Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Theory of mind and neurocognition in early psychosis: a quasi-experimental study

Theory of mind and neurocognition in early psychosis: a quasi-experimental study Background: People with chronic psychosis often display theory of mind impairments that are not fully accounted for by other, more general neurocognitive deficits. In these patients, both theory of mind and neurocognitive deficits contribute to poor functioning, independently of psychotic symptoms. In young people with recent-onset psychosis, however, it is unclear the extent to which theory of mind impairment is independent of neurocognitive deficits. The primary aim of this study was to examine the evidence for specific theory of mind impairments in early psychosis. A secondary aim was to explore the relations between theory of mind, neurocognition, symptom severity, and functional outcomes. Methods: Twenty-three patients who were within two years of their first psychotic episode and 19 healthy controls completed theory of mind and neurocognitive batteries. Social functioning, quality of life, and symptom severity were also assessed in patients. Results: Patients demonstrated deficits in tasks assessing theory of mind and neurocognition relative to controls. Patients’ deficits in theory of mind were evident even after adjusting for their deficits in neurocognition. Neither theory of mind nor neurocognition predicted social functioning or quality of life in this early psychosis sample. Severity of negative symptoms, however, was a significant predictor of both outcomes. Conclusions: While a specific theory of mind impairment was evident in this early psychosis sample, severity of negative symptoms emerged as the best predictor of poor functional outcome. Further early psychosis research is needed to examine the longitudinal progression of theory of mind impairments – independent of neurocognitive deficits – and their impact on psychosocial function. Keywords: Early psychosis, First episode psychosis, Neurocognition, Occupational functioning, Quality of life, Schizophrenia, Social functioning, Theory of mind Background Poor functioning in psychosis may be due, in part, to a Psychosis is usually associated with poor functioning. specific impairment in “theory of mind” (ToM) – the Patients with psychosis, for example, typically display ability to ascribe mental states to others so as to predict poor social skills, report fewer relationships, and are and explain behaviour. ToM is essential to negotiating evaluated more negatively in social situations than social interactions and there is strong evidence that pa- patients without psychosis [1-3]. As a result of this poor tients across all stages of psychosis, including those with functioning, patients with psychosis experience a range at-risk mental states, have impairment in this ability of negative outcomes, including dissatisfaction with their [6,7]. Indeed, social cognitive deficits, including ToM, quality of life, unemployment, and depression [1-3]. appear to be stable over time in patients with early Many interventions for psychosis, therefore, focus on psychosis [8] and across patients at different stages of improving social skills and functional outcomes [4,5]. psychosis [7]. The poor functioning that is associated with psychosis, however, may also be due, in part, to the psychotic symptoms themselves or to other neurocog- * Correspondence: [email protected] nitive deficits. Patients with psychosis typically display ARC Centre of Excellence in Cognition and its Disorders, and Department of deficits in attention, working memory, and many other Cognitive Science, Macquarie University, Sydney, NSW, Australia Full list of author information is available at the end of the article © 2014 Langdon et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Langdon et al. BMC Psychiatry 2014, 14:316 Page 2 of 7 http://www.biomedcentral.com/1471-244X/14/316 aspects of neurocognition, which also predict poor relative independence from neurocognition. Following functioning, independent of severity of negative symp- previous research with patients with chronic psychosis toms [9-11]. [10], our secondary aim was to explore the relations bet- While ToM and neurocognitive deficits appear to be ween theory of mind, neurocognition, symptom severity, present at all stages of psychosis and contribute to poor and functioning in an early psychosis sample. Patients, functioning, the ToM deficits – at least in chronic who were within the first two years of their first psy- patients – are not fully accounted for by the other, more chotic episode, and healthy controls completed batteries general neurocognitive deficits [12]. In addition, the of ToM and neurocognition. The social functioning, negative effects of ToM impairment on functioning in quality of life, and symptom severity of patients were chronic psychosis are present even when severity of also assessed. If ToM was selectively impaired, as it is in other neurocognitive deficits and negative symptoms are people with chronic psychotic symptoms, we expected taken into account [10]. Less is known, however, about that patients and controls would show differences in this these relations at earlier stages of psychosis. Indeed, ability independent of any differences in neurocognition. Bora and Pantelis [6] argue that the extent to which ToM deficits are reducible to other neurocognitive defi- Methods cits at earlier stages of psychosis is unclear. It is possible, Participants for example, that the deterioration of selective theory Twenty-three patients were recruited from two early of mind capacity and neurocognitive functioning follow psychosis intervention programs in New South Wales, different trajectories in psychosis. Australia. All patients were in the first two years of their To address these issues, Sullivan et al. [13] recently first treatment by mental health services. Patients were examined the relations between ToM, general cognition, interviewed using the Diagnostic Interview for Psychosis symptoms and social functioning in a sample of patients [15] to confirm diagnosis according to ICD-10 criteria in their first psychotic episode. Sullivan et al. found that [16]. Seventeen of these patients had a diagnosis of social functioning in their sample was associated with “Paranoid Schizophrenia,” 4had a diagnosis of “Undif- ToM (as measured by the Hinting task) and verbal IQ, ferentiated Schizophrenia,” 1had adiagnosis of “Schizoaf- but not with other general cognitive measures or a mea- fective Disorder – Bipolar Subtype,” and 1 had a diagnosis sure of negative symptoms that excluded symptoms that of “Other Non-Organic Psychotic Disorder.” Patients with overlapped with poor social functioning (e.g. asociality). organic brain disorders or a comorbid diagnosis of sub- These findings suggest that both theory of mind and stance dependence according to the treating clinician aspects of neurocognition contribute to poor social were excluded. All the patients were prescribed low dose functioning in early psychosis. However, later follow-ups atypical neuroleptics but several disclosed their non- found that these variables did not predict functional out- compliance, making it unreliable to explore medication comes at six months or one year [14]. These important effects. Consistent with the gender imbalance in young studies also had some limitations. The approach of cohorts with a schizophrenia-like psychosis [17], 22 of the excluding some negative symptoms, for example, is patients were male and one patient was female. potentially problematic since no evidence was provided Nineteen healthy controls (17 male, 2 female) were to support the categorisation of a negative symptom as recruited from the general community to match the pa- social or not. In addition, Sullivan and colleagues used tient group on age, gender distribution, and formal edu- a rather limited neuropsychological battery. ToM was cation. The controls were screened using the affective, assessed with the Hinting task, for instance, which may psychotic, and substance abuse screening modules from produce skewed data that limits the analyses that