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Pathways between neurocognition, social cognition and emotion regulation in bipolar disorder

Van Rheenen TE, Meyer D, Rossell SL. Pathways between neurocognition, social cognition and emotion regulation in bipolar disorder.

Objective: Converging evidence suggests that in bipolar disorder (BD), social cognition and emotion regulation are affected by the capacity for effective neurocognitive function. Adaptive emotion regulation may also rely on intact social cognition, and it is possible that social cognition acts as a mediator in its relationship with neurocognition. We aimed to address this hypothesis by explicitly examining interrelationships among neurocognition, social cognition and emotion regulation in an out-patient sample meeting criteria for a DSM-IV-TR diagnosis of BD compared with controls. Method: Fifty-one BD patients and 52 healthy controls completed a battery of tests assessing neurocognition, social cognition (emotion perception and theory of mind) and emotion regulation. Results: Path analysis revealed that in BD, neurocognition was associated with social cognition, but social cognition was not associated with emotion regulation as expected. In contrast, a component of social cognition was found to mediate the relationship between neurocognition and emotion regulation in healthy controls. Conclusion: These findings highlight differences in the pattern of associations between neurocognition, social cognition and emotion regulation across BD patients and controls. In the present data, these results appear to indicate that neurocognitive and social cognitive abilities generally operate in isolation from emotion regulation in BD.

T. E. Van Rheenen1,2, D. Meyer1, S. L. Rossell1,2 1Faculty of Health, Arts and Design, School of Health Sciences, Brain and Psychological Sciences Research Centre (BPsyC), Swinburne University, Melbourne, Vic., Australia and 2Cognitive Neuropsychiatry Laboratory, Monash Alfred Psychiatry Research Centre (MAPrc), The Alfred Hospital and Central Clinical School, Monash University, Melbourne, Vic., Australia

Key words: theory of mind; emotion perception; emotion processing; emotional modulation

Tamsyn Van Rheenen, Cognitive Neuropsychology Laboratory, Monash Alfred Psychiatry Research Centre (MAPrc), Level 4, 607 St Kilda Rd, Melbourne, Vic. 3004, Australia. E-mail: [email protected]

Accepted for publication May 1, 2014

Significant outcomes

• Understanding pathways and connections between features of BD is critical to understanding the mechanisms that contribute to episodic relapse and maintenance and for developing necessary psy- chosocial interventions to remediate cognitive or regulatory deficits.

• Neurocognition is significantly predictive of emotion perception and theory of mind performance, but these operate in isolation from emotion regulation in BD.

• These findings may indirectly index dysfunction in the neural circuitry involved in regulating emotions in BD.

Limitations

• We were unable to explicitly investigate the influence of mood on these variables. • An inability to partial out the effects of medication may represent a potential confound.

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Introduction

Bipolar disorder (BD) is a complex mood disorder characterised by abnormalities in emotion regulation. Evidence suggests that patients with the disorder often demonstrate reduced modulatory control over emotions and at times fail to employ productive coping strategies, such that the capacity for overt and covert cognitive, physiological and motivational emotional behaviours is compromised (1–5). Recent interest in the disorders social cognitive profile has also facilitated understandings of patients’ capacity to perceive emotional expres- sions from faces and prosody (emotion percep- tion), and make inferences about others’ emotional and mental states (theory of mind). Growing evidence of mood independent impair- ments in these important social cognitive processes suggests a trait-like dysfunction that may have substantial implications for psychoso- cial outcome in the disorder (6–14). Impor- tantly, abnormalities in both emotion regulation and social cognition may represent modifiable domains of dysfunction (15–17).

There is now also substantial evidence for neuro- cognitive abnormalities in BD (18–21). Further, converging evidence suggests that social cognition and the regulation of emotion in BD may be affected by the capacity for effective neurocogni- tive function, although this has not been empiri- cally investigated (see 22, 23 for discussions). Concurrent neurocognitive, social cognitive and emotion regulatory impairments are evident in the disorder (24, 25), and consistently poor perfor- mance on emotionally relevant cognitive tasks (26) indicates that patients’ aptitude for self-regulatory behaviours including inhibition and flexibility is reduced (27–29).

