REVIEW URRENT C OPINION
Social cognition in serious mental illness Christine M. Hoertnagl a and Alex Hofer b
Purpose of review Social cognition represents a fundamental skill for effective social behavior. It is nowadays widely accepted that individuals suffering from serious mental illness are impaired in this domain. Recent findings Studies published since June 2012 have been reviewed, with a particular focus on theory of mind, social perception, social knowledge, attributional bias, and emotion processing in patients suffering from schizophrenia and mood disorders. Summary The reviewed literature supports previous studies on deficits in social cognition in schizophrenia, major depressive disorder and bipolar disorder, and underscores their relevance in the psychosocial context. Keywords bipolar disorder, major depressive disorder, schizophrenia, serious mental illness, social cognition
INTRODUCTION Social cognition is a multidimensional psychological concept comprising several subdomains and processes that facilitate social interaction, such as the knowledge about the self, perception of others, and interpersonal motivations [1]. Several studies indicate that patients suffering from serious mental illness exhibit impairments in these domains, and that these deficits have a negative impact on social and functional outcomes such as quality of life (QoL), employment status, or social relationships [2,3]. The National Institute of Mental Health consensus statement identified five social cognitive domains to be relevant in patients with schizophrenia: theory of mind (ToM), social perception, social knowledge, attributional bias, and emotion processing [4]. Schizophrenia-related deficits in social cognition and functioning have already been described by Kraepelin in 1919 [5]. Since then, a growing body of evidence has confirmed these impairments. Green et al. [6], for example, investigated three different aspects of social cognition (emotion processing, ToM, and social relationship perception) in prodromal, first episode, and chronically ill patients and found impairments across all domains in all clinical samples. Similarly, social cognitive deficits represent characteristic features of major depressive disorder (MDD) [7,8]. Notably, there is evidence for a mood-congruent negative bias regarding affect perception that is patients
suffering from MDD are mainly impaired in the recognition of positive emotions [9]. As compared with schizophrenia or MDD, the research on social cognition in bipolar disorder, however, is still marginal and provides divergent results. Social cognitive deficits are present during mood episodes, but their occurrence during the euthymic stage of the illness is still unclear [10 ]. &
SOCIAL COGNITION IN SCHIZOPHRENIA AND HIGH-RISK INDIVIDUALS &
Savla et al. [11 ] conducted a meta-analysis of 112 studies providing results from 3908 schizophrenia patients and 3570 healthy control individuals. Patients showed impairments across all social cognitive domains studied (social perception, ToM, emotion perception, and emotion processing) except attributional bias. Greater deficits in social and emotion perception were associated with
a
General and Social Psychiatry Division, and bBiological Psychiatry Division, Department of Psychiatry and Psychotherapy, Medical University Innsbruck, Innsbruck, Austria Correspondence to Christine M. Hoertnagl, MD, General and Social Psychiatry Division, Department of Psychiatry and Psychotherapy, Medical University Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. Tel: +43 512 504 23669; fax: +43 512 504 25267; e-mail: [email protected] Curr Opin Psychiatry 2014, 27:197–202 DOI:10.1097/YCO.0000000000000055
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KEY POINTS Patients suffering from serious mental illness exhibit impairments in social cognition. Impairments in social cognition are negatively associated with patients’ outcomes. Little is known about the effects of medical treatment or nonmedical therapeutic interventions on social cognitive deficits in serious mental illness.
inpatient status, and greater deficits in emotion processing with a longer duration of illness. Similarly, Fiszdon et al. [12 ] investigated emotion processing and ToM in 119 schizophrenia patients and found them to perform worse than healthy control individuals in three out of four tasks. Contrary to Savla et al. [11 ], however, they detected only a weak relationship between task performance and clinical or functional features. Morrison et al. [13] compared social cognition in 36 individuals with psychometrically defined schizotypy and 26 healthy controls and found the former group to perform significantly worse with regard to facial emotion recognition, ToM, and emotion management, but not with regard to social management. Negative schizotypy traits were associated with poorer facial emotion recognition, whereas disorganized schizotypy traits correlated with better social management. Moreover, a poorer facial emotion recognition performance was moderately related with higher levels of general life satisfaction. The authors hypothesized that individuals with impairments in facial emotion recognition may exhibit less insight into poor interpersonal skills such that they may misattribute the cause of interpersonal problems to other people rather than their own impairments, thus preserving their self-esteem and increasing their overall QoL. ToM has been investigated by Langdon et al. [14], Healey et al. [15 ], and Csulky et al. [16]. Patients in early stages of psychosis exhibited impairments in picture-sequencing and jokeappreciation, but not in story-comprehension [14]. The authors, therefore, suggested that tests placing minimal demands on language processing and involving indirect, rather than explicit, instructions to assess ToM might be best suited to detect ToM impairments in early stages of psychosis. Interestingly, in high-risk individuals who were assessed for up to 2 years, baseline ToM performance significantly predicted later conversion to psychosis beyond intelligence quotient (IQ) scores. However, ToM was also significantly correlated with total &
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baseline disorganization and negative symptoms. Accordingly, ToM deficits might predate conversion to psychosis, but one must consider initial symptoms as well [15 ]. Csukly et al. [16] examined potential ToM differences between patients suffering from the deficit syndrome or nondeficit schizophrenia, and healthy controls. Control individuals outperformed both patient groups, but there were no significant differences between the two schizophrenia subgroups. Due to the small number of participants, this finding clearly requires replication. Comparelli et al. [17] investigated facial emotion recognition in a sample of 97 patients meeting the diagnostic criteria for schizophrenia, schizophreniform disorder, or schizoaffective disorder and found patients to perform worse on negative emotions than a healthy control group. In patients, the degree of cognitive/disorganized symptoms correlated with impairments in facial recognition abilities, but no group differences were detected. Next to deficits in facial emotion recognition, Tseng et al. [18] reported on prosodic impairments in schizophrenia patients, particularly with regard to the recognition of fearful emotions. An inverse correlation was found between the degree of positive symptoms and recognition accuracy for happy emotions. In a study performed by Simpson et al. [19 ], emotion recognition was significantly less accurate in patients than in control individuals during both an audio only and a visual only condition, but did not differ during a combined condition. These findings demonstrate that patients benefit from multimodal stimulus presentation of emotion and support hypotheses whereupon visual attention to salient facial features may serve as a mechanism for accurate emotion identification. &
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Social cognition and its relationship with neurocognition Barbato et al. [20] focused on the question whether social cognition serves as a mediator between neurocognition and functional outcome in individuals at clinical high risk for psychosis. Despite their finding of a direct relationship between neurocognition and functioning as well as between social cognition and functioning, social cognition did not seem to mediate the pathway from neurocognition to functional outcome. Similarly, Mehta et al. [21] systematically reviewed 20 studies reporting factor analyses of social cognition and neurocognition in schizophrenia and provided empirical evidence for the distinctiveness of these two domains. Volume 27 Number 3 May 2014
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Santosh et al. [22] reported on significant correlations between social and cognitive functioning. Moreover, cognitive deficits showed a stronger correlation with the degree of negative than with the degree of positive symptoms. Altogether, both positive and negative symptoms as well as verbal fluency performance predicted social functioning.
