Elliot Clayton Brown

Background: Differences in the thalamocortical system have been shown in patients with major depressive disorder (MDD). Given prior evidence of phenotypic heterogeneity by the age of onset in MDD, we examined whether differences in thalamocortical connectivity could identify biological subtypes of MDD defined by the age of illness onset. Methods: A total of 94 subjects including 20 early-onset (EO) MDD (onset, 18 years), 34 adult-onset (AO) MDD, and 40 healthy controls (HCs) underwent resting-state functional MRI. Blood-oxygen-level-dependent time courses were extracted from six cortical regions of interest (ROIs) consisting of frontal, temporal, parietal, and occipital lobes and precentral and postcentral gyri. Each ROI's time course was then correlated with each voxel in thalamus, while covarying out signal from every other ROI. Results: The analysis of variance results showed significant main effects of group in frontal and temporal connectivity with thalamus. Group contrasts showed a right fronto-thalamic hypo-connectivity only in AO-MDD, but not in EO-MDD, when compared to HCs. However, direct comparison between EO-MDD and AO-MDD showed no differences. Furthermore, there was a right temporal-thalamic hyperconnectivity in both EO-MDD and AO-MDD patients relative to HCs. These results were not accounted for by sex, age, or illness burden. Conclusion: The age of illness onset may be a source of heterogeneity in fronto-thalamic intrinsic connectivity in MDD.

Background: Early-onset major depressive disorder (EO-MDD), beginning during childhood and adolescence, is associated with more illness burden and a worse prognosis than adult-onset MDD (AO-MDD), but little is known about the neural features distinguishing these subgroup phenotypes. Functional abnormalities of the amygdala are central to major depressive disorder (MDD) neurobiology; therefore, we examined whether amygdala intrinsic connectivity (IC) can differentiate EO-MDD from AO-MDD in a cohort of adult MDD patients. Subjects and methods: Twenty-one EO-MDD (age of onset #18 years), 31 AO-MDD patients (age of onset $19 years), and 19 healthy controls (HCs) underwent resting-state functional magnetic resonance imaging (7 minutes). Amygdala seed-based resting-state functional connectivity was compared between groups. Results: AO-MDD patients showed loss of inverse left amygdala-left dorsolateral prefrontal cortex IC and increased inverse left amygdala-left inferior parietal IC, compared to both HCs and EO-MDD. EO-MDD showed a switch from inverse to positive IC with right dorsomedial prefrontal cortex, compared to HCs and AO-MDD. This effect was removed when we controlled for illness burden. Conclusion: Alterations in amygdala IC with the default-mode network were specifically related to EO-MDD, whereas amygdala IC with executive cognitive control regions was preferentially disrupted in AO-MDD. Increased illness burden, an important clinical marker of EO-MDD, accounted for its specific effects on amygdala IC. Brain imaging has the potential for validation of clinical subtypes and can provide markers of prognostic value in MDD patients.