Indeed, cognitive processes are responsible for enacting flexible responses to changing environ- mental conditions, inhibiting impulsive actions and configuring a range of sensory inputs necessary for the organisation, monitoring, evalu- ation and modulation of emotions and behav- iours. They also enable the perception, storage and access of emotional information (necessary for emotion perception), and permit its integra- tion with other contextual material to infer behaviour (necessary for theory of mind). Aber- rations of neurocognition could, therefore, inde- pendently impede the capacity for adaptive social cognition and/or emotion regulation. On the other hand, as the regulation of emotional responses is likely to rely on both neurocognitive and social cognitive inputs from observable

(emotion expressions) and inferential (theory of mind) information sources, emotion regulation may also be impacted directly by social cognition itself. It is certainly plausible that impaired neu- rocognition affects emotion perception and the- ory of mind in BD, with impairments in either or both of these social cognitive processes likely to have implications for the regulation of emo- tion (30–32).

In other psychiatric illnesses, poor cognitive function has been associated with deficits in social cognitive abilities, suggesting that cognitive ineffi- ciency confers a liability for poor social cognition (33–36). Aspects of social cognition have also been related to difficulties in emotional regulation (37). However, there is limited previous research directly and explicitly examining these likely inter-relation- ships in BD (38, 39). This is important given that understanding pathways and connections between features of the disorder is critical to understanding the mechanisms that contribute to episodic relapse and maintenance, and for developing necessary psychosocial interventions to remediate cognitive or regulatory deficits.

Aims of the study

To this end, we aimed to examine the relationships between neurocognition, social cognition (emotion perception and theory of mind) and emotion regu- lation by testing an integrated predictive model in an out-patient sample meeting criteria for a DSM- IV-TR diagnosis of BD compared with controls. We hypothesised that neurocognition would influ- ence emotion regulation (Hypothesis 1) as well as emotion perception and theory of mind relevant aspects of social cognition (Hypothesis 2). A fur- ther hypothesis was that social cognition would influence the regulation of emotion and thereby mediate its predicted relationship with neurocogni- tion (Hypothesis 3). Figure 1 presents a pictorial diagram of these hypothesised relationships.

Fig. 1. Hypothesised directional relationships between neuro- cognition, social cognition (EP and ToM) and emotion regula- tion variables; NC, neurocognition; EP, emotion perception; ToM, theory of mind; ER, emotional regulation.

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Material and methods

This study was approved by the Alfred Hospital and Swinburne University Human Ethics Review Boards and abided by the Declaration of Helsinki. Written informed consent was obtained from each participant before the study began.

Participants

The clinical sample comprised 51 patients diag- nosed as having DSM-IV-TR BD using the Mini International Neuropsychiatric Interview (MINI) (40). Patients were recruited via community support groups and general advertisements and were all out-patients. Current symptomology was assessed using the Young Mania Rating Scale (YMRS) (41) and the Montgomery Asberg Depression Rating Scale (MADRS) (42). Patients with visual impairments, neurological disorder and/or a history of substance/alcohol abuse or dependence during the past 6 months were excluded. All participants were fluent in English, were between the ages of 18 and 65 years and had an estimated premorbid IQ as scored by the Wechsler Test Of Adult Reading (WTAR) of >75. At the time of assessment, 33 patients were taking antipsychotics, 16 were taking antidepressants, 16 were taking mood stabilisers and 10 were taking benzodiazepines.

A control sample of 52 healthy participants was recruited for comparison purposes by general advertisement and contacts of the authors. Using the MINI screen, no control participant had a current diagnosis or previous history of psychiatric illness (Axis I). An immediate family history of mood and psychiatric disorder, in addition to a per- sonal history of neurological disorder, current or previous alcohol/substance dependence or abuse, visual impairments and current psychiatric medica- tion use was exclusion criteria for all controls.

All participants were fluent in English, were between the ages of 18 and 65 years and had an estimated premorbid IQ as scored by the Wechsler Test Of Adult Reading (WTAR) of >75.