can be the Structured Clinical Interview for DSM-IV Axis 1 performed. Similarly, neurocognition was assessed using Disorders [18]. In accord with research in this area, only three brief measures. Given these limitations and exclusion criteria for both groups included organic brain the ambiguous findings to date, the current study sought disorders and substance dependence (screened as above). to extend Sullivan et al.’s research using a more detailed All participants were English-speaking and gave written neuropsychological battery. informed consent. Demographic features of both groups and clinical features of patients are summarised in Current study Table 1. As the relations between ToM and neurocognition at The study followed the World Medical Association early stages of psychosis have important implications for Declaration of Helsinki – Ethical Principles for Medical clinical interventions, we aimed to more comprehen- Research Involving Human Subjects, and was approved by sively assess neurocognition and ToM in a first episode the Hunter Area Research Ethics Committee (reference psychosis sample. Our primary aim was to examine number 01/12/12/3.23), South Western Sydney Area theory of mind performance in early psychosis and its Health Service Research Ethics Committee (reference Langdon et al. BMC Psychiatry 2014, 14:316 Page 3 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 1 Demographics of patients and controls Patients Healthy controls Significance test Males:females 22:1 17:2 χ (1) = .599 Age (years) 20.91 ± 1.83 (18-25) 20.79 ± 1.81 (17-24) t(40) = .219 Education (years) 11.43 ± 2.02 (8-18) 12.82 ± 1.94 (9-16) t(40) = 2.247* IQ 96.65 ± 8.41 103.42 ± 9.32 t(40) = 2.472* Age of illness onset (years) 19.91 ± 1.95 (16-24) Duration of illness (weeks) 50.74 ± 29.50 (12-104) SAPS Positive Symptoms 1.25 ± .94 (0.00-3.75) SANS Negative Symptoms 2.18 ± .72 (0.60-3.80) Social Functioning 50.87 ± 12.12 (30-80) Quality of Life 58.22 ± 22.78 (20-120) Note. Data expressed as means ± SD (range in parentheses). *p < .05. Positive and negative symptoms assessed using the Scales for the Assessment of Positive and Negative Symptoms of Schizophrenia (SAPS and SANS: Andreasen, 1983, 1984). The overall Positive and Negative rating is the average of global ratings on the SAPS and SANS respectively (‘0’ = absent; ‘1’ = questionable; ‘2’ = mild; ‘3’ = moderate; ‘4’ = marked; ‘5’ = severe). number 00/082), and the University of Sydney Human eight “ToM” stories that involved understanding the Ethics Committee (reference number 00/10/03). mental states of the characters and eight control stories that required only general comprehension. The length of Materials and procedure the stories and the complexities of the sentences were Theory of Mind (ToM) matched across the two types of story. Responses were The first ToM measure was a non-verbal picture- scored from 0 (an incorrect answer) to 2 (a complete, sequencing task [19-21]. Participants were shown four correct answer). Scores were averaged across the two picture-cards in a fixed, incorrect order. Participants were types of story. asked to reorder the picture-cards to provide a logical sequence of events. There were four types of sequences Neurocognition (four sequences per type): ToM “false belief stories” that Participants also completed a battery of neurocognition required participants to go beyond the immediate ob- tests. IQ was estimated using the National Adult Reading jective information to infer a character’smistaken belief; Test [23]. Visual memory was assessed using the visual “social-script stories” that controlled for simple social rea- memory span test from the Wechsler Adult Intelligence soning; “mechanical stories” that controlled for physical Scale-Revised [24]. Verbal memory was assessed using the cause-and-effect reasoning; and “capture stories” that con- logical memories subtest from the WAIS [24]. Planning trolled for inhibition of an obvious but misleading cue. was assessed using the number of planning moves on a Each sequence scored two points if the first card was posi- computerised Tower of London task [25]. Set shifting was tioned correctly, two points if the last card was positioned assessed using the number of categories achieved on correctly, and one point each if the second and third cards the Wisconsin Card Sort Test [26]. Verbal fluency was were positioned correctly. Scores were averaged across assessed using the Controlled Oral Word Association Test each type of story (range 0–6). [27]. Semantic fluency was assessed by asking participants The second ToM measure was a joke appreciation task to generate the names of as many exemplars of a category [20-22]. Participants were shown a series of visual car- (in this study; food, animals, and furniture) that they could toons and asked to explain the humour. There were 11 think of in 60 seconds. Inhibition was indexed by time “ToM” cartoons in which the joke depended on under- taken on the colour-word interference condition that standing a character’s false belief or mental state, and 11 followed the colour-naming and colour-word reading “control” cartoons in which the joke did not depend on conditions of a bespoke Stroop task [28]. inferring mental states but instead involved situational anomalies. Responses were scored from 0 (an incorrect Clinical interviews or irrelevant answer) to 3 (a complete, correct expla- The scales for Assessment of Positive and Negative Symp- nation). Scores were averaged across the two types of toms of Schizophrenia [29,30] were used to rate symptom cartoon. severity in patients. The social and global functioning of The third ToM measure was a story comprehension patients were also assessed using the Social and Occupa- task [20-22]. Participants were asked to read a series of tional Functioning Assessment Scale [31] and the Quality stories and answer a question about each. There were of Life Scale [32]. Langdon et al. BMC Psychiatry 2014, 14:316 Page 4 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 2 Differences between patients and controls in ToM and neurocognition Patients Healthy controls Significance test: t(40) ToM −1.60 ± 2.16 1.94 ± 1.04 6.55** Picture sequencing 4.80 ± 1.19 5.87 ± .28 3.81** Joke appreciation 1.26 ± .47 1.90 ± .27 5.23** Story comprehension .72 ± .31 1.19 ± .27 5.17** Neurocognition −3.66 ± 3.77 4.21 ± 3.89 6.57** IQ 96.65 ± 8.41 103.42 ± 9.32 2.47* Visual memory 16.78 ± 3.26 19.84 ± 2.73 3.25** Verbal memory 26.39 ± 15.76 54.21 ± 13.44 6.08** Verbal fluency 28.00 ± 9.29 44.58 ± 13.47 4.71** Semantic fluency 32.43 ± 9.45 56.95 ± 12.94 7.09** Inhibition 32.30 ± 9.88 23.24 ± 5.92 3.49** Set-Shifting -.17 ± .93 .20 ± .50 1.54 Planning 60.26 ± 7.84 55.63 ± 6.79 2.02 Note. Data expressed as means ± SD. *p < .05, **p < .01. Statistical analyses score. An ANCOVA was then used to compare ToM The correlations between scores from the three ToM tasks between groups, adjusting for the composite score of were examined first to assess convergent validity. To ob- neurocognition. tain a global index of ToM abilities, scores from the three To explore the relations between ToM, neurocog- ToM measures were then converted to z-scores and aver- nition, symptom severity, and functioning, zero-order aged to produce a single composite ToM score. correlations were assessed between these measures in ToM and neurocognition scores of the patients and patients. To examine predictors of functioning, hierar- controls were compared using independent samples t- chical regression analyses were conducted with social tests. ToM and neurocognitive score differences between functioning and quality of life as the dependent varia- patients and controls were converted to effect sizes in bles, and neurocognition, ToM and severity of negative terms of Cohen’s d. In order to further reduce the data symptoms entered as the predictors. for subsequent analyses, a composite neurocognition score was also calculated by converting scores from the Results individual measures into z-scores across groups, scaled Relationships between ToM measures such that higher scores indicated better function, and All three measures of ToM correlated with each other. averaged to produce