BACKGROUND: Motivational deficits in people with schizophrenia (PSZ) are associated with an inability to integrate the magnitude and probability of previous outcomes. The mechanisms that underlie probability-magnitude integration deficits, however, are poorly understood. We hypothesized that increased reliance on "valueless" stimulus-response associations, in lieu of expected value (EV)-based learning, could drive probability-magnitude integration deficits in PSZ with motivational deficits. METHODS: Healthy volunteers (n = 38) and PSZ (n = 49) completed a learning paradigm consisting of four stimulus pairs. Reward magnitude (3, 2, 1, 0 points) and probability (90%, 80%, 20%, 10%) determined each stimulus's EV. Following a learning phase, new and familiar stimulus pairings were presented. Participants were asked to select stimuli with the highest reward value. RESULTS: PSZ with high motivational deficits made increasingly less optimal choices as the difference in reward value (probability 3 magnitude) between two competing stimuli increased. Using a previously validated computational hybrid model, PSZ relied less on EV ("Q-learning") and more on stimulus-response learning ("actor-critic"), which correlated with Scale for the Assessment of Negative Symptoms motivational deficit severity. PSZ specifically failed to represent reward magnitude, consistent with model demonstrations showing that response tendencies in the actor-critic were preferentially driven by reward probability. CONCLUSIONS: Probability-magnitude deficits in PSZ with motivational deficits arise from underutilization of EV in favor of reliance on valueless stimulus-response associations. Confirmed by our computational hybrid framework, probability-magnitude integration deficits were driven specifically by a failure to represent reward magnitude. This work provides a first mechanistic explanation of complex EV-based learning deficits in PSZ with motivational deficits that arise from an inability to combine information from different reward modalities. Many people with schizophrenia (PSZ) suffer from a reduced tendency to engage in goal-directed behavior (1,2), termed amotivation or avolition. These deficits in motivation can contribute substantially to poor functional capacity and quality of life (3-5). One explanation suggests that motivational deficits result from a specific impairment in the ability to precisely represent the value of an action or choice (expected value [EV]) coupled with overreliance on "valueless" stimulus-response associations (6-8). Support for this computational account, however, comes from studies using reinforcement learning (RL) paradigms in which reward probability (the chance of obtaining a reward) solely determines EV. Importantly, other evidence indicates that EV estimation deficits in PSZ (with motivational deficits) are most prominent when EV depends on the successful integration of reward magnitude (size) and probability. One important line of evidence suggesting prominent deficits in EV representation comes from the Iowa Gambling Task (9), in which participants select from four card decks with varying reward magnitude and probability. Performance deficits on this task, in PSZ, are driven by a reduced ability to integrate long-term outcome magnitude and probability (10-12). These deficits extend to contexts in which participants choose between earning a small certain reward or gamble for a larger reward (a "framing" task) (13). When reward magnitude and probability vary continuously, impaired EV computations in PSZ with motivational deficits are primarily driven by decreased sensitivity to reward magnitude (14). In contrast, 280

BACKGROUND: The current study was designed to test the hypothesis that motivational deficits in schizophrenia (SZ) are tied to a reduced ability to differentially signal gains and instances of loss-avoidance in the brain, leading to reduced ability to form adaptive representations of expected value.
METHODS: We administered a reinforcement learning paradigm to 27 medicated SZ patients and 27 control subjects in which participants learned three probabilistic discriminations. In regions of interest in reward networks identified a priori, we examined contrasts between trial types with different expected values (e.g., expected gain–nonmonetary) and between outcomes with the same prediction error valence but different experienced values (e.g., gain–loss- avoidance outcome, miss–loss outcome).
RESULTS: Both whole-brain and region of interest analyses revealed that SZ patients showed reduced differentiation between gain and loss-avoidance outcomes in the dorsal anterior cingulate cortex and bilateral anterior insula. That is, SZ patients showed reduced contrasts between positive prediction errors of different objective values in these areas. In addition, we observed significant correlations between gain–loss-avoidance outcome contrasts in the ventral striatum and ratings for avolition/anhedonia and between expected gain–nonmonetary contrasts in the ventral striatum and ventromedial prefrontal cortex.
CONCLUSIONS: These results provide further evidence for intact prediction error signaling in medicated SZ patients, especially with regard to loss-avoidance. By contrast, components of frontostriatal circuits appear to show reduced sensitivity to the absolute valence of expected and experienced outcomes, suggesting a mechanism by which motivational deficits may emerge.

Previous studies reported attenuated cortisol reactivity as one explanation for poor social functioning in schi-zophrenia. Recent research has demonstrated that both glucocorticoid and oxytocin systems are central to stress regulation. Here, we studied the associations between basal oxytocin, stress-induced cortisol levels, and social functioning and social support in schizophrenia. A mock job interview was used as an ecologically-valid social stressor in 32 schizophrenia patients. Blood samples were taken before and after stress induction to assess basal oxytocin and cortisol levels. In addition social functioning and social support scales were collected. Patients were divided into cortisol responders and non-responders according to percentage change following stress induction. Our findings revealed a possible subgroup of patients who did not exhibit attenuated cortisol responses. Importantly, cortisol responders had generally better social functioning, but perceived social support was not different between groups. There was also no evidence of a relationship between cortisol and oxytocin. This study highlights the heterogeneity of cortisol responses to stress in a schizophrenia population, and the importance of the relationship between social functioning and cortisol reactivity. These findings could be relevant when considering therapeutic interventions that manipulate endocrinology in order to improve real-world functioning.