Therapeutic interventions In a review by Kucharska-Pietura and Mortimer [23], antipsychotic drugs of either class demonstrated little reliable effect upon social cognition. However, the authors correctly noted that the literature suffers from inconsistencies in study designs and small sample sizes. Hori et al. [24] examined whether switching polypharmacy therapy to monotherapy would improve cognitive and social functioning in patients with schizophrenia. For this purpose, 39 schizophrenia patients receiving two antipsychotics either continued this treatment or were switched to monotherapy. As compared with the continuing group, the switching group showed significantly greater improvement in attention as well as daily living and work skills after switching. Moreover, a significant correlation was noted between improvement in executive function and improvement in daily living as well as between improvement in work skills and improvement in attention. Kaneko and Keshavan [25 ] reviewed cognitive remediation programs targeting neurocognitive and social cognitive impairments and found them to be effective in schizophrenia. Functional outcomes were significantly better when cognitive remediation was combined with some other form of rehabilitation and when it included strategy coaching. In addition, interventions were likely to be more successful when the skills trained closely approximated those needed in daily life. Lastly, cognitive enhancement therapy, a multicomponent cognitive remediation approach designed to provide enriched cognitive experiences through targeted and integrated neurocognitive and social cognitive training, was also successful in improving social and nonsocial cognitive impairments in schizophrenia. &&
SOCIAL COGNITION IN MOOD DISORDERS Several studies indicate that patients suffering from mood disorders exhibit impairments in social cognition.
Major depressive disorder Fischer-Kern et al. [26] investigated the capacity for mentalization in 46 female inpatients suffering
from MDD and found them to be impaired compared with healthy female controls individuals. In addition, correlations with illness duration and number of admissions suggested that a chronic course of depression results in further mentalizing impairments. Schreiter et al. [27] conducted a systematic review of 37 studies on empathy in individuals with MDD. They concluded that depression was related to high levels of emphatic stress but not to abnormal empathic concern. In addition, depression was related to limited cognitive empathy, as indicated by poor perspective taking, empathic accuracy, and ToM. In line with this finding, Cusi et al. [28] found depressed patients to be impaired on second-order, cognitively demanding ToM scenarios. Poorer ToM ability, in turn, was negatively associated with psychosocial functioning. Loi et al. [29 ] investigated emotion recognition from body language and its possible implications to social adjustment in 51 MDD patients, 68 individuals with a history of MDD but in remission, and 69 healthy control individuals. Experimental tasks included emotion recognition from pointlight walkers, body postures as well as movie stills with masked and unmasked faces. Social adjustment was assessed using the Social Adjustment Scale. This study showed a reduced recognition of happy dynamic and static body displays of emotion in MDD compared with remitted patients and healthy comparison participants. Social adjustment was reduced in both currently depressed and remitted patients relative to healthy controls. The authors indicated that previously collected data supported the notion that among a nonclinical population, stimuli conveying happiness are more easily and rapidly recognized than negative or neutral stimuli, which could be due to the working of a cognitive system biased toward the positive appraisal of its surroundings. Accordingly, they hypothesized that this system is altered in MDD because happy stimuli are judged less accurately during the active phase of depression. Beck et al. [30] investigated the ability to identify affect-laden facial expressions in a sample of 52 depressed patients and 72 healthy individuals. Surprisingly, in four out of six tests, depressive individuals achieved significantly better results. The authors inferred from these findings that patients with MDD are able to estimate reality in a better way as it had already been postulated in the concept of depressive emotional realism [31]. Healthy individuals, however, may tend to distort reality into the positive [32]. Aldinger et al. [33 ] were interested in potential associations between depression and emotion
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recognition, affectivity, and interpersonal problems in a sample of 85 women. In this study, depressive symptoms were positively correlated with error rates in anger recognition, but not with recognition of the other basic emotions. This association was moderated by suppression, a strategy of emotion regulation, measured by the emotion regulation questionnaire [34]. In fact, more severely depressed woman who more frequently used suppression to regulate their emotions showed superior recognition of angry faces than those with lower suppression values. This association was unexpected, as suppression is mostly considered as a dysfunctional emotion-regulation strategy. The authors hypothesized that depressive high suppressors may use this regulation strategy due to the maladaptive schema that they ought to restrict their selfexpression in order to avoid any harm. Fehlinger et al. [35], on the other hand, identified emotion regulation to significantly predict the improvement of depressive symptomatology, whereas problem solving, social competence, stress management, relaxation ability, selfefficacy, and self-esteem were not relevant in this context. Moreover, emotion regulation at pretreatment turned out to be a moderator of the association between improvements in skills and the reduction of depressive symptoms. These findings were in line with the views of other researchers [36,37] who considered deficits in emotion regulation a vulnerability factor for developing mood disorders. Therefore, the authors suggested that incorporating emotion regulation trainings in addition to disorder-specific interventions would optimize therapy outcomes.
