Social Dysfunction in Psychosis Is More Than a Matter of Misperception: Advances From the Study of Metacognition

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.

Interventions for social cognitive deficits

Interventions for social cognitive deficits establishes the large impact these deficits exert on psychosocial functioning in major depressive disorder. The chapter reviews a variety of impairments of social cognition and how these may influence psychosocial functioning in the key domains of social performance, emotional/empathic performance, general cognitive functioning, and quality of life. It introduces multiple treatment modalities including antidepressant medication, psychotherapeutic approaches, and procedural interventions with potential treatment efficacy on facial affect recognition, interpretation of affective pictures, theory of mind performance, and prosody. It reviews evidence indicating that many current therapies are shown to have a normalizing effect on the accuracy of interpretation and the reduction of underlying negative interpretative bias. It concludes from evaluating the literature that certain antidepressants seem to correct facial affect recognition deficits, and several psychotherapeutic approaches appear well-suited for addressing impaired theory of mind or mood-congruent interpretive biases.

Social cognition and major depressive disorder: impact on psychosocial function and therapeutic opportunities

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.

Disease-specific contribution of pulvinar dysfunction to impaired emotion recognition in schizophrenia

One important aspect for managing social interactions is the ability to rapidly and accurately perceive and respond to facial expressions, which is highly dependent upon intact processing within both cortical and subcortical components of the early visual pathways. Social cognitive deficits, including face emotion recognition (FER) deficits, are characteristic of several neuropsychiatric disorders, including schizophrenia (Sz) and autism spectrum disorders (ASD). Here, we investigated potential visual sensory contributions to FER deficits in Sz (n=28) and adult ASD (n=20) participants compared to neurotypical (n=30) controls using task-based fMRI during an implicit static/dynamic FER task. Compared to neurotypical controls, both Sz and ASD participants had significantly lower FER scores which interrelated with diminished activation of the superior temporal sulcus (STS). In Sz, STS deficits were predicted by reduced activation of both early visual regions and the pulvinar nucleus of the thalamus, along with impaired cortico-pulvinar interaction. By contrast, ASD participants showed patterns of increased early visual cortical and pulvinar activation. Large effect-size structural and histological abnormalities of pulvinar have previously been documented in Sz. Moreover, we have recently demonstrated impaired pulvinar activation to simple visual stimuli in Sz. Here, we provide the first demonstration of a disease-specific contribution of impaired pulvinar activation to social cognitive impairment in Sz.

Aberrant Activation of the Mentalizing Brain System During Eye Gaze Discrimination in Bipolar Disorder

Bipolar disorder (BD) is associated with a range of social cognitive deficits. This study investigated the functioning of the mentalizing brain system in BD probed by an eye gaze perception task during fMRI. Compared with healthy controls (n = 21), BD participants (n = 14) showed reduced preferential activation for self-directed gaze discrimination in the medial prefrontal cortex (mPFC) and temporo-parietal junction (TPJ), which was associated with poorer cognitive and social functioning. Aberrant functions of the mentalizing system should be further investigated as marker of social dysfunction and treatment targets.

Association of visual motor processing and social cognition in schizophrenia

Patients with schizophrenia have difficulties in social cognitive domains including emotion recognition and mentalization, and in sensorimotor processing and learning. The relationship between social cognitive deficits and sensorimotor function in patients with schizophrenia remains largely unexplored. With the hypothesis that impaired visual motor processing may decelerate information processing and subsequently affects various domains of social cognition, we examined the association of nonverbal emotion recognition, mentalization, and visual motor processing in schizophrenia. The study examined mentalization using the verbal subset of the Chinese version of Theory of Mind (CToM) Task, an equivalent task of the Faux Pas Test; emotion recognition using the Diagnostic Analysis of Nonverbal Accuracy 2-Taiwan version (DANVA-2-TW), and visual motor processing using a joystick tracking task controlled for basic motor function in 34 individuals with chronic schizophrenia in the community and 42 healthy controls. Patients with schizophrenia had significantly worse performance than healthy controls in social cognition, including facial, prosodic emotion recognition, and mentalization. Visual motor processing was also significantly worse in patients with schizophrenia. Only in patients with schizophrenia, both emotion recognition (mainly in prosodic modality, happy, and sad emotions) and mentalization were positively associated with their learning capacity of visual motor processing. These findings suggest a prospective role of sensorimotor function in their social cognitive deficits. Despite that the underlying neural mechanism needs further research, our findings may provide a new direction for restoration of social cognitive function in schizophrenia by enhancing visual motor processing ability.

Neurofeedback Training for Social Cognitive Deficits: A Systematic Review

<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>

Frontal Pole Hypometabolism Linked to Reduced Prosocial Sexual Behaviors in Frontotemporal Dementia and Corticobasal Syndrome

Background: Changes in sexual behaviors in frontotemporal dementia (FTD) are common and multifaceted, but not well characterized. Objective: To characterize changes in sexual behaviors and intimacy in FTD compared to corticobasal syndrome (CBS) and normal controls (NC), and to evaluate the neuroanatomical associations of these changes. Methods: Spouses of 30 FTD patients, 20 CBS patients, and 35 NC completed the Sexual Symptoms in Neurological Illness and Injury Questionnaire (SNIQ), which captures changes in sexual interest, inappropriate sexual behaviors, and prosocial sexual behaviors. 25 patients with FTD and 14 patients with CBS also received 18-flouorodeoxyglucose positron-emission topography (18FDG-PET) scans to determine the metabolic changes associated with these symptoms. Results: FTD patients showed a greater increase in inappropriate sexual behaviors than CBS patients [p = 0.009] and NC [p < 0.001] and a greater decrease in prosocial sexual behaviors than CBS patients [p = 0.026] and NC [p < 0.001]. Groups did not differ in change in sexual interest. Among both patient groups, the most common change was decreased prosocial sexual behaviors p < 0.01. Hypometabolism in Brodmann’s Area 10 (BA10), within the right frontal pole, correlated with decreased prosocial sexual behaviors [p(FWE-corr) <0.05, k = 44]. No anatomical associations were found with other sexual changes. Conclusion: Decreased prosocial sexual behavior was associated with hypometabolism in BA 10, an area tied to social knowledge and theory of mind, supporting the idea that changes reflect social-cognitive deficits due to frontal dysfunction.