Impairments in the mirror neuron system (MNS) have been implicated as a possible underlying neurological basis for deficits in higher-level social cognition in schizophrenia. Previous work testing this hypothesis has used the electroencephalographic mu rhythm as an index of MNS activity, with studies showing mixed results. Here we investigated the role that reward plays in modulating the mu rhythm, and its association with empathy and emotional mental state reasoning. A group of schizophrenia patients and a healthy control group completed an action observation paradigm in which they watched actions that were financially rewarding, punishing, or neutral. Patients showed intact reward-related modulation of the mu rhythm, and greater mu suppression was associated with greater negative symptoms. There was also a trend for reduced mu suppression in patients. Furthermore, both empathy and emotional mental state reasoning were associated with the degree of mu suppression, but only in healthy controls. These findings confirm the association between the mu suppression and high-level social cognition. It is possible that schizophrenia patients utilize different cognitive routes to infer mental states. The demonstration that reward influences the degree of mu suppression in schizophrenia patients may help to account for previous conflicting findings in the literature.

Sufi meditation is a spiritual form of physically active meditation in which performers (Semazens) whirl without losing conscious awareness and while internally focusing on reaching an ecstatic state, thus requiring substantial motor and cognitive control and monitoring. Studies have argued that the experience of the meditator may affect the strength of the brain activations because more experienced meditators may need less cognitive effort to reach the ecstatic state. Despite this, our knowledge about the associations between emotional states of the meditators and activated brain areas during meditation remains unknown. With this in mind, fourteen male Semazens were recruited for this study. All Semazens performed Sema meditation under the scanner using imagined whirling techniques. An active control condition was used to explore brain areas specific to Sema meditation. Measures of affective states and psychiatric symptoms were also collected. Statistical parametric maps were created to compare the meditation vs. control conditions. Accordingly, Sema meditation specifically evoked activations in left anterior cingulate cortex (ACC) and left orbitofrontal areas. Activations in ACC were negatively correlated with the positive affect of the Semazens suggesting that less cognitive effort required to reach the meditative state in Semazens was associated with more positive affect. Despite previous studies highlighting the experience of the meditators as a predictor of brain activation, we found that affective state may also be an important factor that may facilitate emotion regulation and cognitive monitoring in the brain. Our findings may also be applicable to the effects of meditation on psychological and emotional wellbeing.

Objective: Recent studies in patients with Bipolar Disorder (BD) have revealed problems in emotion recognition, specifically for negative emotions, which have been subsequently related to amygdala activity. Previously, the prosocial neuropeptide oxytocin has been shown to be one hormone that alters emotion perception capacities and modulates amygdala response. Accordingly, the aim of this study was to see if plasma oxytocin levels have specific effects on predicting emotion recognition patterns in BD.
Methods: Twenty-eight remitted BD patients were recruited for this study and the Vienna Emotion Recognition Task was given. In addition, blood samples were collected for plasma oxytocin analysis.
Results: Strong associations were found between fearful emotions and basal oxytocin levels, which were supported by a stepwise regression analysis. Patients with higher levels of basal oxytocin also exhibited greater recognition of fearful emotions.
Conclusions: The relationship between recognition of fearful faces and individual endogenous oxytocin levels may contribute to explaining individual differences in social functioning and amygdala dysfunction in BD.

Introduction: Understanding the biological underpinnings of unipolar (UD) and bipolar depression (BD) is vital for avoiding inappropriate treatment through the misdiagnosis of bipolar patients in their first depressive episode. One plausible way to distinguish between UD and BD is to compare EEG brain dynamics to identify potential neurophysiological biomarkers. Here we aimed to test group differences in EEG power, cordance and coherence values between UD and BD.
Methods:Twenty-five bipolar and 56 unipolar depression patients were recruited. Sociodemographic and clinical variables were collected in addition to resting state EEG. Data was analyzed with multivariate and repeated analyses of variance where parametric assumptions were met.
Results: Accordingly, we did not find any differences in the EEG absolute power and frontal asymmetry indexes between UD and BD. Regarding cordance, significant group differences were observed in the right theta cordance values (p=0.031). Regarding coherence, BD patients (as compared to UD) exhibited greater central–temporal theta (p=0.003), and parietal–temporal alpha (p=0.007) and theta (p=0.001) coherence. Lastly, less alpha coherence in BD was present at right frontal–central (p=0.007) and central inter-hemispheric (p=0.019) regions.
Conclusions: Our results demonstrate that EEG cordance and coherence values have potential to discriminate between UD and BD. The loss of temporal synchronization in the frontal interhemispheric and right sided frontolimbic neuronal networks may be a unique feature that distinguishes between BD and UD.