Bipolar disorder In a review, Samame´ [38] states that although it is well documented that bipolar disorder is frequently associated with cognitive deficits and suboptimal social adjustment, the social cognitive profile of the illness through its three phases remains unclear. For this purpose, she evaluated 51 studies comparing social cognitive performance of bipolar disorder patients with that of healthy control individuals and found patients to be impaired in emotion recognition and ToM during manic, depressed as well as euthymic phases. In another review, Samame` et al. [10 ] evaluated solely data on euthymic bipolar disorder and healthy individuals to clarify whether patients suffered from deficits in social cognition or not. Next to impairments of moderate magnitude across mentalizing skills small but significant effect sizes were observed for facial emotion recognition. However, no between-group differences were found &
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regarding decision-making. Mercer and Becerra [39], on the other hand, reviewed the literature on a number of dimensions of emotion processing in remitted bipolar disorder patients, including facial emotion recognition, emotional memory, affective ToM, affective attention, and affective auditory information processing. Euthymic patients’ abilities to process emotional material were compromised in three of six studies on affective attention, whereas they did not differ from healthy control individuals with regard to the recall of emotional or neutral information. Findings on facial emotion recognition abilities provided divergent results with 12 studies reporting no deficits, six studies describing deficits, and two studies reporting better performance in remitted bipolar disorder patients than in healthy individuals. Concerning ToM, all studies found deficits in this domain. Altogether, the authors concluded that bipolar disorder patients continue to exhibit some emotion processing deficits during the euthymic phase of the illness. Purcell et al. [40] investigated ToM abilities in 26 bipolar disorder patients in remission and compared them with 29 remitted individuals with MDD and 28 healthy control individuals. They found no group differences regarding ToM accuracy; however, bipolar disorder patients showed a significantly shorter mean response time than the other groups. The authors concluded that ToM is preserved in remitted bipolar disorder, which is in accordance with the literature [41]. Furthermore, the pattern of quicker responding may support the growing research linking impulsivity with bipolar disorder [42]. Fulford et al. [43] found that emotion perception protected QoL in bipolar disorder patients and suggested that it could, therefore, serve as a potential treatment target in this population. Lahera et al. [44 ] investigated the effect of an 18-week social cognition and interaction training in a mixed group of bipolar disorder and schizoaffective patients and compared them with a treatment as usual patient group. Analysis of covariance revealed significant group effects for emotion perception, ToM, and depressive symptoms. The group who received the social cognition and functioning training showed a large increase of face emotion discrimination and face emotion identification as well as a mild increase on emotion recognition capability relative to those who got treatment as usual. As stated by the authors, this study suffered from notable limitations. First, the sample was heterogeneous, as both groups composed of individuals with bipolar disorder I, bipolar disorder II, and schizoaffective disorder. Secondly, no follow-up assessment was conducted. Accordingly, &
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it is unknown whether training effects persist over time.
COMPARISON: SOCIAL COGNITION IN SCHIZOPHRENIA AND BIPOLAR DISORDER Baez et al. [45] evaluated the performance of 15 schizophrenia and 15 bipolar disorder patients compared with 30 healthy control individuals on several social cognition tasks, including emotion processing, empathy, and social knowledge. Impairments were found in both patient groups. They were more severe in schizophrenia than in bipolar disorder patients. Similarly, Goghari and Sponheim [46] who examined facial emotion recognition in 27 schizophrenia and 16 bipolar disorder patients compared with 30 healthy control individuals found more pronounced deficits in schizophrenia than in bipolar disorder. They suggested that this result may be a reflection of a greater degree of brain abnormities in regions associated with facial emotion recognition, such as in the amygdala and hippocampus, in schizophrenia patients. Yalcin-Siedentopf et al. [47] directly contrasted facial emotion recognition abilities in remitted patients with bipolar disorder or schizophrenia, and healthy volunteers. Their findings again indicate that during periods of remission the recognition of facial affect may be less impaired in bipolar disorder patients. Interestingly, associations with residual symptomatology were only present in bipolar disorder but not in schizophrenia patients.
