ between ADHD and ASD as social cognitive deficits in ADHD might be improving with age in most individuals. There is a need for studies investigating a potential subtype of ADHD with persistent social cognitive deficits and exploring longitudinal changes in social cognition during development.


2019 ◽  
Vol 46 (2) ◽  
pp. 236-241 ◽  
Author(s):  
Andrea Pelletier-Baldelli ◽  
Daphne J Holt

Abstract Many investigations have demonstrated that negative symptoms and social cognitive deficits in schizophrenia play a large role in determining functional outcomes and ultimately long-term prognosis. Given this, there is increasing interest in understanding the relationship between these two symptom domains, particularly since studies have consistently found moderate to large associations between them. This shared variance raises a key question: to what degree do these two categories of symptoms arise from overlapping or identical changes in brain function? In other words, do some or all negative symptoms represent merely the downstream effects of social cognition deficits on daily functioning? In this commentary, the evidence for and against this possibility, limitations of currently validated empirical measurements of these symptoms, and directions for further investigation of this hypothesis are discussed. Understanding the shared and distinct mechanisms of these disabling deficits will have important implications for the design of novel, personalized treatments for psychotic illness.


2014 ◽  
Vol 29 (S3) ◽  
pp. 543-544
Author(s):  
P. Roux ◽  
P. Smith ◽  
C. Passerieux ◽  
F. Ramus

Individuals with schizophrenia have been shown to be impaired in their ability to attribute intentions to others. However, the mentalizing tasks usually used impose large demands on explicit reasoning, thus leaving the large domain of implicit social cognition largely unexplored in schizophrenia. Yet, Frith has suggested that social cognitive deficits in schizophrenia were characterized by dissociation between an impaired explicit mentalization and a spared implicit mentalization [1]. Another question that remains open is whether schizophrenic patients’ difficulties in those tasks can be characterized as hypo- [2] or as hyper mentalization deficits [3]. In order to test these two questions, mentalization was tested in individuals with schizophrenia (n = 29) and in control subjects (n = 29) with the Frith-Happé paradigm [4], while eye movements were recorded. Explicit mentalizing was measured from participants’ verbal descriptions and was contrasted with implicit mentalization measured through eyetracking. As a group, schizophrenia cases made less accurate and intentional descriptions of the intentional animations whereas no differences where found for the random animations. These differences were not explained by lower verbal or performance IQ or impaired executive function measured by cognitive contextual control. However, eyetracking results revealed that individuals with and without schizophrenia showed a similar modulation of eye movements in response to the different condition of Frith-Happé animations. To conclude, participants with schizophrenia showed an explicit deficit in mentalization in the direction of a hypomentalization, whereas their implicit mentalization was preserved, thus suggesting dissociation between explicit and implicit attribution of intentions in schizophrenia.


2014 ◽  
Vol 20 (11) ◽  
pp. 1478-1484 ◽  
Author(s):  
LE Charvet ◽  
RE Cleary ◽  
K Vazquez ◽  
AL Belman ◽  
LB Krupp ◽  
...  

Background: Pediatric-onset multiple sclerosis (MS) patients represent a subpopulation who are diagnosed during the course of development. Social cognitive deficits have recently been recognized in adults with MS. It is critical to identify whether these youngest patients with the disorder are also at risk. Objective: To determine whether pediatric-onset MS is associated with social cognitive deficits. Methods: Consecutively-recruited participants with pediatric-onset MS were compared to a group of age- and gender-matched healthy controls on Theory of Mind (ToM) task performance. Tasks measured facial affect recognition (Reading the Mind in the Eyes Test), detecting social faux pas (Faux Pas Test), and understanding the perspective of another (False Beliefs Task). Results: Twenty-eight (28) pediatric-onset MS participants (median age 17 years) and 32 healthy controls (median age 16 years) completed the study. The MS participants performed worse than controls on all three ToM tasks: Reading the Mind in the Eyes Test ( p = 0.008), the Faux Pas Test ( p = 0.009), and the False Beliefs Task ( p = 0.06). While more MS than control participants were impaired on a measure of information processing speed (the Symbol Digit Modalities Test; 38% versus 6%), it did not account for the differences in ToM performance. Conclusions: Social cognition may represent an area of cognitive functioning affected by MS in the pediatric-onset population. These processes are especially important to study in younger patients as they may have long range implications for social adjustment, employment, and well-being.


Sign in / Sign up

Export Citation Format

Share Document