With the contribution of social neuroscience in neuropsychiatry, a large body of literature has suggested that schizophrenia is a product of a dysfunction in the ‘social brain’. The rising interest in the field of social neuroscience has provided an instrumental foundation for understanding how the social brain may be going wrong in schizophrenia, and how neurobiologic abnormalities may help to explain deficits in social cognition. So far, work using animal disease models and neuroimaging in patients has already made progress in uncovering some of the neurobiologic factors related to social cognitive deficits in schizophrenia. This chapter will summarize the work to date in this area, while also raising some crucial unresolved issues in this field by taking a critical view on the literature, and making future suggestions for research.

Exciting new research has revealed that the administration of oxytocin can improve empathetic abilities, increase trustworthiness and other attachment-related behaviors, and reduce social anxiety in both healthy and some clinical populations. A growing body of work has explored the potential therapeutic benefit of oxytocin for improving deficits in social cognition in schizophrenia. The aim of this chapter is to review the current state of this work, including current limitations and issues for future work.

Positive and negative reinforcers guide our behaviors as we interact with others in our social environment. Here, we present evidence that highlights a central role for reward in the general functioning of the mirror neuron system (MNS). We also discuss the relevance of reward-related modulation on other previous findings revealing certain properties of the MNS, and on social context and psychopathology.

" Patients with anxiety spectrum disorders are a highly heterogeneous group, requiring new therapeutic strategies and individualized treatment monitoring. Today, there is a growing interest for implementing biological approaches to clinical practice in psychiatry. Quantitative EEG is an excellent tool in this regard, though it has been widely underestimated when compared to recent neuroimaging techniques. In this case series, we presented four cases with a different diagnosis of anxiety spectrum disorder and evaluated their qEEG changes before and after the treatment. In addition, we also calculated the so-called EEG cordance values as an index of cerebral perfusion and cingulate cortex activity. According to the results, there appears to be an increase in the frontal beta and theta band in our cases, which has responded to treatment. In regards to the cordance values, we found that there was a reduction in the prefrontal regions up to %38 percent following the treatment. Based on previous studies, this may also indirectly suggest reduction in the cingulate cortex activity. The possible implications of these findings were discussed. Taken together, this case series highlighted the potential use of qEEG power values, normative z-scores and cordance values in treatment response monitoring of anxiety spectrum disorders."

Interpreting others' actions is essential for understanding the intentions and goals in social interactions. Activity in the motor cortex is evoked when we see another person performing actions, which can also be influenced by the intentions and context of the observed action. No study has directly explored the influence of reward and punishment on motor cortex activity when observing others' actions, which is likely to have substantial relevance in different social contexts. In this experiment, EEG was recorded while participants watched movie clips of a person performing actions that led to a monetary reward, loss or no change for the observer. Using the EEG mu rhythm as an index of motor resonance, our results demonstrate that observation of rewarding actions produce significantly greater motor cortex activity than punishing or neutral actions, with punishing actions producing greater activity than neutral ones. In addition, the dynamic change in the mu rhythm over sensorimotor cortex is modulated by reward and punishment, with punishing actions producing a prolonged suppression. These findings demonstrate that the associated reward value of an observed action may be crucial in determining the strength of the representation of the action in the observer's brain. Consequently, reward and punishment is likely to drive observational learning through changes in the action observation network, and may also influence how we interpret, understand, engage in and empathize with others' actions in social interaction.

Research has shown that the brain is constantly making predictions about future events. Theories of prediction in perception, action and learning suggest that the brain serves to reduce the discrepancies between expectation and actual experience, i.e., by reducing the prediction error. Forward models of action and perception propose the generation of a predictive internal representation of the expected sensory outcome, which is matched to the actual sensory feedback. Shared neural representations have been found when experiencing one's own and observing other's actions, rewards, errors, and emotions such as fear and pain. These general principles of the "predictive brain" are well established and have already begun to be applied to social aspects of cognition. The application and relevance of these predictive principles to social cognition are discussed in this article. Evidence is presented to argue that simple non-social cognitive processes can be extended to explain complex cognitive processes required for social interaction, with common neural activity seen for both social and non-social cognitions. A number of studies are included which demonstrate that bottom-up sensory input and top-down expectancies can be modulated by social information. The concept of competing social forward models and a partially distinct category of social prediction errors are introduced. The evolutionary implications of a "social predictive brain" are also mentioned, along with the implications on psychopathology. The review presents a number of testable hypotheses and novel comparisons that aim to stimulate further discussion and integration between currently disparate fields of research, with regard to computational models, behavioral and neurophysiological data. This promotes a relatively new platform for inquiry in social neuroscience with implications in social learning, theory of mind, empathy, the evolution of the social brain, and potential strategies for treating social cognitive deficits.