CONCLUSION The reviewed literature supports previous studies on social cognitive impairments in schizophrenia, MDD, and bipolar disorder; however, impairments differ in occurrence and severity. As social cognition is a multidimensional psychological concept comprising several subdomains, an operationalization of them is necessary. The heterogeneity of social cognition tasks clearly impedes the comparability of studies. Therefore, a consensus battery assessing more thoroughly the wide range of social cognitive components is strongly needed. Acknowledgements None. Conflicts of interest A.H. has received payment for lectures from Janssen and Lundbeck. There are no conflicts of interest for C.M.H.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Amodio DM, Frith CD. Meeting of minds: the medial frontal cortex and social cognition. Nat Rev Neurosci 2006; 7:268–277. 2. Fulford D, Peckham AD, Johnson K, et al. Emotion perception and quality of life in bipolar disorder. J Affect Disord 2014; 152–154:491–497. 3. Fett AK, Viechtbauer W, Dominguez MD, et al. The relationship between neurocognition and social cognition with functional outcomes in schizophrenia: a meta-analysis. Neurosci Biobehav Rev 2011; 35:573–588. 4. Green MF, Penn DL, Bentall R, et al. Social cognition in schizophrenia: an NIMH workshop on definitions, assessment, and research opportunities. Schizophr Bull 2008; 34:1211–1220. 5. Kraepelin E. Dementia praecox and paraphrenia. Huntington, NY: Robert E. Krieger Publishing Co. Inc; 1919. 6. Green MF, Bearden CE, Cannon TD. Social cognition in schizophrenia, Part I: performance across phase of illness. Schizophr Bull 2012; 38:854–864. 7. Fischer JE, Sass SM, Heller W, et al. Time course of processing emotional stimuli as a function of perceived emotional intelligence, anxiety, and depression. Emotion 2010; 10:486–497. 8. Leppanen JM. Emotional information processing in mood disorder: a review of behavioural and neuroimaging findings. Curr Opin Psychiatry 2006; 19: 34–39. 9. Suslow J, Junghanns K, Arolt V. Detection of facial expression of emotions in depression. Percept Mot Skills 2001; 92:857–868. 10. Samame` C, Martino DJ, Strejilevich SA. Social cognition in euthymic bipolar & disorder: systematic review and meta-analytic approach. Acta Psychiatr Scand 2012; 125:266–280. This review summarizes the findings of a large number of reports on social cognition in euthymic bipolar disorder patients. 11. Savla GN, Vella L, Armstrong CC, et al. Deficits in domains of social cognition & in schizophrenia: a meta-analysis of the empirical evidence. Schizophr Bull 2013; 39:979–992. This meta-analysis investigated all domains of social cognition in schizophrenia with a huge sample size. 12. Fiszdon JM, Fanning JR, Johannesen JK, et al. Social cognition deficits in & schizophrenia and their relationship to clinical and functional status. Psychiatry Res 2013; 205:25–29. Social cognition and its clinical and functional correlates are investigated in a good sample size of 119 patients. 13. Morrison SC, Brown LA, Cohen AS. A multidimensional assessment of social cognition in psychometrically defined schizotypy. Psychiatry Res 2013; 210:1014–1019. 14. Langdon R, Still M, Connors MH. Theory of mind in early psychosis. Early Interv Psychiatry 2013. doi: 10.1111/eip.12072. 15. Healy KM, Penn DL, Perkins D, et al. Theory of mind and social judgement in & people at clinical high risk of psychosis. Schizophr Res 2013; 150:498–504. This study evaluates the longitudinal correlation of baseline ToM performance and later conversion to psychosis beyond IQ scores. 16. Csukly G, Polga´r P, Tombor L, et al. Theory of mind impairments in patients with deficit schizophrenia. Compr Psychiatry 2014; 55:349–356. 17. Comparelli A, De Carolis A, Corgiliano V, et al. Symptom correlates of facial emotion recognition impairment in schizophrenia. Psychopathology 2014; 47:65–70. 18. Tseng HH, Chen SH, Liu CM, et al. Facial and prosodic emotion recognition deficits associate with specific clusters of psychotic symptoms in schizophrenia. PLoS One 2013; 8:e66571. 19. Simpson C, Pinkham AE, Kelsven S, et al. Emotion recognition abilities && across stimulus modalities in schizophrenia and the role of visual attention. Schizophr Res 2013; 151:102–106. This study investigates emotion recognition abilities in three different conditions: audio only; visual only; and combined audiovisual so that a broad domain of emotion recognition is covered. 20. Barbato M, Liu L, Penn DL, et al. Social cognition as a mediator between neurocognition and functional outcome in individuals at clinical high risk for psychosis. Schizophr Res 2013; 150:542–546. 21. Mehta UM, Thirthalli J, Subbakrishna DK, et al. Social and neurocognition as distinct cognitive factors in schizophrenia: a systematic review. Schizophr Res 2013; 148:3–11. 22. Santosh S, Dutta Roy D, Kundu PS. Psychopathology, cognitive function, and social functioning of patients with schizophrenia. East Asian Arch Psychiatry 2013; 23:65–70. 23. Kucharska-Pietura K, Mortimer A. Can antipsychotics improve social cognition in patients with schizophrenia? CNS Drugs 2013; 27:335–343. 24. Hori H, Yoshimura R, Katsuki A, et al. Switching to antipsychotic monotherapy can improve attention and processing speed, and social activity in chronic schizophrenia patients. J Psychiatr Res 2013; 47: 1843–1848.