Materials

Neurocognition. A composite score reflecting cog- nitive functioning across the domains of speed of processing, attention/vigilance, working memory, verbal learning, visual learning and executive func- tion performance was used as the neurocognitive measure. It was derived from the summation of standardised z scores from the Trail Making Test-Part B (43), the Colour-Word Stroop (44) and

all subtests, except the Mayor–Salovey–Caruso Emotional Intelligence Test from the MATRICS consensus cognitive battery [MCCB: described elsewhere by (45)]; although the Mayor–Salovey– Caruso Emotional Intelligence Test is an impor- tant aspect of the MCCB, it is designed to measure social cognition. Thus, in the interests of maintain- ing a pure neurocognitive measure, it was excluded from the neurocognitive score in this study. Higher composite neurocognitive scores reflect better neu- rocognitive ability. A comprehensive assessment of performance using this battery in the two cohorts reported upon in the current paper can be found in Van Rheenen and Rossell (18).

Social cognition. Two components of social cogni- tion were measured: a composite reflecting facial emotion perception was used as the emotion per- ception measure. The score was derived from the summation of percentage correct responses on a static facial emotion labelling task. This task required participants to accurately identify a series of high intensity facial emotional expressions (depicting happy, sad, angry, fear, neutral) pre- sented sequentially (11), with higher scores repre- senting better emotion perception ability.

A score reflecting performance on the false- belief stories from the picture sequencing task (46) was used to assess theory of mind. The task required participants to make false-belief infer- ences to logically sequence a series of stories. Higher scores represent better theory of mind ability.

Emotion regulation. The global score of the Diffi- culties in Emotion Regulation Scale (DERS) (47) was used as the emotion regulation measure. The DERS is a 36-item self-report scale for the assess- ment of non-acceptance of emotional responses, difficulties engaging in goal-directed behaviours when experiencing negative emotions, difficulties in impulse control, lack of emotional awareness, limited access to emotion regulation strategies and lack of emotional clarity. Higher scores represent greater difficulties in emotion regulation.

Statistical analysis

Missing data was imputed using the IBM SPSS (48) missing values imputation function. Indepen- dent samples t-tests and chi-squared tests were used to examine between group differences on demographic variables. Bivariate correlations bet- ween variables of interest (and mood symptom- atology in the patient group) were estimated using Pearson’s r. Path analysis was used to estimate the

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directional relationships between variables of interest in this study. Path analysis is a statistical technique used to model the magnitude and strength of theoretical associations between con- structs. It can facilitate understanding about which causal structure best fits correlational patterns in the data, and is advantageous over regression because it accounts for measurement error and allows for the specification of any number of dependent, independent and mediating variables of which both indirect and direct effects can be cap- tured. It also allows for the concurrent estimation of pathways between distinct groups and permits the examination of path moderation based on group membership (49, 50).

We used SPSS AMOS version 20 (51) to test our hypotheses and employed the chi-squared test, and the following well-recognised fit indices to test the overall model fit; The normed fit index, the relative fit index, the incremental fit index, the Tucker-Lewis coefficient and the comparative fit index (a score above 0.9 on all fit indices indicates a good fit). Bentler and Chou (52) pro- posed that a ratio of five cases (participants) to each free parameter (i.e., measured variables and paths) is necessary for appropriate statistical power using path analysis. As our model com- prised four measured variables and five path- ways, the samples of 51 BD and 52 control participants was sufficient.

We ran an initial predictor model simulta- neously testing all of our hypotheses in each group, and trimmed insignificant pathways one at a time until we reached an appropriate model fit where all paths were statistically significant. A multi-group

analysis strategy was used to test for symptomatic status (symptomatic n = 33, defined as those that met criteria for YMRS and MADRS scores >8; euthymic n = 18; defined as those that met strict criteria for YMRS and MADRS scores ≤8) and diagnostic subtype (BD I n = 39, BD II n = 12) moderation of pathways in the patient group for the final BD predictor model.

Results

No significant differences in age, gender, education level completed or premorbid IQ were found between the BD patients and controls (see Table 1).

Initial correlational analyses

Bivariate correlations between neurocognition, social cognition and emotion regulation scores (and mood severity in the patient group) are pre- sented in Table 2. Depressive and manic symptom- atology was related only to emotion regulation (the dependent variable) and not to the indepen- dent variable (neurocognition) or mediators (emo- tion perception and theory of mind) in the BD group. In this group, better neurocognition was also associated with better emotion perception and better theory of mind, but was not associated with emotion regulation. In contrast, better neurocogni- tion (the independent variable) was associated with better emotion perception and theory of mind (the mediators) as well as with better emotion regula- tion (the dependent variable) in the control group. In this group, better emotion perception (the

