Elsevier

Journal of Affective Disorders

Volume 207, 1 January 2017, Pages 268-275
Journal of Affective Disorders

Autistic and schizotypal traits and global functioning in bipolar I disorder

https://doi.org/10.1016/j.jad.2016.09.059Get rights and content

Highlights

  • Bipolar disorder individuals show clinically significant levels of autistic traits.

  • Bipolar disorder individuals show elevated levels of positive schizotypal traits.

  • Autistic and positive schizotypal traits interactively improve global functioning.

Abstract

Objective

To determine the expression of autistic and positive schizotypal traits in a large sample of adults with bipolar I disorder (BD I), and the effect of co-occurring autistic and positive schizotypal traits on global functioning in BD I.

Method

Autistic and positive schizotypal traits were self-assessed in 797 individuals with BD-I recruited by the Bipolar Disorder Research Network. Differences in global functioning (rated using the Global Assessment Scale) during lifetime worst depressive and manic episodes (GASD and GASM respectively) were calculated in groups with high/low autistic and positive schizotypal traits. Regression analyses assessed the interactive effect of autistic and positive schizotypal traits on global functioning.

Results

47.2% (CI=43.7–50.7%) showed clinically significant levels of autistic traits, and 23.22% (95% CI=20.29–26.14) showed clinically significant levels of positive schizotypal traits. In the worst episode of mania, the high autistic, high positive schizotypal group had better global functioning compared to the other groups. Individual differences analyses showed that high levels of both traits were associated with better global functioning in both mood states.

Limitations

Autistic and schizotypal traits were assessed using self-rated questionnaires.

Conclusions

Expression of autistic and schizotypal traits in adults with BD I is prevalent, and may be important to predict illness aetiology, prognosis, and diagnostic practices in this population. Future work should focus on replicating these findings in independent samples, and on the biological and/or psychosocial mechanisms underlying better global functioning in those who have high levels of both autistic and positive schizotypal traits.

Introduction

Bipolar disorder (BD) is a major affective disorder characterised by chronically recurring episodes of mania (or hypomania) and depression, which in their severe forms may present with psychotic symptoms, such as hallucinations or delusions (Weissman et al., 1996). This complex condition is often exacerbated by the presence of one or more comorbid conditions, in addition to a number of clinical factors such long duration of illness (Altamura et al., 2010, Altamura et al., 2015). While BD, schizophrenia spectrum disorders (SSD) and autism spectrum disorders (ASD) are considered distinct conditions, there is evidence for an overlap between BD and SSD (Altamura et al., 2014, Carroll and Owen, 2009, Moller, 2003), as well as between ASD and BD (Carroll and Owen, 2009, Stahlberg et al., 2004). Indeed, BD has a number of genetic, symptomatological and epidemiological overlaps with SSD (Laursen et al., 2009, Lichtenstein et al., 2009, Murray et al., 2004), and psychosis has been recognised as an important dimension in the psychopathology of BD (van Os and Kapur, 2009). In addition, schizotypy, which encompasses a set of personality traits that reflect subclinical expression of schizophrenia (Ettinger et al., 2015), is recognised as genetically related to SSD and is considered an endophenotype common to both SSD and BD (Ettinger et al., 2014, Mahon et al., 2013, Schurhoff et al., 2005). Schizotypy has been reported at elevated rates in individuals with BD compared to healthy controls, although this was conducted in a relatively small BD sample (N=92) (Heron et al., 2003).

Furthermore, there is growing evidence of an association between ASD and BD (Cross-Disorder Group of the Psychiatric Genomics, 2013; Vannucchi et al., 2014). ASD is defined by its cardinal impairments in social interaction, language and communication, and restricted behaviour and interests. To date, the majority of reports of ASD-BD comorbidity are in ASD samples, with prevalences ranging from 6% to 21.4% (Vannucchi et al., 2014). Only two studies have assessed ASD in BD samples: in youths (aged 7–17 years, N=157), 30% met diagnostic criteria for ASD (Joshi et al., 2013); and in a small sample of adults (N=56), 50% had high levels of autistic traits as measured with the Social Responsiveness Scale (Matsuo et al., 2015). Thus, the extant literature reporting the expression of autistic or schizotypal traits in BD has been limited by small samples, and requires replication in large, well-characterised, adult samples of BD.