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Schizophrenia and related disorders 25. Kaneko Y, Keshavan M. Cognitive remediation in schizophrenia. Clin Psychopharmacol Neurosci 2012; 10:125–135. This study reports on a new promising training program to improve social cognition in schizophrenia. 26. Fischer-Kern M, Fonagy P, Kapusta ND, et al. Mentalizing in female inpatients with major depressive disorder. J Nerv Ment Dis 2013; 201:202–207. 27. Schreiter S, Pijnenborg GHM, Aan Het Rot M. Empathy in adults with clinical or subclinical depressive symptoms. J Affect Disord 2013; 150:1–16. 28. Cusi AM, Nazarov A, MacQueen M, et al. Theory of mind deficits in patients with mild symptoms of major depressive disorder. Psychiatry Res 2013; 210:672–674. 29. Loi F, Vaidya JG, Paradiso S. Recognition of emotion from body language && among patients with unipolar depression. Psychiatry Res 2013; 209:40–49. This innovative study is the only one which investigates emotion recognition from body language. 30. Beck T, Mitmansgruber H, Kumning M, et al. Depressives have the better view: the influence of mood in the recognition of emotional expression. Psychosom Med Psychother 2013; 59:247–253. 31. Dobson K, Franche RL. A conceptual and empirical review of the depressive realism hypotheses. Can J Behav Sci 1989; 21:419–433. 32. Allen LG, Siegl S, Hannah S. The sad truth about depressive realism. Q J Exp Psychol 2007; 60:482–495. 33. Aldinger M, Stopsack M, Barnow S, et al. The association between & depressive symptoms and emotion recognition is moderated by emotion regulation. Psychiatry Res 2013; 205:59–66. This study investigates the effect of emotion regulation on depression and emotion recognition by using a comprehensive test battery. 34. Abler B, Kessler H. Emotion regulation questionnaire: Eine deutschsprachige Fassung von Gross und John. Diagnostica 2009; 55:144–152. 35. Fehlinger T, Stumpenhorst M, Stenzel N, et al. Emotion regulation is the essential skill for improving depressive symptoms. J Affect Disord 2013; 144:116–122. &&
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36. Campbell-Sills L, Barlow D. Incorporation emotion regulation into conceptualizations and treatments of anxiety and mood disorder. In: Gross JJ, editor. Handbook of emotion regulation. The Guilford Press; 2009. pp. 542–559. 37. Davidson R, Pizzagalli D, Nitschke J, et al. Depression: perspectives from affective neuroscience. Ann Rev Psychol 2002; 53:545–574. 38. Samame´ C. Social cognition throughout the three phases of bipolar disorder: a state of the art overview. Psychiatry Res 2013; 210:1275– 1286. 39. Mercer L, Becerra R. A unique emotional processing profile of euthymic bipolar disorder? A critical review. J Affect Disord 2013; 146:295–309. 40. Purcell AL, Phillips M, Gruber J. In your eyes: does theory of mind predict impaired life functioning in bipolar disorder? J Affect Disord 2013; 151:1113–1119. 41. Montag C, Ehrlich A, Neuhaus K, et al. Theory of mind impairments in euthymic bipolar patients. J Affect Disord 2010; 123:264–269. 42. Lombardo LE, Bearden CE, Barrett J, et al. Trait impulsivity as an endophenotype for bipolar I disorder. Bip Disord 2012; 14:565–570. 43. Fulford D, Peckham AD, Johnson K, et al. Emotion perception and quality of life in bipolar I disorder. J Affect Disord 2014; 152-154:491–497. 44. Lahera G, Benito A, Montes JM, et al. Social cognition and interaction training & for outpatients with bipolar disorder. J Affect Disord 2013; 146:132–136. This study reports on a promising training program for deficits in social cognition in patients suffering from bipolar disorder and schizoaffective disorder. 45. Baez S, Herrera E, Villarin L, et al. Contextual social cognition impairments in schizophrenia and bipolar disorder. PLoS One 2013; 8:e57664. 46. Goghari VM, Sponheim SR. More pronounced deficits in facial emotion recognition for schizophrenia than bipolar disorder. Compr Psychiatry 2013; 54:388–397. 47. Yalcin-Siedentopf N, Hoertnagl CM, Biedermann F, et al. Facial affect recognition in symptomatically remitted patients with schizophrenia and bipolar disorder. Schizophr Res 2014; 152:440–445.
Volume 27 Number 3 May 2014
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Social cognition in serious mental illness Christine M. Hoertnagl a and Alex Hofer b
Purpose of review Social cognition represents a fundamental skill for effective social behavior. It is nowadays widely accepted that individuals suffering from serious mental illness are impaired in this domain. Recent findings Studies published since June 2012 have been reviewed, with a particular focus on theory of mind, social perception, social knowledge, attributional bias, and emotion processing in patients suffering from schizophrenia and mood disorders. Summary The reviewed literature supports previous studies on deficits in social cognition in schizophrenia, major depressive disorder and bipolar disorder, and underscores their relevance in the psychosocial context. Keywords bipolar disorder, major depressive disorder, schizophrenia, serious mental illness, social cognition
INTRODUCTION Social cognition is a multidimensional psychological concept comprising several subdomains and processes that facilitate social interaction, such as the knowledge about the self, perception of others, and interpersonal motivations [1]. Several studies indicate that patients suffering from serious mental illness exhibit impairments in these domains, and that these deficits have a negative impact on social and functional outcomes such as quality of life (QoL), employment status, or social relationships [2,3]. The National Institute of Mental Health consensus statement identified five social cognitive domains to be relevant in patients with schizophrenia: theory of mind (ToM), social perception, social knowledge, attributional bias, and emotion processing [4]. Schizophrenia-related deficits in social cognition and functioning have already been described by Kraepelin in 1919 [5]. Since then, a growing body of evidence has confirmed these impairments. Green et al. [6], for example, investigated three different aspects of social cognition (emotion processing, ToM, and social relationship perception) in prodromal, first episode, and chronically ill patients and found impairments across all domains in all clinical samples. Similarly, social cognitive deficits represent characteristic features of major depressive disorder (MDD) [7,8]. Notably, there is evidence for a mood-congruent negative bias regarding affect perception that is patients
suffering from MDD are mainly impaired in the recognition of positive emotions [9]. As compared with schizophrenia or MDD, the research on social cognition in bipolar disorder, however, is still marginal and provides divergent results. Social cognitive deficits are present during mood episodes, but their occurrence during the euthymic stage of the illness is still unclear [10 ]. &
SOCIAL COGNITION IN SCHIZOPHRENIA AND HIGH-RISK INDIVIDUALS &
Savla et al. [11 ] conducted a meta-analysis of 112 studies providing results from 3908 schizophrenia patients and 3570 healthy control individuals. Patients showed impairments across all social cognitive domains studied (social perception, ToM, emotion perception, and emotion processing) except attributional bias. Greater deficits in social and emotion perception were associated with
a
General and Social Psychiatry Division, and bBiological Psychiatry Division, Department of Psychiatry and Psychotherapy, Medical University Innsbruck, Innsbruck, Austria Correspondence to Christine M. Hoertnagl, MD, General and Social Psychiatry Division, Department of Psychiatry and Psychotherapy, Medical University Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. Tel: +43 512 504 23669; fax: +43 512 504 25267; e-mail: [email protected] Curr Opin Psychiatry 2014, 27:197–202 DOI:10.1097/YCO.0000000000000055
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Schizophrenia and related disorders
KEY POINTS Patients suffering from serious mental illness exhibit impairments in social cognition. Impairments in social cognition are negatively associated with patients’ outcomes. Little is known about the effects of medical treatment or nonmedical therapeutic interventions on social cognitive deficits in serious mental illness.