a single composite neurocognition The picture sequencing ToM score correlated with ToM 2.5 1.5 0.5 Figure 1 Patients’ deficits in ToM and different neurocognitive domains relative to controls. Effect Size (Cohen's d) Langdon et al. BMC Psychiatry 2014, 14:316 Page 5 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 3 Zero-order correlations between ToM, neurocognition, symptom severity, and social functioning in patients ToM Neurocognition Negative symptoms Positive symptoms Quality of life Social functioning ToM .70** -.50* -.01 .26 .16 Neurocognition .70** -.47* −.06 .53* .30 Negative symptoms -.50* -.47* .18 -.50* -.51* Positive symptoms -.01 -.06 .18 .02 -.09 Quality of Life .26 .53* -.50* .02 .85** Social Functioning .16 .30 -.51* -.09 .85** Note. *p < .05, **p < .01. scores from both the joke appreciation task, r(42) = .52, Predictors of social functioning and quality of life p < .01, and the story comprehension task, r(42) = .47, Since previous research indicates that neurocognitive p < .01. The latter two measures also correlated signifi- deficits contribute to theory of mind impairment which, cantly, r(42) = .59, p < .01. in turn, associates with negative symptoms (in accord with our zero-order correlation results), we conducted follow-up hierarchical regression analyses to examine Specificity of ToM deficits in patients the cumulative effects of these measures when pre- Patients performed worse than controls in ToM tasks dicting patients’ social functioning and quality of life. and in all measures of neurocognition. These differences, Table 4 summarises the results. While acknowledging however, did not reach statistical significance for set the need for caution given our small sample size and the shifting and planning (see Table 2). Effect sizes are intercorrelations between predictors, findings indicate shown in Figure 1. Patients showed particularly large im- that neither neurocognition, nor the combination of pairments in ToM, verbal memory, and semantic fluency neurocognition and ToM, predicted our functioning relative to controls. To determine whether ToM deficits were evident when neurocognitive performance was Table 4 Summary of hierarchical regression analyses accounted for, we compared patients and controls’ com- predicting social functioning and quality of life in early posite ToM scores using an ANCOVA with the compos- psychosis patients ite score of neurocognition as a covariate. Patients still ßt p R displayed a significant deficit in ToM compared to con- Predicting SOFAS Scores of Social Functioning trols, F(1, 38) = 5.60, p = .02, η = .13. There was also a Step 1 .09 significant effect of neurocognition on ToM independent 2 Neurocognition .30 1.39 .18 of group, F(1, 38) = 25.81, p < .01, η = .41. Levene’s test Step 2 .09 indicated that the assumption of equality of error varian- Neurocognition .34 1.12 .28 ces was met for this analysis, F(1, 39) = 3.83, p = .06. Patients and controls did not differ on any of the control ToM -.07 .21 .83 conditions in the ToM tasks (all ps > .05). Step 3 .30 Neurocognition .20 .70 .49 ToM, neurocognition, symptom severity, and functioning ToM -.22 .76 .46 in patients Negative symptoms -.53 2.30 .03* Correlations between ToM, neurocognition, symptom Predicting QLS Scores of Life Satisfaction severity, and functional outcomes are shown in Table 3. Step 1 .29 Focusing on correlations with the latter, ToM did not Neurocognition .53 2.83 .01 correlate significantly with either quality of life or the Step 2 .29 SOFAS social functioning measure. Neurocognition was significantly correlated with quality of life. This relation- Neurocognition .60 2.22 .04 ship, however, was not significant in a partial correlation ToM -.09 .33 .74 that controlled for negative symptoms (r = .70, p = .76). Step 3 .42 Negative symptoms were associated with poorer social Neurocognition .48 1.89 .08 functioning and quality of life, as well as lower ToM and ToM -.21 .81 .43 neurocognition. Positive symptoms were not signifi- Negative symptoms -.42 2.00 .06 cantly correlated with any of the other domains assessed (all ps > .42). *p < .05; p < .10. Langdon et al. BMC Psychiatry 2014, 14:316 Page 6 of 7 http://www.biomedcentral.com/1471-244X/14/316 measures in this early psychosis sample. In contrast, seve- more sensitive and targeted measures of functioning, rity of negative symptoms was a significant predictor of including scales that require direct observation of actual poor social functioning and showed a similar trend for or role-played functioning, to assess different domains of reduced quality of life, having adjusted for the effects of functional outcomes. Future research could also examine neurocognition and ToM. Subsequent backward regres- whether subtypes of negative symptoms differentially sion analyses reduced the full models in each case to leave impact functioning [34]. negative symptoms as the sole predictor, F(1,20) = 7.37, In conclusion, patients in our early psychosis sample p =.01 and F(2,19) = 6.25, p = .01 respectively. displayed deficits in ToM, which were independent of their neurocognitive deficits. Negative symptoms, and Discussion not these cognitive deficits, were the strongest predictor Consistent with previous research [6], patients in the of poor functioning. This is in contrast with the evidence early stages of psychosis demonstrated deficits in both that ToM deficits are the strongest predictors of social ToM and neurocognition. Importantly, however, while dysfunction in patients living with chronic psychotic ToM deficits co-occurred with deficits in neurocogni- symptoms [10]. In addition, the significant correlations tion – particularly deficits in verbal memory and seman- in our sample between negative symptoms and impaired tic fluency – they were not fully accounted for by these ToM and neurocognition indicate the challenges of neurocognitive deficits. This evidence for specificity of separating their effects on functioning. While our results ToM impairment at early stages of psychosis is consis- require replication with a larger, more gender-balanced tent with evidence elsewhere that ToM deficits may be a early psychosis sample, they reinforce the need for future trait marker of schizophrenia [6,25]. early psychosis research to examine the developmental Nevertheless, neither ToM nor neurocognitive deficits progression of ToM deficits and their real-world conse- in the early psychosis patients predicted poor functional quences over time. outcomes. This is consistent with Sullivan et al.’s [14] Competing interests finding that ToM does not predict poor outcomes longi- The authors declare that they have no competing interests. tudinally in the early stages of psychosis. The findings, however, are in contrast to other cross-sectional research Authors’ contributions which has found that ToM deficits are associated with RL designed the study, tested participants, and helped to draft the manuscript. MC performed the statistical analyses and drafted the poor social functioning in both early [13] and chro- manuscript. MS helped to recruit participants and also collected data. MS, nic psychosis [10]. These divergent findings may reflect PW, and SC helped to design the study. All authors read and approved the differences in methodology. The current study used dif- final manuscript. ferent measures of ToM to those employed in Sullivan Acknowledgements et al.’s [13] cross-sectional study, which used the Hinting This work was supported in part by the Australian Research Council task to test sensitivity to intended meanings of indirect Centre of Excellence for Cognition and its Disorders (CE110001021) hints. It is possible that the Hinting task taps social <http://www.ccd.edu.au>. knowledge in addition to ToM and so better predicts Author details functional outcomes. Sullivan et al.’s [14] failure, how- ARC Centre of Excellence in Cognition and its Disorders, and Department of ever, to find an association longitudinally, together with Cognitive Science, Macquarie University, Sydney, NSW, Australia. Rehabilitation Services, Division of Mental Health, Sydney & South Western the current findings, suggests that other factors, inclu- Sydney Local