Impairments in social functioning commonly seen in schizophrenia are thought to be mediated by deficits in the domains of social cognition. Some previous research has explored how social cognitive skills and psychotic symptoms are associated with social functioning, however these associations are still under debate. The main aim of this study was to investigate the relationship between different domains of social cognition and psychotic symptomatology, and also to look at the relationships with individual subdomains of social functioning within a clinically stable schizophrenia population. 45 outpatients were recruited and symptoms were assessed with the PANSS, and measures of emotion processing, affective and cognitive theory of mind (ToM), mental state reasoning attributional biases, and social functioning were taken. A correlational analysis was performed with the data. Following this, a regression analysis was used to reveal which domains of social cognition best predicted psychotic symptoms. In this stable group of patients, our results support the suggestion of a likely distinction between affective and cognitive components of ToM. The study also demonstrated that ToM and mental state reasoning were the best predictors of psychotic symptoms. Here we reveal that cognitive ToM had the most widespread relationship with social functioning, across multiple subdomains, while only some specific subdomains of social functioning correlated with other domains of social cognition and symptomatology. Further to this, positive symptoms were associated with much fewer subdomains of social functioning than negative and general symptoms. These findings imply that different aspects of social functioning may be served by different domains of social cognition and symptomatology.

The group of schizophrenias concerns heterogeneous psychopathological syndromes that are often associated with neurocognitive impairment and poor functional outcome. Research suggests that many symptoms associated with schizophrenia can be interpreted as a result of poor social cognition and “metacognition”, two related concepts that refer to the ability to recognise and interpret social signals, to reflect upon mental states of oneself and others, and to flexibly entertain this knowledge in social interaction and problem-solving. The present article reviews the evidence for social cognitive and metacognitive deficits in schizophrenia and whether training in these domains may improve poor social functioning. In schizophrenia social cognition and metacognition are intrinsically linked with social functioning, yet partly dependent on neurocognition. In addition, there is some evidence to suggest that social and metacognitive training can improve social functioning, possibly depending on patients' learning potential and motivation. Future studies may aim at resolving the question which syndromal subgroups within the schizophrenia phenotype benefit best from social and metacognitive training, and which groups may need additional neurocognitive training to improve social functioning.

BACKGROUND: Previous research has suggested that neurocognitive functioning predicts best the potential of patients with schizophrenia to acquire newly learned material, which, in turn may impact patients' social functioning. Recent studies have also shown that intrinsic motivation and metacognitive abilities play a decisive role in social functioning in schizophrenia. Accordingly, the present study sought to examine the relationship between intelligence, motivation, metacognition, and learning during a cognitive remediation experimental training. We hypothesized that metacognition and intrinsic motivation would have a strong relationship and independently predict learning potential.
METHOD: Thirty-two patients with schizophrenia who fulfilled the criteria of functional remission were recruited. In a pre-training-post experimental design, patients' learning potential was assessed using previously defined cognitive remediation training for WCST. Intrinsic motivation was examined using Intrinsic Motivation Inventory for schizophrenia; mastery, a domain of metacognition, was measured using the Metacognitive Assessment Scale.
RESULTS: Metacognition significantly correlated with subdomains of intrinsic motivation. Patients with higher intrinsic motivation and preserved metacognition improved more in the learning paradigm compared to poorly motivated patients and patients with reduced metacognitive abilities. In particular, "mastery" was determined as an independent predictor of learning potential.
CONCLUSIONS: Motivation and metacognition are important predictors of learning in schizophrenia. Psychological interventions in schizophrenia may therefore consider incorporating techniques to stimulate metacognitive and motivational abilities as well as developing individualized training programs.