inpatient status, and greater deficits in emotion processing with a longer duration of illness. Similarly, Fiszdon et al. [12 ] investigated emotion processing and ToM in 119 schizophrenia patients and found them to perform worse than healthy control individuals in three out of four tasks. Contrary to Savla et al. [11 ], however, they detected only a weak relationship between task performance and clinical or functional features. Morrison et al. [13] compared social cognition in 36 individuals with psychometrically defined schizotypy and 26 healthy controls and found the former group to perform significantly worse with regard to facial emotion recognition, ToM, and emotion management, but not with regard to social management. Negative schizotypy traits were associated with poorer facial emotion recognition, whereas disorganized schizotypy traits correlated with better social management. Moreover, a poorer facial emotion recognition performance was moderately related with higher levels of general life satisfaction. The authors hypothesized that individuals with impairments in facial emotion recognition may exhibit less insight into poor interpersonal skills such that they may misattribute the cause of interpersonal problems to other people rather than their own impairments, thus preserving their self-esteem and increasing their overall QoL. ToM has been investigated by Langdon et al. [14], Healey et al. [15 ], and Csulky et al. [16]. Patients in early stages of psychosis exhibited impairments in picture-sequencing and jokeappreciation, but not in story-comprehension [14]. The authors, therefore, suggested that tests placing minimal demands on language processing and involving indirect, rather than explicit, instructions to assess ToM might be best suited to detect ToM impairments in early stages of psychosis. Interestingly, in high-risk individuals who were assessed for up to 2 years, baseline ToM performance significantly predicted later conversion to psychosis beyond intelligence quotient (IQ) scores. However, ToM was also significantly correlated with total &
&
&
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baseline disorganization and negative symptoms. Accordingly, ToM deficits might predate conversion to psychosis, but one must consider initial symptoms as well [15 ]. Csukly et al. [16] examined potential ToM differences between patients suffering from the deficit syndrome or nondeficit schizophrenia, and healthy controls. Control individuals outperformed both patient groups, but there were no significant differences between the two schizophrenia subgroups. Due to the small number of participants, this finding clearly requires replication. Comparelli et al. [17] investigated facial emotion recognition in a sample of 97 patients meeting the diagnostic criteria for schizophrenia, schizophreniform disorder, or schizoaffective disorder and found patients to perform worse on negative emotions than a healthy control group. In patients, the degree of cognitive/disorganized symptoms correlated with impairments in facial recognition abilities, but no group differences were detected. Next to deficits in facial emotion recognition, Tseng et al. [18] reported on prosodic impairments in schizophrenia patients, particularly with regard to the recognition of fearful emotions. An inverse correlation was found between the degree of positive symptoms and recognition accuracy for happy emotions. In a study performed by Simpson et al. [19 ], emotion recognition was significantly less accurate in patients than in control individuals during both an audio only and a visual only condition, but did not differ during a combined condition. These findings demonstrate that patients benefit from multimodal stimulus presentation of emotion and support hypotheses whereupon visual attention to salient facial features may serve as a mechanism for accurate emotion identification. &
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Social cognition and its relationship with neurocognition Barbato et al. [20] focused on the question whether social cognition serves as a mediator between neurocognition and functional outcome in individuals at clinical high risk for psychosis. Despite their finding of a direct relationship between neurocognition and functioning as well as between social cognition and functioning, social cognition did not seem to mediate the pathway from neurocognition to functional outcome. Similarly, Mehta et al. [21] systematically reviewed 20 studies reporting factor analyses of social cognition and neurocognition in schizophrenia and provided empirical evidence for the distinctiveness of these two domains. Volume 27 Number 3 May 2014
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Santosh et al. [22] reported on significant correlations between social and cognitive functioning. Moreover, cognitive deficits showed a stronger correlation with the degree of negative than with the degree of positive symptoms. Altogether, both positive and negative symptoms as well as verbal fluency performance predicted social functioning.