Health Districts, Liverpool, NSW, Australia. School of Psychiatry, ding severity of negative symptoms, may play a greater University of New South Wales and Schizophrenia Research Unit, South role in determining real-world functioning, at least in Western Sydney Local Health District, Liverpool, NSW, Australia. School of Psychiatry, University of Queensland, Brisbane, QLD, Australia. the early stages of psychosis. The current study was limited by its relatively small Received: 7 June 2014 Accepted: 24 October 2014 sample size and the fact that it did not consider the effects of general psychopathology and comorbid Axis-II symptomatology. With regard to the latter, borderline References 1. Couture SM, Penn DL, Roberts DL: The functional significance of social traits in adolescents are associated with ‘hyper-mentalis- cognition in schizophrenia: a review. Schizophr Bull 2006, 32:S44–S63. ing’ errors (i.e., errors of inferring mental states in others 2. Green MF, Penn DL, Bentall R, Carpenter WT, Gaebel W, Gur RC, Kring AM, without reasonable justification) [33], rather than the Park S, Silverstein SM, Heinssen R: Social cognition in schizophrenia: An NIMH workshop on definitions, assessment, and research opportunities. ‘hypo-mentalising’ errors (i.e., errors of failing to infer Schizophr Bull 2008, 34:1211–1220. mental states) seen in our early psychosis sample. In 3. Hooley JM: Interpersonal functioning and schizophrenia. In Oxford addition, we could not examine medication effects and Textbook of Psychopathology. 2nd edition. Edited by Millon T, Blaney P, Davis R. New York: Oxford University Press; 2008:333–360. relied on the SOFAS and QLS, which although widely- 4. Marsh PJ, Langdon R, Harris A, Coltheart M: The case for social-cognitive used, are based on interview and provide only gross glo- remediation in schizophrenia: a life well lived is more than remission bal estimates of functioning. Future research could use from psychosis. Aust N Z J Psychiatry 2013, 47:512–515. Langdon et al. BMC Psychiatry 2014, 14:316 Page 7 of 7 http://www.biomedcentral.com/1471-244X/14/316 5. Roberts DL, Velligan DI: Can social functioning in schizophrenia be 31. American Psychiatric Association: Social and Occupational Functioning improved through targeted social cognitive intervention? Rehabil Res Pract Assessment Scale (SOFAS). In Diagnostic and Statistical Manual of Mental 2012, 2012:8. Disorders. 4th edition. Washington: Author; 1994. 6. Bora E, Pantelis C: Theory of mind impairments in first-episode psychosis, 32. Heinrichs DW, Hanlon TE, Carpenter WT: The quality of life scale: an individuals at ultra-high risk for psychosis and in first-degree relatives of instrument for rating the schizophrenic deficit syndrome. Schizophr Bull schizophrenia: systematic review and meta-analysis. Schizophr Res 2013, 1984, 10:388–398. 144:31–36. 33. Sharp C, Pane H, Ha C, Venta A, Patel AB, Sturek J, Fonagy P: Theory of 7. Green MF, Bearden CE, Cannon TD, Fiske AP, Hellemann GS, Horan WP, mind and emotion regulation difficulties in adolescents with borderline Kee K, Kern RS, Lee J, Sergi MJ, Subotnik KL, Sugar CA, Ventura J, Yee CM, traits. J Am Acad Child Adolesc Psychiatry 2011, 50:563–573.e561. Nuechterlein KH: Social cognition in schizophrenia, part 1: performance 34. Green MF, Horan WP, Mathis KI, Wynn JK: Neurocognition and functional across phase of illness. Schizophr Bull 2012, 38:854–864. outcome in schizophrenia: filling in the gap. In Cognitive Impairment in 8. Horan WP, Green MF, DeGroot M, Fiske A, Hellemann G, Kee K, Kern RS, Schizophrenia. Edited by Harvey PD. New York: Cambridge University Press; Lee J, Sergi MJ, Subotnik KL, Sugar CA, Ventura J, Nuechterlein KH: Social 2013:85–97. cognition in schizophrenia, part 2: 12-month stability and prediction of functional outcome in first-episode patients. Schizophr Bull 2012, doi:10.1186/s12888-014-0316-6 38:865–872. Cite this article as: Langdon et al.: Theory of mind and neurocognition 9. Bowie CR, Harvey PD: Cognitive deficits and functional outcome in in early psychosis: a quasi-experimental study. BMC Psychiatry 2014 14:316. schizophrenia. Neuropsychiatr Dis Treat 2006, 2:531–536. 10. Brüne M, Schaub D, Juckel G, Langdon R: Social skills and behavioral problems in schizophrenia: the role of mental state attribution, neurocognition and clinical symptomatology. Psychiatry Res 2011, 190:9–17. 11. Fett A-KJ, Viechtbauer W, Dominguez M-d-G, Penn DL, van Os J, Krabbendam L: The relationship between neurocognition and social cognition with functional outcomes in schizophrenia: a meta-analysis. Neurosci Biobehav Rev 2011, 35:573–588. 12. Bora E, Yucel M, Pantelis C: Theory of mind impairment in schizophrenia: meta-analysis. Schizophr Res 2009, 109:1–9. 13. Sullivan S, Herzig D, Mohr C, Lewis G, Corcoran R, Drake R, Evans J: Theory of mind and social functioning in first episode psychosis. Cognit Neuropsychiatry 2012, 18:219–242. 14. Sullivan S, Lewis G, Mohr C, Herzig D, Corcoran R, Drake R, Evans J: The longitudinal association between social functioning and theory of mind in first-episode psychosis. Cognit Neuropsychiatry 2013, 19:58–80. 15. Castle DJ, Jablensky A, McGrath JJ, Carr V, Morgan V, Waterreus A, Valuri G, Stain H, McGuffin P, Farmer A: The diagnostic interview for psychoses (DIP): development, reliability and applications. Psychol Med 2006, 36:69–80. 16. World Health Organisation: ICD-10: International Statistical Classification of Diseases and Related Health Problems 10th Rev. edn. New York: Author; 2008. 17. Ochoa S, Usall J, Cobo J, Labad X, Kulkarni J: Gender differences in schizophrenia and first-episode psychosis: a comprehensive literature review. Schizophr Res Treat 2012, 2012:1–9. 18. First MB, Spitzer RL, Gibbon M, Williams JBW: Structured Clinical Interview for DSM-IV Axis I Disorders - Patient edition (SCID-I P, Version 2.0). New York: New York State Psychiatric Institute, Biometrics Research Department; 1996. 19. Langdon R, Coltheart M: Mentalising, schizotypy, and schizophrenia. Cognition 1999, 71:43–71. 20. Langdon R, Ward PB, Coltheart M: Reasoning anomalies associated with delusions in schizophrenia. Schizophr Bull 2010, 36:321–330. 21. Langdon R, Still M, Connors MH, Ward PB, Catts SV: Theory of mind in early psychosis. Early Interv Psychiatry 2014, 8:286–290. 22. Happé F, Brownell H, Winner E: Acquired ‘theory of mind’ impairments following stroke. Cognition 1999, 70:211–240. 23. Nelson HE, Willison J: National Adult Reading Test (NART): Test manual. 2nd edition. Windsor: NFER Nelson; 1991. 24. Wechsler D: Manual of the Wechsler Adult Intelligence Scale. 3rd edition. San Antonio: The Psychological Corporation; 1997. Submit your next manuscript to BioMed Central 25. Langdon R, Coltheart M, Ward PB, Catts SV: Disturbed communication in and take full advantage of: schizophrenia: the role of poor pragmatics and poor mind-reading. Psychol Med 2002, 32:1273–1284. • Convenient online submission 26. Heaton RK: Wisconsin Card Sorting Test Manual. Odessa: Psychological • Thorough peer review Assessment Resources Inc.; 1981. 27. Spreen O, Strauss E: A Compendium of Neuropsychological Tests: Administration, • No space constraints or color figure charges Norms and Commentary. Tucson: Neuropsychological Press; 1998. • Immediate publication on acceptance 28. Golden CJ: Stroop Color and Word Test: Manual for Clinical and Experimental Uses. Chicago: Stoelting; 1978. • Inclusion in PubMed, CAS, Scopus and Google Scholar 29. Andreasen NC: Scale for the Assessment of Negative Symptoms (SANS). • Research which is freely available for redistribution Iowa City: University of Iowa; 1983. 30. Andreasen NC: Scale for the Assessment of Positive Symptoms (SAPS). Submit your manuscript at Iowa City: University of Iowa; 1984. www.biomedcentral.com/submit http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png BMC Psychiatry Springer Journals

Theory of mind and neurocognition in early psychosis: a quasi-experimental study

Loading next page...
 
/lp/springer-journals/theory-of-mind-and-neurocognition-in-early-psychosis-a-quasi-DKXzbY1HFj

References (48)

Publisher
Springer Journals
Copyright
Copyright © 2014 by Langdon et al.; licensee BioMed Central Ltd.