Table 1. Demographic and clinical characteristics of the sample

Group n

Control

BD Group comparisons

M SD M SD t/v2 df P

N 52 51 Age 33.98 14.27 38.45 12.89 �1.67 101 0.10 Gender (M/F)† 20/32 17/34 0.29 1 0.59 WTAR (scaled) 111.65 7.24 109.40 12.06 1.13 79.96 0.26 Education standard completed† 8.05 4 0.09 Completed secondary 12 – – 7 – – – – Completed TAFE/diploma 3 – – 11 – – – – Completed trade qualification 3 – – 5 – – – – Completed tertiary degree 28 – – 20 – – – – Other 5 – – 7 – – – –

No. of Symptomatic/Euthymic – 33/18 No. of BD I/BD II 39/12 YMRS – – 6.22 5.47 – – – MADRS – – 11.82 10.02 – – –

†Group comparisons all independent samples t-tests except gender and education which was chi-squared; M/F, Male/Female; Premorbid IQ as measured by the WTAR = Wechsler Test of Adult Intelligence; YMRS = Young Mania Rating Scale; MADRS = Montgomery Asberg depression Rating Scale; symptomatic patients are defined as those that met criteria for YMRS and MADRS scores >8; euthymic patients are defined as those that met strict criteria for YMRS and MADRS scores <8.

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mediator) was also associated with better emotion regulation (the dependent variable).

Hypothesis testing

Table 3 summarises the process of model develop- ment when testing our hypotheses in both groups. It should be noted as there is a fundamental link between variability in mood and emotion regula- tion (that is, as emotion regulation decreases mood symptoms may become worse), co-varying out cur- rent depression and mania symptoms was not pos- sible. Variables can only be used as covariates if they are related to both independent and depen- dent variables (not clearly only to the dependent variable as shown in Table 2). Thus, we chose not to control for mood symptomatology in the subse- quent BD path analysis. In the control group, the initial model fit the data well (see fit indices in Table 3). However, despite all of the direct

pathways occurring in the expected direction, only three of the five paths were significant. The non-significant pathways from neurocognition to emotion regulation and from theory of mind to emotion regulation were therefore eliminated from the model. The overall model fit did not deteriorate significantly as a result of the elimination of these paths, and bootstrapped testing of indirect effects indicated that emotion perception was fully medi- ating the effect of neurocognition on emotion regu- lation (b = �0.16, P ≤ 0.02). In the final predictor model, neurocognition explained 19% of the vari- ance in emotion perception and 20% of the vari- ance in theory of mind, while emotion perception explained 14% of the variance in emotion regula- tion. The fit indices for this model indicated that this more parsimonious model fit the data well. Figure 2 presents a graphical representation of the final model for the control group.

In the patient group, the initial model was not a good fit for the data (see fit indices in Table 3). The proposed direct paths from neurocognition, emotion perception and theory of mind to emotion regulation were not statistically significant, and these were eliminated from the model. This signifi- cantly improved the model fit. In the final model, neurocognition explained 13% of the variance in emotion perception and 30% of the variance in theory of mind. The fit indices for this model indi- cated a good fit for the data. Figure 3 presents a graphical depiction of the final model for the patient group.

Symptomatic status and diagnostic subtype moderation testing

The final BD predictor model was a good fit of the data for the symptomatic (v2(8) = 12.19, P = 0.14), euthymic (v2(4) = 8.01, P = 0.09), BD I (v2(4) = 1.92, P = 0.75) and BD II (v2(4) = 6.87,

Table 2. Correlations between predictor variables, dependent variables and current mood symptomatology

NC EP ToM ER† Depression Mania

BD NC 1.00 0.36** 0.55** 0.03 �0.15 0.05 EP 1.00 0.37** 0.04 �0.08 0.02 ToM 1.00 �0.01 0.08 0.20 ER† 1.00 0.51** 0.36** Depression 1.00 0.39** Mania 1.00

Controls NC 1.00 EP 0.43** 1.00 ToM 0.44** 0.20 1.00 ER† �0.33* �0.37** �0.25 1.00

**P < 0.01. †Higher scores represent greater difficulties in emotion regulation. NC, neurocognition; EP, emotion perception; ToM, theory of mind; ER, emotion regu- lation.