Therapeutic interventions In a review by Kucharska-Pietura and Mortimer [23], antipsychotic drugs of either class demonstrated little reliable effect upon social cognition. However, the authors correctly noted that the literature suffers from inconsistencies in study designs and small sample sizes. Hori et al. [24] examined whether switching polypharmacy therapy to monotherapy would improve cognitive and social functioning in patients with schizophrenia. For this purpose, 39 schizophrenia patients receiving two antipsychotics either continued this treatment or were switched to monotherapy. As compared with the continuing group, the switching group showed significantly greater improvement in attention as well as daily living and work skills after switching. Moreover, a significant correlation was noted between improvement in executive function and improvement in daily living as well as between improvement in work skills and improvement in attention. Kaneko and Keshavan [25 ] reviewed cognitive remediation programs targeting neurocognitive and social cognitive impairments and found them to be effective in schizophrenia. Functional outcomes were significantly better when cognitive remediation was combined with some other form of rehabilitation and when it included strategy coaching. In addition, interventions were likely to be more successful when the skills trained closely approximated those needed in daily life. Lastly, cognitive enhancement therapy, a multicomponent cognitive remediation approach designed to provide enriched cognitive experiences through targeted and integrated neurocognitive and social cognitive training, was also successful in improving social and nonsocial cognitive impairments in schizophrenia. &&
SOCIAL COGNITION IN MOOD DISORDERS Several studies indicate that patients suffering from mood disorders exhibit impairments in social cognition.
Major depressive disorder Fischer-Kern et al. [26] investigated the capacity for mentalization in 46 female inpatients suffering
from MDD and found them to be impaired compared with healthy female controls individuals. In addition, correlations with illness duration and number of admissions suggested that a chronic course of depression results in further mentalizing impairments. Schreiter et al. [27] conducted a systematic review of 37 studies on empathy in individuals with MDD. They concluded that depression was related to high levels of emphatic stress but not to abnormal empathic concern. In addition, depression was related to limited cognitive empathy, as indicated by poor perspective taking, empathic accuracy, and ToM. In line with this finding, Cusi et al. [28] found depressed patients to be impaired on second-order, cognitively demanding ToM scenarios. Poorer ToM ability, in turn, was negatively associated with psychosocial functioning. Loi et al. [29 ] investigated emotion recognition from body language and its possible implications to social adjustment in 51 MDD patients, 68 individuals with a history of MDD but in remission, and 69 healthy control individuals. Experimental tasks included emotion recognition from pointlight walkers, body postures as well as movie stills with masked and unmasked faces. Social adjustment was assessed using the Social Adjustment Scale. This study showed a reduced recognition of happy dynamic and static body displays of emotion in MDD compared with remitted patients and healthy comparison participants. Social adjustment was reduced in both currently depressed and remitted patients relative to healthy controls. The authors indicated that previously collected data supported the notion that among a nonclinical population, stimuli conveying happiness are more easily and rapidly recognized than negative or neutral stimuli, which could be due to the working of a cognitive system biased toward the positive appraisal of its surroundings. Accordingly, they hypothesized that this system is altered in MDD because happy stimuli are judged less accurately during the active phase of depression. Beck et al. [30] investigated the ability to identify affect-laden facial expressions in a sample of 52 depressed patients and 72 healthy individuals. Surprisingly, in four out of six tests, depressive individuals achieved significantly better results. The authors inferred from these findings that patients with MDD are able to estimate reality in a better way as it had already been postulated in the concept of depressive emotional realism [31]. Healthy individuals, however, may tend to distort reality into the positive [32]. Aldinger et al. [33 ] were interested in potential associations between depression and emotion
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recognition, affectivity, and interpersonal problems in a sample of 85 women. In this study, depressive symptoms were positively correlated with error rates in anger recognition, but not with recognition of the other basic emotions. This association was moderated by suppression, a strategy of emotion regulation, measured by the emotion regulation questionnaire [34]. In fact, more severely depressed woman who more frequently used suppression to regulate their emotions showed superior recognition of angry faces than those with lower suppression values. This association was unexpected, as suppression is mostly considered as a dysfunctional emotion-regulation strategy. The authors hypothesized that depressive high suppressors may use this regulation strategy due to the maladaptive schema that they ought to restrict their selfexpression in order to avoid any harm. Fehlinger et al. [35], on the other hand, identified emotion regulation to significantly predict the improvement of depressive symptomatology, whereas problem solving, social competence, stress management, relaxation ability, selfefficacy, and self-esteem were not relevant in this context. Moreover, emotion regulation at pretreatment turned out to be a moderator of the association between improvements in skills and the reduction of depressive symptoms. These findings were in line with the views of other researchers [36,37] who considered deficits in emotion regulation a vulnerability factor for developing mood disorders. Therefore, the authors suggested that incorporating emotion regulation trainings in addition to disorder-specific interventions would optimize therapy outcomes.