Subject
Medicine & Public Health; Psychiatry; Psychotherapy
eISSN
1471-244X
DOI
10.1186/s12888-014-0316-6
pmid
25472859
Publisher site
See Article on Publisher Site

Abstract

Background: People with chronic psychosis often display theory of mind impairments that are not fully accounted for by other, more general neurocognitive deficits. In these patients, both theory of mind and neurocognitive deficits contribute to poor functioning, independently of psychotic symptoms. In young people with recent-onset psychosis, however, it is unclear the extent to which theory of mind impairment is independent of neurocognitive deficits. The primary aim of this study was to examine the evidence for specific theory of mind impairments in early psychosis. A secondary aim was to explore the relations between theory of mind, neurocognition, symptom severity, and functional outcomes. Methods: Twenty-three patients who were within two years of their first psychotic episode and 19 healthy controls completed theory of mind and neurocognitive batteries. Social functioning, quality of life, and symptom severity were also assessed in patients. Results: Patients demonstrated deficits in tasks assessing theory of mind and neurocognition relative to controls. Patients’ deficits in theory of mind were evident even after adjusting for their deficits in neurocognition. Neither theory of mind nor neurocognition predicted social functioning or quality of life in this early psychosis sample. Severity of negative symptoms, however, was a significant predictor of both outcomes. Conclusions: While a specific theory of mind impairment was evident in this early psychosis sample, severity of negative symptoms emerged as the best predictor of poor functional outcome. Further early psychosis research is needed to examine the longitudinal progression of theory of mind impairments – independent of neurocognitive deficits – and their impact on psychosocial function. Keywords: Early psychosis, First episode psychosis, Neurocognition, Occupational functioning, Quality of life, Schizophrenia, Social functioning, Theory of mind Background Poor functioning in psychosis may be due, in part, to a Psychosis is usually associated with poor functioning. specific impairment in “theory of mind” (ToM) – the Patients with psychosis, for example, typically display ability to ascribe mental states to others so as to predict poor social skills, report fewer relationships, and are and explain behaviour. ToM is essential to negotiating evaluated more negatively in social situations than social interactions and there is strong evidence that pa- patients without psychosis [1-3]. As a result of this poor tients across all stages of psychosis, including those with functioning, patients with psychosis experience a range at-risk mental states, have impairment in this ability of negative outcomes, including dissatisfaction with their [6,7]. Indeed, social cognitive deficits, including ToM, quality of life, unemployment, and depression [1-3]. appear to be stable over time in patients with early Many interventions for psychosis, therefore, focus on psychosis [8] and across patients at different stages of improving social skills and functional outcomes [4,5]. psychosis [7]. The poor functioning that is associated with psychosis, however, may also be due, in part, to the psychotic symptoms themselves or to other neurocog- * Correspondence: [email protected] nitive deficits. Patients with psychosis typically display ARC Centre of Excellence in Cognition and its Disorders, and Department of deficits in attention, working memory, and many other Cognitive Science, Macquarie University, Sydney, NSW, Australia Full list of author information is available at the end of the article © 2014 Langdon et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Langdon et al. BMC Psychiatry 2014, 14:316 Page 2 of 7 http://www.biomedcentral.com/1471-244X/14/316 aspects of neurocognition, which also predict poor relative independence from neurocognition. Following functioning, independent of severity of negative symp- previous research with patients with chronic psychosis toms [9-11]. [10], our secondary aim was to explore the relations bet- While ToM and neurocognitive deficits appear to be ween theory of mind, neurocognition, symptom severity, present at all stages of psychosis and contribute to poor and functioning in an early psychosis sample. Patients, functioning, the ToM deficits – at least in chronic who were within the first two years of their first psy- patients – are not fully accounted for by the other, more chotic episode, and healthy controls completed batteries general neurocognitive deficits [12]. In addition, the of ToM and neurocognition. The social functioning, negative effects of ToM impairment on functioning in quality of life, and symptom severity of patients were chronic psychosis are present even when severity of also assessed. If ToM was selectively impaired, as it is in other neurocognitive deficits and negative symptoms are people with chronic psychotic symptoms, we expected taken into account [10]. Less is known, however, about that patients and controls would show differences in this these relations at earlier stages of psychosis. Indeed, ability independent of any differences in neurocognition. Bora and Pantelis [6] argue that the extent to which ToM deficits are reducible to other neurocognitive defi- Methods cits at earlier stages of psychosis is unclear. It is possible, Participants for example, that the deterioration of selective theory Twenty-three patients were recruited from two early of mind capacity and neurocognitive functioning follow psychosis intervention programs in New South Wales, different trajectories in psychosis. Australia. All patients were in the first two years of their To address these issues, Sullivan et al. [13] recently first treatment by mental health services. Patients were examined the relations between ToM, general cognition, interviewed using the Diagnostic Interview for Psychosis symptoms and social functioning in a sample of patients [15] to confirm diagnosis according to ICD-10 criteria in their first psychotic episode. Sullivan et al. found that [16]. Seventeen of these patients had a diagnosis of social functioning in their sample was associated with “Paranoid Schizophrenia,” 4had a diagnosis of “Undif- ToM (as measured by the Hinting task) and verbal IQ, ferentiated Schizophrenia,” 1had adiagnosis of “Schizoaf- but not with other general cognitive measures or a mea- fective Disorder – Bipolar Subtype,” and 1 had a diagnosis sure of negative symptoms that excluded symptoms that of “Other Non-Organic Psychotic Disorder.” Patients with overlapped with poor social functioning (e.g. asociality). organic brain disorders or a comorbid diagnosis of sub- These findings suggest that both theory of mind and stance dependence according to the treating clinician aspects of neurocognition contribute to poor social were excluded. All the patients were prescribed low dose functioning in early psychosis. However, later follow-ups atypical neuroleptics but several disclosed their non- found that these variables did not predict functional out- compliance, making it unreliable to explore medication comes at six months or one year [14]. These important effects. Consistent with the gender imbalance in young studies also had some limitations. The approach of cohorts with a schizophrenia-like psychosis [17], 22 of the excluding some negative symptoms, for example, is patients were male and one patient was female. potentially problematic since no evidence was provided Nineteen healthy controls (17 male, 2 female) were to support the categorisation of a negative symptom as recruited from the general community to match the pa- social or not. In addition, Sullivan and colleagues used tient group on age, gender distribution, and formal edu- a rather limited neuropsychological battery. ToM was cation. The controls were screened using the affective, assessed with the Hinting task, for instance, which may psychotic, and substance abuse screening modules from produce