The term "schizophrenia" refers to a debilitating group of disorders that usually results in a severely impaired quality of life (QoL). Symptomatology appears to have a substantial role in determining QoL, although the relationship between QoL and specific psychotic symptoms is still unclear and has demonstrated mixed results. Due to the intrinsic importance of social functioning in QoL, and the mediating effect of social cognition on social functioning, the aim of this study was to try to investigate QoL in schizophrenia, not only in terms of symptomatology, but also in consideration of potential neurocognitive and social cognitive contributing factors. Twenty-eight clinically stable patients with schizophrenia performed a broad range of neurocognitive and social cognitive assessments, and also participated in a semi-structured interview of QoL, assessing four partially independent subdomains of QoL. A stepwise regression model was used to determine the best predictors of QoL, and additionally a mediator analysis was performed to test for the mediating power of social cognition on QoL. Negative symptoms, intelligence, executive functioning and social cognition all had some power in predicting QoL in schizophrenia. Though most interestingly, mental state reasoning was specifically found to be most strongly related with the Intrapsychic Foundation subdomain of QoL, whereas neurocognition and symptom severity were associated with other subdomains of QoL. The association between mental state reasoning and the more "internal" aspects of QoL in schizophrenia may reflect a specific role for social cognition in introspective and subjective judgments of one's own QoL, whereas neurocognition and negative symptomatology may be more predictive of the external or extrinsic aspects of QoL. In conclusion, social cognitive skills appear to play a crucial role in the experience of one's own subjective well-being, which could help to explain previous inconsistencies in the literature investigating QoL in schizophrenia.

Therapeutic strategies for improving social cognition in patients with schizophrenia have shown much promise in improving social functioning, as well as remediating core psychotic symptoms. However, the efficacy of previous interventions has often been limited by the ambiguity and inconsistency of the categorized subdomains of social cognition, including theory of mind, emotion processing, social perception and attributional bias. Recent research in social and cognitive neuroscience has revealed many new issues that could contribute to the development of more integrated approaches for improving social functioning. The application of such neuroscientific work to a therapeutic and diagnostic context is likely to encourage more effective transference of learned skills to real-world social functioning. This article seeks to provide a comprehensive review of previous social cognitive interventions for schizophrenia, highlight some crucial limitations of these and present the relevance of recent advances in neuroscientific research in possible future treatment strategies. It is emphasized that a more integrated and naturalistic approach for improving social functioning with greater sensitivity for neuroscientific findings related to the psychopathology of schizophrenia is warranted.

Activity in the motor cortex is induced when we watch others performing actions (Gallese et al., 1996), and can also be influenced by the intentions and context of the observed action (Iacoboni et al., 2005; Perry et al., 2010). The effect of reward and punishment on motor resonance has not yet been directly explored, though it is likely that different social contexts will be associated with different degrees of reward and punishment. EEG was recorded from 17 healthy right-handed females while they passively observed video clips of a person performing actions that led to a monetary reward, loss (i.e. punishment) or no change for the observer. The study compared the EEG mu rhythm suppression between conditions and showed that it was modulated by the motivational value of the observed action, with activity being the largest for rewarding actions and the least for neutral actions. We also show temporal dynamic changes in the mu rhythm power of these effects, with punishing actions producing delayed and prolonged mu suppression. This provides evidence for reward-related modulation of motor cortex activity during action observation. Our findings suggest that future studies investigating the neural activity related to the observation of others' actions may need to consider the effect of the reward (and punishment) associations made with the observed actions when comparing across conditions. The presence of reward-related modulation in motor resonance may also help to explain some previous inconsistent findings comparing mu rhythm activity in different clinical groups such as autism spectrum disorders (Oberman et al., 2012) and in schizophrenia (Singh et al., 2011). The reward and punishment associated with the actions we see in our social environment is likely to drive observational learning and may also influence how we interpret, understand, engage in and empathize with others’ actions in social interaction.

Background:
An NIMH workshop has identified 5 key domains of social cognition that are at a deficit in people with schizophrenia (Green et al., 2008). These include emotion processing, theory of mind, attributional style, social perception and social knowledge. The efficacy of future social cognition training strategies is likely to be substantially influenced by the degree of independence and overlap between these social cognitive domains. The aim of this study is to address this very issue with a factor analysis that looks at the grouping of measures of three main social cognitive domains.   

Methods:
Forty-five patients diagnosed with schizophrenia were recruited and given a battery of measures for social cognition performance. For theory of mind, both the Hinting Task and the Mind in the Eyes test were done. For emotion processing skills, facial emotion recognition and discrimination tasks were administered. Attributional style was assessed with Internal Personal Situational Attributions Questionnaire (IPSAQ).  An exploratory factor analysis was performed using the scree test to select the number of factors and an oblique rotation algorithm was chosen. Indexes were highlighted based on the strength of their loadings.