Table 3. Process of model development during hypothesis testing

v2 statistics

Fit indices

Steps takenNFI RFI IFI TLI CFI

Controls v2(1) = 0.01, P = 0.91 1.00 1.00 1.03 1.23 1.00 Remove non-significant path from ToM?ER v2(2) = 0.80, P = 0.67 0.97 0.93 1.04 1.14 1.00 Remove non-significant path from NC?ER v2(3) = 2.937, P = 0.40 0.90 0.82 1.00 1.01 1.00 All paths significant?No further action required

BD v2(1) = 2.64, P = 0.10 0.91 0.43 0.94 0.55 0.93 Remove non-significant path from ToM?ER v2(2) = 2.64, P = 0.27 0.91 0.72 0.98 0.91 0.97 Remove non-significant path from NC?ER v2(3) = 2.77, P = 0.43 0.90 0.80 1.01 1.02 1.00 Remove non-significant path from EP?ER v2(4) = 2.85, P = 0.58 0.90 0.85 1.05 1.08 1.00 All paths significant?No further action required

Non-significant v2 and all fit indices above 0.9 indicate a good model fit. NFI, normed fit index: RFI, relative fit index; IFI, incremental fit index; TLI, Tucker-Lewis index; CFI, comparative fit index; EP, emotion perception; ER, emotion regulation; NC, neu- rocognition; ToM, theory of mind.

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P = 0.14) subgroups. There was no significant moderation of regression weights as a function of symptom status (v2(2) = 1.98, P = 0.37) nor diag- nostic group (v2(2) = 2.89, P = 0.24).

Discussion

Given disturbed emotional regulation is proposed to be a contributor to negative clinical/psychoso- cial outcomes in BD, understanding the connec- tions it has with other features of the disorder is important (4, 23, 53). Likewise, as growing evi- dence indicates that both neurocognitive and social cognitive impairments are stable features of the disorder, establishing the relationship between them is fundamental for the development of psy- chosocial and cognitive remediation programmes (7, 21). The aim of this study was to examine inter-relationships between neurocognition, social

cognition and emotion regulation in a sample of DSM-IV-TR diagnosed BD patients compared with controls.

In the patient group, correlational analysis revealed relationships between neurocognitive and social cognitive variables, but not between neuro- cognitive/social cognitive and emotion regulation variables. This pattern of associations was largely replicated when we tested a model including neuro- cognition and social cognition as direct and indi- rect predictors of emotion regulation in a path analysis. Specifically, we found support for the hypothesis that neurocognition directly predicts variance in both emotion perception and theory of mind (Hypothesis 2) in BD. However, the direct pathways from social cognition (both emotion per- ception and theory of mind) to emotion regulation were not significant, and thus we did not obtain support for the prediction that social cognition influences emotion regulation and thereby medi- ates its predicted relationship with neurocognition (Hypothesis 3). The lack of association between social cognition and emotion regulation could not be explained as a result of emotion regulatory function relying directly on neurocognitive as opposed to social cognitive skills, given that a sta- tistically significant path directly from neurocogni- tion to emotion regulation was also absent (Hypothesis 1). Thus, the prediction that emotion regulation is underpinned by neurocognition in BD was also not supported.

In the control group however, the associations between neurocognition, social cognition and emo- tion regulation were largely consistent with our hypotheses. Specifically, we found that neurocog- nition directly predicted variance in social cogni- tion (both emotion perception and theory of mind). Emotion perception was also found to directly predict variance in emotion regulation, such that it appeared to be mediating the effect of neurocognition on emotion regulation. This sug- gests that in the healthy population, better neuro- cognitive skills are related to better emotion perception and theory of mind. Better emotion perception in turn, appears to improve the regula- tion of emotion.

Taken together, these findings highlight differ- ences in the pattern of associations between neuro- cognition, social cognition and emotion regulation across BD patients and controls. In the present data, these results appear to indicate that neuro- cognitive and social cognitive abilities generally operate in isolation from emotion regulation in BD. Given that there were no overall differences between euthymic and symptomatic patients or those meeting criteria for BD I or BD II in the final

Fig. 2. Final predictor model representing directional relation- ships between neurocognition, social cognition and emotion regulation variables in the control group: * indicates variance explained in dependent variable by predictors; values on paths represent standardised regression coefficients; the indirect effect of neurocognition on emotion regulation is calculated by multiplying the path coefficients of each direct effect from predictor to dependent variable; NC, neurocognition; EP, emotion perception; ToM, theory of mind; ER, emotion regu- lation.

