Neurocognition and social cognition training as treatments for violence and aggression in people with severe mental illness

CNS Spectrums ◽  
2019 ◽  
Vol 25 (2) ◽  
pp. 145-153
Author(s):  
Mackenzie T. Jones ◽  
Philip D. Harvey

Aggressive and violent behavior, including both verbal and physical aggression, have considerable adverse consequences for people with schizophrenia. There are several potential causes of violent behavior on the part of people with severe mental illness, which include intellectual impairments, cognitive and social-cognitive deficits, skills deficits, substance abuse, antisocial features, and specific psychotic features. This review explores the interventions that have been tested to this date. Computerized Cognitive Training (CCT) or Computerized Social-Cognitive Training (CSCT) have been associated with reductions in violence. Combined CCT and CSCT have been found to improve social cognition and neurocognition, as well as everyday functioning when combined with rehabilitation interventions. These interventions have been shown to reduce violence in schizophrenia patients across multiple environments, including forensic settings. The reductions in violence and aggression have manifested in various ways, including reduced violent thinking and behavior, reduced physical and violent assaults, and reduced disruptive and aggressive behaviors. Effects of cognitive training may be associated with improvements in problem-solving and the increased ability to deploy alternative strategies. The effect of social cognition training on violence reduction appears to be direct, with improvements in violence related to the extent of improvement in social cognition. There are still remaining issues to be addressed in the use of CCT and CSCT, and the benefits should not be overstated; however, the results of these interventions are very promising.

2017 ◽  
Vol 23 (7) ◽  
pp. 577-583 ◽  
Author(s):  
Beatrice Frajo-Apor ◽  
Georg Kemmler ◽  
Silvia Pardeller ◽  
Markus Huber ◽  
Christian Macina ◽  
...  

AbstractObjectives:Social cognitive deficits have been discussed to be endophenotypes for schizophrenia and other serious mental illnesses. The current study aimed to assess emotional intelligence (EI) in unaffected siblings of schizophrenia patients to investigate its potential role as endophenotype for schizophrenia.Methods:EI was measured in 56 schizophrenia patients, 57 unaffected siblings, and 127 healthy control subjects by using the Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT). In addition, non-social cognition was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS). Linear mixed models with compound symmetric correlation structure were used for of the three groups with respect to EI and non-social cognition.Results:Schizophrenia patients showed significantly lower overall EI and performed significantly worse in three out of four MSCEIT branches compared to unaffected siblings and control subjects, whereas the two latter groups had comparable EI levels. Similar performance patterns (patients<unaffected siblings=control subjects) were found with respect to non-social cognition. Solely in the “Tower of London” test, siblings achieved significantly lower task scores compared to control subjects.Conclusions:Based on our results, EI as measured with the MSCEIT does not seem to represent a marker of risk for schizophrenia. Further investigations should concentrate on other EI measures to reassess this finding. (JINS, 2017,23, 577–583)


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.


2002 ◽  
Vol 92 (9) ◽  
pp. 1523-1531 ◽  
Author(s):  
Jeffrey W. Swanson ◽  
Marvin S. Swartz ◽  
Susan M. Essock ◽  
Fred C. Osher ◽  
H. Ryan Wagner ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Paul H. Lysaker ◽  
Ilanit Hasson-Ohayon ◽  
Courtney Wiesepape ◽  
Kelsey Huling ◽  
Aubrie Musselman ◽  
...  

Many with psychosis experience substantial difficulties forming and maintaining social bonds leading to persistent social alienation and a lack of a sense of membership in a larger community. While it is clear that social impairments in psychosis cannot be fully explained by symptoms or other traditional features of psychosis, the antecedents of disturbances in social function remain poorly understood. One recent model has proposed that deficits in social cognition may be a root cause of social dysfunction. In this model social relationships become untenable among persons diagnosed with psychosis when deficits in social cognition result in inaccurate ideas of what others feel, think or desire. While there is evidence to support the influence of social cognition upon social function, there are substantial limitations to this point of view. Many with psychosis have social impairments but not significant deficits in social cognition. First person and clinical accounts of the phenomenology of psychosis also do not suggest that persons with psychosis commonly experience making mistakes when trying to understand others. They report instead that intersubjectivity, or the formation of an intimate shared understanding of thoughts and emotions with others, has become extraordinarily difficult. In this paper we explore how research in metacognition in psychosis can transcend these limitations and address some of the ways in which intersubjectivity and more broadly social function is compromised in psychosis. Specifically, research will be reviewed on the relationship between social cognitive abilities and social function in psychosis, including measurement strategies and limits to its explanatory power, in particular with regard to challenges to intersubjectivity. Next, we present research on the integrated model of metacognition in psychosis and its relation to social function. We then discuss how this model might go beyond social cognitive models of social dysfunction in psychosis by describing how compromises in intersubjectivity occur as metacognitive deficits leave persons without an integrated sense of others' purposes, relative positions in the world, possibilities and personal complexities. We suggest that while social cognitive deficits may leave persons with inaccurate ideas about others, metacognitive deficits leave persons ill equipped to make broader sense of the situations in which people interact and this is what leaves them without a holistic sense of the other and what makes it difficult to know others, share experiences, and sustain relationships. The potential of developing clinical interventions focused on metacognition for promoting social recovery will finally be explored.


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. 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.


2016 ◽  
Vol 18 (1) ◽  
pp. 138-173 ◽  
Author(s):  
Renée L. Roelofs ◽  
Ellen Wingbermühle ◽  
Jos I.M. Egger ◽  
Roy P.C. Kessels

Social cognitive deficits are common in neuropsychiatric disorders. Given the proximity of social cognition (SC) to everyday functioning, many intervention studies (including targeted, comprehensive, and broad-based approaches) have focussed on SC. The aim of this paper was to quantitatively meta-analyse the efficacy of SC interventions in adult neuropsychiatric patients. Databases Pubmed, PsycINFO, Web of Knowledge, and Embase were searched for controlled SC intervention studies published between 01-01-2003 and 01-01-2016. Forty-one studies, comprising 1,508 patients with schizophrenia, autism spectrum disorders, or acquired brain injury were included. Outcome measures evaluated emotion perception (EP), social perception (SP), Theory of Mind (ToM), and social functioning (SF). The meta-analyses showed that interventions were effective in improving SC (Cohen'sd=.71). Interventions targeting one specific SC function were found to be most effective (d=.89), followed by broad-based interventions, targeting non-SC domains in addition to SC (d=.65), and comprehensive interventions, that target multiple SC processes (d=.61). Targeted interventions were especially effective in improving EP and ToM. Comprehensive interventions were able to ameliorate EP, ToM, and SF. Broad-based interventions were especially effective in improving SF, but also showed effects on EP and ToM.


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.


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