Bipolar disorder In a review, Samame´ [38] states that although it is well documented that bipolar disorder is frequently associated with cognitive deficits and suboptimal social adjustment, the social cognitive profile of the illness through its three phases remains unclear. For this purpose, she evaluated 51 studies comparing social cognitive performance of bipolar disorder patients with that of healthy control individuals and found patients to be impaired in emotion recognition and ToM during manic, depressed as well as euthymic phases. In another review, Samame` et al. [10 ] evaluated solely data on euthymic bipolar disorder and healthy individuals to clarify whether patients suffered from deficits in social cognition or not. Next to impairments of moderate magnitude across mentalizing skills small but significant effect sizes were observed for facial emotion recognition. However, no between-group differences were found &
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regarding decision-making. Mercer and Becerra [39], on the other hand, reviewed the literature on a number of dimensions of emotion processing in remitted bipolar disorder patients, including facial emotion recognition, emotional memory, affective ToM, affective attention, and affective auditory information processing. Euthymic patients’ abilities to process emotional material were compromised in three of six studies on affective attention, whereas they did not differ from healthy control individuals with regard to the recall of emotional or neutral information. Findings on facial emotion recognition abilities provided divergent results with 12 studies reporting no deficits, six studies describing deficits, and two studies reporting better performance in remitted bipolar disorder patients than in healthy individuals. Concerning ToM, all studies found deficits in this domain. Altogether, the authors concluded that bipolar disorder patients continue to exhibit some emotion processing deficits during the euthymic phase of the illness. Purcell et al. [40] investigated ToM abilities in 26 bipolar disorder patients in remission and compared them with 29 remitted individuals with MDD and 28 healthy control individuals. They found no group differences regarding ToM accuracy; however, bipolar disorder patients showed a significantly shorter mean response time than the other groups. The authors concluded that ToM is preserved in remitted bipolar disorder, which is in accordance with the literature [41]. Furthermore, the pattern of quicker responding may support the growing research linking impulsivity with bipolar disorder [42]. Fulford et al. [43] found that emotion perception protected QoL in bipolar disorder patients and suggested that it could, therefore, serve as a potential treatment target in this population. Lahera et al. [44 ] investigated the effect of an 18-week social cognition and interaction training in a mixed group of bipolar disorder and schizoaffective patients and compared them with a treatment as usual patient group. Analysis of covariance revealed significant group effects for emotion perception, ToM, and depressive symptoms. The group who received the social cognition and functioning training showed a large increase of face emotion discrimination and face emotion identification as well as a mild increase on emotion recognition capability relative to those who got treatment as usual. As stated by the authors, this study suffered from notable limitations. First, the sample was heterogeneous, as both groups composed of individuals with bipolar disorder I, bipolar disorder II, and schizoaffective disorder. Secondly, no follow-up assessment was conducted. Accordingly, &
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it is unknown whether training effects persist over time.
COMPARISON: SOCIAL COGNITION IN SCHIZOPHRENIA AND BIPOLAR DISORDER Baez et al. [45] evaluated the performance of 15 schizophrenia and 15 bipolar disorder patients compared with 30 healthy control individuals on several social cognition tasks, including emotion processing, empathy, and social knowledge. Impairments were found in both patient groups. They were more severe in schizophrenia than in bipolar disorder patients. Similarly, Goghari and Sponheim [46] who examined facial emotion recognition in 27 schizophrenia and 16 bipolar disorder patients compared with 30 healthy control individuals found more pronounced deficits in schizophrenia than in bipolar disorder. They suggested that this result may be a reflection of a greater degree of brain abnormities in regions associated with facial emotion recognition, such as in the amygdala and hippocampus, in schizophrenia patients. Yalcin-Siedentopf et al. [47] directly contrasted facial emotion recognition abilities in remitted patients with bipolar disorder or schizophrenia, and healthy volunteers. Their findings again indicate that during periods of remission the recognition of facial affect may be less impaired in bipolar disorder patients. Interestingly, associations with residual symptomatology were only present in bipolar disorder but not in schizophrenia patients.
CONCLUSION The reviewed literature supports previous studies on social cognitive impairments in schizophrenia, MDD, and bipolar disorder; however, impairments differ in occurrence and severity. As social cognition is a multidimensional psychological concept comprising several subdomains, an operationalization of them is necessary. The heterogeneity of social cognition tasks clearly impedes the comparability of studies. Therefore, a consensus battery assessing more thoroughly the wide range of social cognitive components is strongly needed. Acknowledgements None. Conflicts of interest A.H. has received payment for lectures from Janssen and Lundbeck. There are no conflicts of interest for C.M.H.
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36. Campbell-Sills L, Barlow D. Incorporation emotion regulation into conceptualizations and treatments of anxiety and mood disorder. In: Gross JJ, editor. Handbook of emotion regulation. The Guilford Press; 2009. pp. 542–559. 37. Davidson R, Pizzagalli D, Nitschke J, et al. Depression: perspectives from affective neuroscience. Ann Rev Psychol 2002; 53:545–574. 38. Samame´ C. Social cognition throughout the three phases of bipolar disorder: a state of the art overview. Psychiatry Res 2013; 210:1275– 1286. 39. Mercer L, Becerra R. A unique emotional processing profile of euthymic bipolar disorder? A critical review. J Affect Disord 2013; 146:295–309. 40. Purcell AL, Phillips M, Gruber J. In your eyes: does theory of mind predict impaired life functioning in bipolar disorder? J Affect Disord 2013; 151:1113–1119. 41. Montag C, Ehrlich A, Neuhaus K, et al. Theory of mind impairments in euthymic bipolar patients. J Affect Disord 2010; 123:264–269. 42. Lombardo LE, Bearden CE, Barrett J, et al. Trait impulsivity as an endophenotype for bipolar I disorder. Bip Disord 2012; 14:565–570. 43. Fulford D, Peckham AD, Johnson K, et al. Emotion perception and quality of life in bipolar I disorder. J Affect Disord 2014; 152-154:491–497. 44. Lahera G, Benito A, Montes JM, et al. Social cognition and interaction training & for outpatients with bipolar disorder. J Affect Disord 2013; 146:132–136. This study reports on a promising training program for deficits in social cognition in patients suffering from bipolar disorder and schizoaffective disorder. 45. Baez S, Herrera E, Villarin L, et al. Contextual social cognition impairments in schizophrenia and bipolar disorder. PLoS One 2013; 8:e57664. 46. Goghari VM, Sponheim SR. More pronounced deficits in facial emotion recognition for schizophrenia than bipolar disorder. Compr Psychiatry 2013; 54:388–397. 47. Yalcin-Siedentopf N, Hoertnagl CM, Biedermann F, et al. Facial affect recognition in symptomatically remitted patients with schizophrenia and bipolar disorder. Schizophr Res 2014; 152:440–445.
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