skewed data that limits the analyses that can be the Structured Clinical Interview for DSM-IV Axis 1 performed. Similarly, neurocognition was assessed using Disorders [18]. In accord with research in this area, only three brief measures. Given these limitations and exclusion criteria for both groups included organic brain the ambiguous findings to date, the current study sought disorders and substance dependence (screened as above). to extend Sullivan et al.’s research using a more detailed All participants were English-speaking and gave written neuropsychological battery. informed consent. Demographic features of both groups and clinical features of patients are summarised in Current study Table 1. As the relations between ToM and neurocognition at The study followed the World Medical Association early stages of psychosis have important implications for Declaration of Helsinki – Ethical Principles for Medical clinical interventions, we aimed to more comprehen- Research Involving Human Subjects, and was approved by sively assess neurocognition and ToM in a first episode the Hunter Area Research Ethics Committee (reference psychosis sample. Our primary aim was to examine number 01/12/12/3.23), South Western Sydney Area theory of mind performance in early psychosis and its Health Service Research Ethics Committee (reference Langdon et al. BMC Psychiatry 2014, 14:316 Page 3 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 1 Demographics of patients and controls Patients Healthy controls Significance test Males:females 22:1 17:2 χ (1) = .599 Age (years) 20.91 ± 1.83 (18-25) 20.79 ± 1.81 (17-24) t(40) = .219 Education (years) 11.43 ± 2.02 (8-18) 12.82 ± 1.94 (9-16) t(40) = 2.247* IQ 96.65 ± 8.41 103.42 ± 9.32 t(40) = 2.472* Age of illness onset (years) 19.91 ± 1.95 (16-24) Duration of illness (weeks) 50.74 ± 29.50 (12-104) SAPS Positive Symptoms 1.25 ± .94 (0.00-3.75) SANS Negative Symptoms 2.18 ± .72 (0.60-3.80) Social Functioning 50.87 ± 12.12 (30-80) Quality of Life 58.22 ± 22.78 (20-120) Note. Data expressed as means ± SD (range in parentheses). *p < .05. Positive and negative symptoms assessed using the Scales for the Assessment of Positive and Negative Symptoms of Schizophrenia (SAPS and SANS: Andreasen, 1983, 1984). The overall Positive and Negative rating is the average of global ratings on the SAPS and SANS respectively (‘0’ = absent; ‘1’ = questionable; ‘2’ = mild; ‘3’ = moderate; ‘4’ = marked; ‘5’ = severe). number 00/082), and the University of Sydney Human eight “ToM” stories that involved understanding the Ethics Committee (reference number 00/10/03). mental states of the characters and eight control stories that required only general comprehension. The length of Materials and procedure the stories and the complexities of the sentences were Theory of Mind (ToM) matched across the two types of story. Responses were The first ToM measure was a non-verbal picture- scored from 0 (an incorrect answer) to 2 (a complete, sequencing task [19-21]. Participants were shown four correct answer). Scores were averaged across the two picture-cards in a fixed, incorrect order. Participants were types of story. asked to reorder the picture-cards to provide a logical sequence of events. There were four types of sequences Neurocognition (four sequences per type): ToM “false belief stories” that Participants also completed a battery of neurocognition required participants to go beyond the immediate ob- tests. IQ was estimated using the National Adult Reading jective information to infer a character’smistaken belief; Test [23]. Visual memory was assessed using the visual “social-script stories” that controlled for simple social rea- memory span test from the Wechsler Adult Intelligence soning; “mechanical stories” that controlled for physical Scale-Revised [24]. Verbal memory was assessed using the cause-and-effect reasoning; and “capture stories” that con- logical memories subtest from the WAIS [24]. Planning trolled for inhibition of an obvious but misleading cue. was assessed using the number of planning moves on a Each sequence scored two points if the first card was posi- computerised Tower of London task [25]. Set shifting was tioned correctly, two points if the last card was positioned assessed using the number of categories achieved on correctly, and one point each if the second and third cards the Wisconsin Card Sort Test [26]. Verbal fluency was were positioned correctly. Scores were averaged across assessed using the Controlled Oral Word Association Test each type of story (range 0–6). [27]. Semantic fluency was assessed by asking participants The second ToM measure was a joke appreciation task to generate the names of as many exemplars of a category [20-22]. Participants were shown a series of visual car- (in this study; food, animals, and furniture) that they could toons and asked to explain the humour. There were 11 think of in 60 seconds. Inhibition was indexed by time “ToM” cartoons in which the joke depended on under- taken on the colour-word interference condition that standing a character’s false belief or mental state, and 11 followed the colour-naming and colour-word reading “control” cartoons in which the joke did not depend on conditions of a bespoke Stroop task [28]. inferring mental states but instead involved situational anomalies. Responses were scored from 0 (an incorrect Clinical interviews or irrelevant answer) to 3 (a complete, correct expla- The scales for Assessment of Positive and Negative Symp- nation). Scores were averaged across the two types of toms of Schizophrenia [29,30] were used to rate symptom cartoon. severity in patients. The social and global functioning of The third ToM measure was a story comprehension patients were also assessed using the Social and Occupa- task [20-22]. Participants were asked to read a series of tional Functioning Assessment Scale [31] and the Quality stories and answer a question about each. There were of Life Scale [32]. Langdon et al. BMC Psychiatry 2014, 14:316 Page 4 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 2 Differences between patients and controls in ToM and neurocognition Patients Healthy controls Significance test: t(40) ToM −1.60 ± 2.16 1.94 ± 1.04 6.55** Picture sequencing 4.80 ± 1.19 5.87 ± .28 3.81** Joke appreciation 1.26 ± .47 1.90 ± .27 5.23** Story comprehension .72 ± .31 1.19 ± .27 5.17** Neurocognition −3.66 ± 3.77 4.21 ± 3.89 6.57** IQ 96.65 ± 8.41 103.42 ± 9.32 2.47* Visual memory 16.78 ± 3.26 19.84 ± 2.73 3.25** Verbal memory 26.39 ± 15.76 54.21 ± 13.44 6.08** Verbal fluency 28.00 ± 9.29 44.58 ± 13.47 4.71** Semantic fluency 32.43 ± 9.45 56.95 ± 12.94 7.09** Inhibition 32.30 ± 9.88 23.24 ± 5.92 3.49** Set-Shifting -.17 ± .93 .20 ± .50 1.54 Planning 60.26 ± 7.84 55.63 ± 6.79 2.02 Note. Data expressed as means ± SD. *p < .05, **p < .01. Statistical analyses score. An ANCOVA was then used to compare ToM The correlations between scores from the three ToM tasks between groups, adjusting for the composite score of were examined first to assess convergent validity. To ob- neurocognition. tain a global index of ToM abilities, scores from the three To explore the relations between ToM, neurocog- ToM measures were then converted to z-scores and aver- nition, symptom severity, and functioning, zero-order aged to produce a single composite ToM score. correlations were assessed between these measures in ToM and neurocognition scores of the patients and patients. To examine predictors of functioning, hierar- controls were compared using independent samples t- chical regression analyses were conducted with social tests. ToM and neurocognitive score differences between functioning and quality of life as the dependent varia- patients and controls were converted to effect sizes in bles, and neurocognition, ToM and severity of negative terms of Cohen’s d. In order to further reduce the data symptoms entered as the predictors. for subsequent analyses, a composite neurocognition score was also calculated by converting scores from the Results individual measures into z-scores across groups, scaled Relationships between ToM measures