Social cognition in schizophrenia in comparison to bipolar disorder: A meta-analysis

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Abstract

Objective

Cognitive dysfunction is a common characteristic of both schizophrenia and bipolar disorder (BP). While these deficits are more severe in schizophrenia, there is a significant overlap between conditions. However, it was hypothesized that social cognitive deficits might be more specific to schizophrenia.

Methods

We conducted a meta-analysis of studies comparing facial emotion recognition and theory of mind (ToM) abilities in schizophrenia and BP. 26 studies comparing 1301 patients with schizophrenia and 1075 with BP were included.

Results

Schizophrenia patients significantly underperformed compared with BP patients in both facial emotion recognition (d = 0.39) and ToM (d = 0.57). Neurocognitive deficits significantly contributed to schizophrenia-BP group differences for ToM. However, between-group differences for social cognition were not statistically more severe than neurocognition.

Conclusion

Social cognitive impairment is more severe in schizophrenia in comparison to BP. However, between-group differences are modest and are comparable to other neurocognitive differences between schizophrenia and BP. There is significant overlap in social cognitive performance deficits observed in both schizophrenia and BP.

Introduction

Neurocognitive impairment is a well-established and persistent feature of schizophrenia (Bora et al., 2010, Heinrichs and Zakzanis, 1998). Similar cognitive deficits, albeit less severe, are also clearly evident in BP, even during remission (Bora et al., 2009a, Bourne et al., 2013). The magnitude of cognitive differences between schizophrenia and BP are modest (Bora et al., 2009b, Krabbendam et al., 2005). Therefore, it seems that cognitive impairment, as assessed with traditional neuropsychological batteries, is a common feature of both disorders.

On the other hand, schizophrenia but not BP has been associated with persistent poor social and occupational recovery since the early days of modern psychiatry. Kraepelin considered manic or depressive disorder as an illness that is periodic in nature and typically characterized by a return to normal functioning after remission from the episode (Kraepelin, 1921). More modern studies have shown that a significant proportion of patients with BP also has poor functioning (Burdick et al., 2010, Sanchez-Moreno et al., 2009). However, it is well accepted that severe functional impairment is much more specific to schizophrenia in comparison to BP. In schizophrenia, functional impairment has been associated not only with intellectual deficits and executive dysfunction but also with social cognitive deficits. Social cognitive abilities, including emotion recognition and theory of mind, might be more directly related to some aspects of functioning and some studies have suggested that these deficits can predict social dysfunction better than traditional cognitive tests in schizophrenia (Bora et al., 2006, Fett et al., 2011, Green et al., 2012). For example, difficulties in recognizing others' emotional expressions, empathic abilities, reading their complex mental states and understanding pragmatic language statements (such as irony) in schizophrenia can contribute to interpersonal problems in the work environment and other social settings. Given that there are only modest cognitive differences between schizophrenia and BP, it can be hypothesized that robust differences in social functioning between schizophrenia and BP might be related to social cognitive deficits which might be specific to schizophrenia.

Deficits in emotion recognition and ToM are well-established findings in schizophrenia (Bliksted et al., 2014, Bora et al., 2009c, Bora and Pantelis, 2013, Koelkebeck et al., 2010, Kohler et al., 2010, Lee et al., 2015). More recent studies have shown that social cognitive deficits are also evident in BP (Bora et al., 2005, Samamé et al., 2012). This might not be surprising as both disorders are associated with structural and functional abnormalities in brain regions (i.e., ventromedial prefrontal cortex) which important for social cognitive abilities (Bora et al., 2012, Delvecchio et al., 2013). However, Lee et al. (2013) has proposed that social cognitive impairment might be more specific to schizophrenia than neurocognitive impairment. In their study, Lee et al. (2013) found that BP patients showed less impairment on social cognition relative to neurocognition, whereas schizophrenia patients showed more impairment on social cognition relative to neurocognition. Recently, several meta-analyses of social cognition in BP in comparison to controls have been conducted (Bora et al., 2016, Samamé et al., 2012). These meta-analyses suggested that BP is associated with social cognitive deficits with medium effect sizes. This finding is similar to the outcome of meta-analyses of neurocognition in BP. These findings can be interpreted as evidence for quantitative rather than qualitative differences between schizophrenia and BP for social cognition. The performance of BP patients on social cognitive tasks, similar to neurocognition, can be intermediate between schizophrenia and healthy controls. However, indirect comparisons of findings of social cognition studies in schizophrenia and BP might be misleading due to significant limitations including potential methodological differences in sample selection. Relative specificity of social cognition to schizophrenia should be investigated by studies directly comparing social cognitive (and neurocognitive) abilities in schizophrenia and BP.

A number of recent studies have compared social cognitive, particularly facial emotion recognition and ToM, performances of schizophrenia and BP. However, the available evidence is contradictory regarding the extent of differences in social cognition deficits between schizophrenia and BP and whether social cognition, in comparison to neurocognition, is a more specific feature of schizophrenia. No meta-analyses have compared social cognitive performances of schizophrenia and BP or investigated the relationship between social cognition and neurocognition. In this meta-analysis, we aimed to investigate emotion recognition and ToM deficits (and their relationship to neurocognition) in schizophrenia compared to BP.

Section snippets

Study selection

We followed MOOSE and PRISMA guidelines in conducting this meta-analysis (Moher et al., 2009, Stroup et al., 2000). A literature search was conducted using the databases Pubmed, PsycINFO, ProQuest and Scopus to identify the relevant studies (January 1990 to March 2016) using the combination of keywords as follows: (emotion recognition or theory of mind or mentalizing or social cognition) and (bipolar disorder, schizophrenia). Reference lists of published reports were also reviewed for

Results

Social cognition was significantly impaired (d = 0.45) in schizophrenia in comparison to BP (Table 2). When two social cognitive domains were investigated separately, the performance of schizophrenia patients was significantly poorer than BP patients for both emotion recognition (d = 0.39, Fig. 1) and ToM (d = 0.57, Fig. 2) (Table 2). Distributions of effect sizes of these measures were heterogeneous (p for Q < 0.001 and I2 = 61–68%) but the magnitude of this heterogeneity was modest on the

Discussion

The current meta-analysis investigated social cognitive deficits in schizophrenia in comparison with individuals with BP. Our findings showed that emotion recognition and ToM deficits are significantly more severe in schizophrenia compared to BP. The magnitude of differences between schizophrenia and BP were similar in social cognitive and neurocognitive tasks. More severe neurocognitive deficits and the higher ratio of males in schizophrenia than BP significantly contributed to between-group

Role of funding source

Funding body agreements and policies: not relevant for authors.

Contributors

EB conducted the analyses and wrote the first draft. All authors (EB, CP) contributed to the planning of the study. All authors critically reviewed the paper. All authors contributed to and have approved the final manuscript.

Conflict of interest

Over the last two years, Christos Pantelis has participated on Advisory Boards for Janssen-Cilag and Lundbeck. He has received honoraria for talks presented at educational meetings organized by Janssen-Cilag, Astra-Zeneca, Shire and Lundbeck. EB have no conflict of interests to be reported. None of the authors have financial or personal relationships, interests and affiliations relevant to the subject matter of the manuscript.

Acknowledgements

Prof Christos Pantelis was supported by a NHMRC Senior Principal Research Fellowship (ID: 628386).

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