Fig. 3. Final predictor model representing directional relation- ships between neurocognition, social cognition and emotion regulation variables in the BD group: * indicates variance explained in dependent variable by predictors; values on paths represent standardised regression coefficients; NC, neurocogni- tion; EP, emotion perception; ToM, theory of mind; ER, emo- tional regulation.

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path model, it appears this pattern of relationships is independent of mood and clinical subtype.

These findings are in accordance with a growing neurobiological literature suggesting a disruption in frontolimbic neural networks in the disorder (54–56). The dissociation between cognitive (both neurocognition and social cognition) and emotion regulatory abilities certainly seem to reflect under- lying dysfunction in this neural circuitry. It closely supports the results of recent BD studies, where a resting state imaging paradigm indicated reduced connectivity within prefrontal brain regions and between amygdala and dorsolateral regions, and a behavioural paradigm indicated that links between social cognition and adaptive emotion regulation strategies were missing (3, 57).

Nevertheless, our findings did indicate that neu- rocognition and social cognition in BD are related. Specifically, neurocognition predicted substantial variance in social cognition even after accounting for measurement error; a one-point decrease in neurocognitive capacity was reflective of a decrease in both emotion perception and theory of mind to the order of between 0.3 and 0.5 standard devia- tions, respectively, indicating that intact neurocog- nition is a necessary precursor to good social cognition in BD. These findings are consistent with research indicating that dysfunction in the same brain networks involved in neurocognition mediate dysfunctions in social cognition as well (see 23 for a review).

These findings should be interpreted with cau- tion however, as they are limited by at least three factors. First, we were unable to explicitly investi- gate the influence of current mood state on these variables as comparisons between different sub- groups (manic, depressive and euthymic patients) were not possible given the small sample. Although we did compare patients that were symptomatic to those that were euthymic and found no significant differences in the pattern of relationships, the sub- group sizes were still small and caution is war- ranted when interpreting these subgroup findings. Increasing mood severity may exacerbate cognitive and emotional symptoms, and it is certainly possi- ble that the inclusion of both symptomatic and eu- thymic patients in the primary path model may have influenced the present results. Future studies would certainly do well to compare the pattern of inter-relationships between neurocognition, social cognition and emotion regulation in explicitly defined manic, depressed and euthymic mood phases of the illness to determine state versus trait effects. Second, an inability to partial out the effects of medication may represent a potential confound. Therefore, future studies should aim to

explicitly compare inter-relationships between these variables in patients on and off different clas- ses of medications. Finally, we did not include a measure of functioning as an outcome in the analy- sis, although this would be very helpful to inform psychosocial or cognitive remediation therapies that are focused on the functional recovery of BD patients. As these variables are likely to impact psychosocial outcomes in BD (53), we recommend that future studies in the area take functioning into account when assessing similar models of interac- tion. Further research including larger samples to replicate the current findings would also be helpful to study the inter-relationships between neurocog- nition, social cognition and emotion regulation.

In sum, this study was among the first of its kind to explicitly examine inter-relationships between neurocognition, social cognition and emotion reg- ulation in a sample of BD patients. Our results reveal that in BD, neurocognitive ability is predic- tive of social cognition, yet associations between neurocognition and emotion regulation appear to be absent. As these findings provide indirect sup- port for neurobiological theories of disrupted neu- ral circuitry, future studies should aim to replicate these findings using both behavioural and neuroi- maging measures. Further, the finding that neuro- cognition predicts social cognition in BD has substantial implications for psychosocial therapies for the disorder. Specifically, they suggest that the remediation of neurocognitive deficits may at least partially remediate social cognitive deficits in BD too. On the basis of these results, it would be wise for researchers and clinicians developing treat- ments that target psychosocial dysfunctions plausi- bly linked to poor social cognitive function, to consider the impact of neurocognitive deficits on social perception and to adjust current treatments to reduce cognitive load.

Acknowledgements

The authors would like to acknowledge the Australian Rotary Health/Bipolar Expedition (SR and TVR), the Helen McPher- son Smith Trust (SR and TVR) and an Australian Postgradu- ate Award to TVR for providing financial assistance for the completion of this work.

Declaration of interest

None.

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