such that higher scores indicated better function, and All three measures of ToM correlated with each other. averaged to produce a single composite neurocognition The picture sequencing ToM score correlated with ToM 2.5 1.5 0.5 Figure 1 Patients’ deficits in ToM and different neurocognitive domains relative to controls. Effect Size (Cohen's d) Langdon et al. BMC Psychiatry 2014, 14:316 Page 5 of 7 http://www.biomedcentral.com/1471-244X/14/316 Table 3 Zero-order correlations between ToM, neurocognition, symptom severity, and social functioning in patients ToM Neurocognition Negative symptoms Positive symptoms Quality of life Social functioning ToM .70** -.50* -.01 .26 .16 Neurocognition .70** -.47* −.06 .53* .30 Negative symptoms -.50* -.47* .18 -.50* -.51* Positive symptoms -.01 -.06 .18 .02 -.09 Quality of Life .26 .53* -.50* .02 .85** Social Functioning .16 .30 -.51* -.09 .85** Note. *p < .05, **p < .01. scores from both the joke appreciation task, r(42) = .52, Predictors of social functioning and quality of life p < .01, and the story comprehension task, r(42) = .47, Since previous research indicates that neurocognitive p < .01. The latter two measures also correlated signifi- deficits contribute to theory of mind impairment which, cantly, r(42) = .59, p < .01. in turn, associates with negative symptoms (in accord with our zero-order correlation results), we conducted follow-up hierarchical regression analyses to examine Specificity of ToM deficits in patients the cumulative effects of these measures when pre- Patients performed worse than controls in ToM tasks dicting patients’ social functioning and quality of life. and in all measures of neurocognition. These differences, Table 4 summarises the results. While acknowledging however, did not reach statistical significance for set the need for caution given our small sample size and the shifting and planning (see Table 2). Effect sizes are intercorrelations between predictors, findings indicate shown in Figure 1. Patients showed particularly large im- that neither neurocognition, nor the combination of pairments in ToM, verbal memory, and semantic fluency neurocognition and ToM, predicted our functioning relative to controls. To determine whether ToM deficits were evident when neurocognitive performance was Table 4 Summary of hierarchical regression analyses accounted for, we compared patients and controls’ com- predicting social functioning and quality of life in early posite ToM scores using an ANCOVA with the compos- psychosis patients ite score of neurocognition as a covariate. Patients still ßt p R displayed a significant deficit in ToM compared to con- Predicting SOFAS Scores of Social Functioning trols, F(1, 38) = 5.60, p = .02, η = .13. There was also a Step 1 .09 significant effect of neurocognition on ToM independent 2 Neurocognition .30 1.39 .18 of group, F(1, 38) = 25.81, p < .01, η = .41. Levene’s test Step 2 .09 indicated that the assumption of equality of error varian- Neurocognition .34 1.12 .28 ces was met for this analysis, F(1, 39) = 3.83, p = .06. Patients and controls did not differ on any of the control ToM -.07 .21 .83 conditions in the ToM tasks (all ps > .05). Step 3 .30 Neurocognition .20 .70 .49 ToM, neurocognition, symptom severity, and functioning ToM -.22 .76 .46 in patients Negative symptoms -.53 2.30 .03* Correlations between ToM, neurocognition, symptom Predicting QLS Scores of Life Satisfaction severity, and functional outcomes are shown in Table 3. Step 1 .29 Focusing on correlations with the latter, ToM did not Neurocognition .53 2.83 .01 correlate significantly with either quality of life or the Step 2 .29 SOFAS social functioning measure. Neurocognition was significantly correlated with quality of life. This relation- Neurocognition .60 2.22 .04 ship, however, was not significant in a partial correlation ToM -.09 .33 .74 that controlled for negative symptoms (r = .70, p = .76). Step 3 .42 Negative symptoms were associated with poorer social Neurocognition .48 1.89 .08 functioning and quality of life, as well as lower ToM and ToM -.21 .81 .43 neurocognition. Positive symptoms were not signifi- Negative symptoms -.42 2.00 .06 cantly correlated with any of the other domains assessed (all ps > .42). *p < .05; p < .10. Langdon et al. BMC Psychiatry 2014, 14:316 Page 6 of 7 http://www.biomedcentral.com/1471-244X/14/316 measures in this early psychosis sample. In contrast, seve- more sensitive and targeted measures of functioning, rity of negative symptoms was a significant predictor of including scales that require direct observation of actual poor social functioning and showed a similar trend for or role-played functioning, to assess different domains of reduced quality of life, having adjusted for the effects of functional outcomes. Future research could also examine neurocognition and ToM. Subsequent backward regres- whether subtypes of negative symptoms differentially sion analyses reduced the full models in each case to leave impact functioning [34]. negative symptoms as the sole predictor, F(1,20) = 7.37, In conclusion, patients in our early psychosis sample p =.01 and F(2,19) = 6.25, p = .01 respectively. displayed deficits in ToM, which were independent of their neurocognitive deficits. Negative symptoms, and Discussion not these cognitive deficits, were the strongest predictor Consistent with previous research [6], patients in the of poor functioning. This is in contrast with the evidence early stages of psychosis demonstrated deficits in both that ToM deficits are the strongest predictors of social ToM and neurocognition. Importantly, however, while dysfunction in patients living with chronic psychotic ToM deficits co-occurred with deficits in neurocogni- symptoms [10]. In addition, the significant correlations tion – particularly deficits in verbal memory and seman- in our sample between negative symptoms and impaired tic fluency – they were not fully accounted for by these ToM and neurocognition indicate the challenges of neurocognitive deficits. This evidence for specificity of separating their effects on functioning. While our results ToM impairment at early stages of psychosis is consis- require replication with a larger, more gender-balanced tent with evidence elsewhere that ToM deficits may be a early psychosis sample, they reinforce the need for future trait marker of schizophrenia [6,25]. early psychosis research to examine the developmental Nevertheless, neither ToM nor neurocognitive deficits progression of ToM deficits and their real-world conse- in the early psychosis patients predicted poor functional quences over time. outcomes. This is consistent with Sullivan et al.’s [14] Competing interests finding that ToM does not predict poor outcomes longi- The authors declare that they have no competing interests. tudinally in the early stages of psychosis. The findings, however, are in contrast to other cross-sectional research Authors’ contributions which has found that ToM deficits are associated with RL designed the study, tested participants, and helped to draft the manuscript. MC performed the statistical analyses and drafted the poor social functioning in both early [13] and chro- manuscript. MS helped to recruit participants and also collected data. MS, nic psychosis [10]. These divergent findings may reflect PW, and SC helped to design the study. All authors read and approved the differences in methodology. The current study used dif- final manuscript. ferent measures of ToM to those employed in Sullivan Acknowledgements et al.’s [13] cross-sectional study, which used the Hinting This work was supported in part by the Australian Research Council task to test sensitivity to intended meanings of indirect Centre of Excellence for Cognition and its Disorders (CE110001021) hints. It is possible that the Hinting task taps social <http://www.ccd.edu.au>. knowledge in addition to ToM and so better predicts Author details functional outcomes. Sullivan et al.’s [14] failure, how- ARC Centre of Excellence in Cognition and its Disorders, and Department of ever, to find an association longitudinally, together