Results:
The factor analysis including measures of social cognition and symptomatology converged on a four-factor solution. Our four-factor solution explained a total of 70% of the variance with factor one contributing to 29% , factor two to 16%, factor three to 13%  and factor four to 12% of the variance. The first factor appears to be strongly loaded by emotion processing and affective theory of mind measures with the grouping of emotion recognition and discrimination and reading the mind in the eyes. Reasoning skills (UOT) are shown to be strongly loaded on the second factor, while externalizing bias, PANSS scores and cognitive theory of mind (Hinting Task) also loaded on to factor 2 but also contributed more weakly to loading in the first and third factors. Personalizing bias appears to be the only measure strongly loaded in the third factor and need for closure in the fourth.

Discussion:
It is clear from these results that the different domains of social cognition are not easily nor definitively separable or independent. In particular, the loadings of externalizing bias and cognitive theory of mind in the factor analysis are spread over three factors with little difference between factor loads. Negative symptomatology may also be more closely associated with cognitive theory of mind, as opposed to affective theory of mind and emotional processing, which is a surprising result. Affective theory of mind as measured by the Mind in the Eyes test appears to be strongly grouped with emotion processing rather than theory of mind as such. Therefore this test may actually be only accounting for deficits in emotion processing. According to our results, reasoning skills could be having a substantial mediating effect on more cognitive social domains. Interestingly, need for closure is independent from currently defined social cognitive domains altogether, as confirmed by previous research. Current definitions of social cognitive domains using existing measures may not be sufficient for assessing specific and distinct social cognitive skills in a population suffering from schizophrenia. Future research in social cognition that aims to inform therapeutic interventions to improve social functioning in schizophrenia will benefit from including more integrated approaches for assessment.

Background: Previous research has concluded that the capacity to work is an important component of real life social functioning for patients suffering from schizophrenia. A few studies have investigated predictors of occupational outcome in schizophrenia, though most have used neurocognitive scores in their regression models. Without disregarding the effect of individual neurocognitive performance on occupational outcome, our aim with this study is to investigate the effect of intrinsic motivation and metacognition on occupational functioning.

Method: Thirty schizophrenia patients in symptomatic remission according to Andreasen’s remission criteria (2005) were recruited.  Occupational outcome was assessed by the employment/occupation subscale of the Social Functioning Scale (Birchwood et al., 1990). Metacognition was measured with the Metacognition Assessment Scale (Lysaker et al., 2005).Intrinsic motivation was measured with the IMI-SC scale (Choi et al., 2008) in this case, after cognitive remediation training of WCST skills. IQ levels and baseline WCST number of completed groups was measured as neurocognitive variables.

Results: Occupation- employment found as significantly correlated with WCST completed categories (r=.46,  p= .007) ,  mastery levels of metacognition (r=.48,  p= 004)  and  metacognitive self-reflectivity (r=.68,  p= <.001). Controversially, no significant correlation found between intrinsic motivation (r=.041, p= 414) and IQ levels (r=.24, p= .102).  A hierarchical regression model, after ruling out inflation of variance by multi-collinearity analysis, explained a large proportion of the variance (R2adj= .483, df=1, 24, p=.001, see Table 1). Metacognitive self-reflectivity independently predicted occupational functioning after variance from other variables was controlled in each step. Mastery levels of metacognition and executive functioning were also found as independent predictors. Total intrinsic motivation failed to explain overall variance independently in any of the steps, although it seems to have a contributing role in the last step.

Discussion: Previous studies of occupational functioning found that executive functioning explained a significant proportion of the variance (Dickerson et al., 2008). In contrast, in our study it seemed to have less importance in a symptomatically remitted group of patients. According to the results, metacognitive self-reflectivity and mastery levels of metacognition appeared to have a more crucial contribution towards accomplishing remission of social functioning after symptomatic remission. However, our results showed less importance of intrinsic motivation as compared to other studies (Choi et al., 2010).We believe that, while perceived lack of interest and enjoyment of a particular task may be related to the core symptoms of schizophrenia, perceived value and usefulness, which supports intrinsic motivation, has the potential to be improved by targeted interventions for metacognition.