with Cognitive Science, Macquarie University, Sydney, NSW, Australia. Rehabilitation Services, Division of Mental Health, Sydney & South Western the current findings, suggests that other factors, inclu- Sydney Local Health Districts, Liverpool, NSW, Australia. School of Psychiatry, ding severity of negative symptoms, may play a greater University of New South Wales and Schizophrenia Research Unit, South role in determining real-world functioning, at least in Western Sydney Local Health District, Liverpool, NSW, Australia. School of Psychiatry, University of Queensland, Brisbane, QLD, Australia. the early stages of psychosis. The current study was limited by its relatively small Received: 7 June 2014 Accepted: 24 October 2014 sample size and the fact that it did not consider the effects of general psychopathology and comorbid Axis-II symptomatology. With regard to the latter, borderline References 1. Couture SM, Penn DL, Roberts DL: The functional significance of social traits in adolescents are associated with ‘hyper-mentalis- cognition in schizophrenia: a review. Schizophr Bull 2006, 32:S44–S63. ing’ errors (i.e., errors of inferring mental states in others 2. Green MF, Penn DL, Bentall R, Carpenter WT, Gaebel W, Gur RC, Kring AM, without reasonable justification) [33], rather than the Park S, Silverstein SM, Heinssen R: Social cognition in schizophrenia: An NIMH workshop on definitions, assessment, and research opportunities. ‘hypo-mentalising’ errors (i.e., errors of failing to infer Schizophr Bull 2008, 34:1211–1220. mental states) seen in our early psychosis sample. In 3. Hooley JM: Interpersonal functioning and schizophrenia. In Oxford addition, we could not examine medication effects and Textbook of Psychopathology. 2nd edition. Edited by Millon T, Blaney P, Davis R. New York: Oxford University Press; 2008:333–360. relied on the SOFAS and QLS, which although widely- 4. Marsh PJ, Langdon R, Harris A, Coltheart M: The case for social-cognitive used, are based on interview and provide only gross glo- remediation in schizophrenia: a life well lived is more than remission bal estimates of functioning. Future research could use from psychosis. Aust N Z J Psychiatry 2013, 47:512–515. Langdon et al. BMC Psychiatry 2014, 14:316 Page 7 of 7 http://www.biomedcentral.com/1471-244X/14/316 5. Roberts DL, Velligan DI: Can social functioning in schizophrenia be 31. American Psychiatric Association: Social and Occupational Functioning improved through targeted social cognitive intervention? Rehabil Res Pract Assessment Scale (SOFAS). In Diagnostic and Statistical Manual of Mental 2012, 2012:8. Disorders. 4th edition. Washington: Author; 1994. 6. Bora E, Pantelis C: Theory of mind impairments in first-episode psychosis, 32. Heinrichs DW, Hanlon TE, Carpenter WT: The quality of life scale: an individuals at ultra-high risk for psychosis and in first-degree relatives of instrument for rating the schizophrenic deficit syndrome. Schizophr Bull schizophrenia: systematic review and meta-analysis. Schizophr Res 2013, 1984, 10:388–398. 144:31–36. 33. Sharp C, Pane H, Ha C, Venta A, Patel AB, Sturek J, Fonagy P: Theory of 7. Green MF, Bearden CE, Cannon TD, Fiske AP, Hellemann GS, Horan WP, mind and emotion regulation difficulties in adolescents with borderline Kee K, Kern RS, Lee J, Sergi MJ, Subotnik KL, Sugar CA, Ventura J, Yee CM, traits. J Am Acad Child Adolesc Psychiatry 2011, 50:563–573.e561. Nuechterlein KH: Social cognition in schizophrenia, part 1: performance 34. Green MF, Horan WP, Mathis KI, Wynn JK: Neurocognition and functional across phase of illness. Schizophr Bull 2012, 38:854–864. outcome in schizophrenia: filling in the gap. In Cognitive Impairment in 8. Horan WP, Green MF, DeGroot M, Fiske A, Hellemann G, Kee K, Kern RS, Schizophrenia. Edited by Harvey PD. New York: Cambridge University Press; Lee J, Sergi MJ, Subotnik KL, Sugar CA, Ventura J, Nuechterlein KH: Social 2013:85–97. cognition in schizophrenia, part 2: 12-month stability and prediction of functional outcome in first-episode patients. Schizophr Bull 2012, doi:10.1186/s12888-014-0316-6 38:865–872. Cite this article as: Langdon et al.: Theory of mind and neurocognition 9. Bowie CR, Harvey PD: Cognitive deficits and functional outcome in in early psychosis: a quasi-experimental study. BMC Psychiatry 2014 14:316. schizophrenia. Neuropsychiatr Dis Treat 2006, 2:531–536. 10. Brüne M, Schaub D, Juckel G, Langdon R: Social skills and behavioral problems in schizophrenia: the role of mental state attribution, neurocognition and clinical symptomatology. Psychiatry Res 2011, 190:9–17. 11. Fett A-KJ, Viechtbauer W, Dominguez M-d-G, Penn DL, van Os J, Krabbendam L: The relationship between neurocognition and social cognition with functional outcomes in schizophrenia: a meta-analysis. Neurosci Biobehav Rev 2011, 35:573–588. 12. Bora E, Yucel M, Pantelis C: Theory of mind impairment in schizophrenia: meta-analysis. Schizophr Res 2009, 109:1–9. 13. Sullivan S, Herzig D, Mohr C, Lewis G, Corcoran R, Drake R, Evans J: Theory of mind and social functioning in first episode psychosis. Cognit Neuropsychiatry 2012, 18:219–242. 14. Sullivan S, Lewis G, Mohr C, Herzig D, Corcoran R, Drake R, Evans J: The longitudinal association between social functioning and theory of mind in first-episode psychosis. Cognit Neuropsychiatry 2013, 19:58–80. 15. Castle DJ, Jablensky A, McGrath JJ, Carr V, Morgan V, Waterreus A, Valuri G, Stain H, McGuffin P, Farmer A: The diagnostic interview for psychoses (DIP): development, reliability and applications. Psychol Med 2006, 36:69–80. 16. World Health Organisation: ICD-10: International Statistical Classification of Diseases and Related Health Problems 10th Rev. edn. New York: Author; 2008. 17. Ochoa S, Usall J, Cobo J, Labad X, Kulkarni J: Gender differences in schizophrenia and first-episode psychosis: a comprehensive literature review. Schizophr Res Treat 2012, 2012:1–9. 18. First MB, Spitzer RL, Gibbon M, Williams JBW: Structured Clinical Interview for DSM-IV Axis I Disorders - Patient edition (SCID-I P, Version 2.0). New York: New York State Psychiatric Institute, Biometrics Research Department; 1996. 19. Langdon R, Coltheart M: Mentalising, schizotypy, and schizophrenia. Cognition 1999, 71:43–71. 20. Langdon R, Ward PB, Coltheart M: Reasoning anomalies associated with delusions in schizophrenia. Schizophr Bull 2010, 36:321–330. 21. Langdon R, Still M, Connors MH, Ward PB, Catts SV: Theory of mind in early psychosis. Early Interv Psychiatry 2014, 8:286–290. 22. Happé F, Brownell H, Winner E: Acquired ‘theory of mind’ impairments following stroke. Cognition 1999, 70:211–240. 23. Nelson HE, Willison J: National Adult Reading Test (NART): Test manual. 2nd edition. Windsor: NFER Nelson; 1991. 24. Wechsler D: Manual of the Wechsler Adult Intelligence Scale. 3rd edition. San Antonio: The Psychological Corporation; 1997. Submit your next manuscript to BioMed Central 25. Langdon R, Coltheart M, Ward PB, Catts SV: Disturbed communication in and take full advantage of: schizophrenia: the role of poor pragmatics and poor mind-reading. Psychol Med 2002, 32:1273–1284. • Convenient online submission 26. Heaton RK: Wisconsin Card Sorting Test Manual. Odessa: Psychological • Thorough peer review Assessment Resources Inc.; 1981. 27. Spreen O, Strauss E: A Compendium of Neuropsychological Tests: Administration, • No space constraints or color figure charges Norms and Commentary. Tucson: Neuropsychological Press; 1998. • Immediate publication on acceptance 28. Golden CJ: Stroop Color and Word Test: Manual for Clinical and Experimental Uses. Chicago: Stoelting; 1978. • Inclusion in PubMed, CAS, Scopus and Google Scholar 29. Andreasen NC: Scale for the Assessment of Negative Symptoms (SANS). • Research which is freely available for redistribution Iowa City: University of Iowa; 1983. 30. Andreasen NC: Scale for the Assessment of Positive Symptoms (SAPS). Submit your manuscript at Iowa City: University of Iowa; 1984. www.biomedcentral.com/submit

Journal

BMC PsychiatrySpringer Journals

Published: Dec 4, 2014

There are no references for this article.