The interplay between BD, SSD and ASD or expression of their traits may have significant consequences on global functioning in patients with BD. Global functioning, a measure of illness severity, provides an overall picture of an individual's combined psychological, social and occupational functioning, such as how adaptive the patient is in dealing with social and interpersonal problems (Endicott et al., 1976). Poor functioning has been reported in individuals with schizotypal personality disorder (Henry et al., 2008, Skodol et al., 2002), schizophrenia (Robertson et al., 2013) and ASD (Engstrom et al., 2003, Kastner et al., 2015). Hence a combined worsening effect may be expected in BD patients with high levels of co-occurring autistic and schizotypal traits. A recent study evaluated the effect of co-occurring autistic and positive schizotypal (i.e. relating to psychotic-like experiences) traits on the ability to appreciate the perspective of others (or mentalising) in the general population (N=201) (Abu-Akel et al., 2015). It showed that while autistic and positive schizotypal traits independently induced perspective-taking errors, their interaction was associated with fewer errors, reflecting an improvement in mentalising abilities. The authors proposed that this unexpected finding may be explained by the diametric model (Crespi and Badcock, 2008), which postulates that ASD and SSD have opposing effects on mentalising abilities, whereby autism is associated with reduced or no mentalising, and schizophrenia with dysfunctional overmentalising. While global functioning is not a test of mentalising per se, it has been shown to be associated with socio-cognitive abilities (Bo et al., 2015) and improve following mentalising-based treatments (Bateman and Fonagy, 2008). To-date, no study has investigated the effect of co-occurring autistic and schizotypal traits on an outcome of clinical value in a psychiatric population.

Thus the present study has two main objectives: (1) to determine the expression of autistic and positive schizotypal traits in a large sample of adults with BD, and (2) to examine whether co-occurring autistic and positive schizotypal traits interact to affect global functioning in this population. The assessment of positive schizotypy only, rather than the general construct of schizotypy (comprising both positive and negative traits), is based on evidence that autistic and schizotypal traits cannot be distinguished by the presence or absence of negative traits, due to similarities in impaired social and communicative functioning (Spek and Wouters, 2010). Moreover, given that ASD is more prevalent in males compared to females (Lehnhardt et al., 2016), the expression of autism traits in our sample was analysed for male and female patients separately.

Investigating the prevalence of autistic and schizotypal traits in BD has management implications for individuals with BD, and may contribute to understanding the aetiology of BD. Moreover, isolating and characterising the expression of autistic and schizotypal traits is important to understanding the nature of their effect on the course, outcome and treatment of the index condition (i.e. BD).

Section snippets

Participants

Participants were recruited by the Bipolar Disorder Research Network (BDRN) to an on-going programme of research into the genetic and non-genetic causes of BD. The study has UK National Health Service (NHS) Research Ethics Committee approval and local Research and Development approval in all participating NHS Trusts/Health Boards. Participants were recruited systematically via NHS mental health services, and non-systematically via advertisements on the BDRN website, in general practitioner

Expression of autistic and positive schizotypal traits

On the AQ-Short, the sample scored a mean of 65.02 (SD=11.51; 95% CI 64.22–65.82). When comparing males and females, the males (Mean±SD=68.66±10.76) scored significantly higher than the females (Mean±SD=63.79±11.50) (tdf=795=5.28, p<0.001, Cohen's d=0.44).

Using the AQ-Short cut-off of >65, 47.2% (95% CI=43.7–50.7%) of the entire sample scored positive for clinically significant levels of autistic traits, 60.20% (95% CI=53.43–66.97%) in males, and 42.79% (95% CI=38.82–46.75%) in females. When

Discussion

This study sought to assess the expression of autistic and positive schizotypal traits in a large, well-characterised, adult sample of BD (N=797), and their concurrent effect on global functioning. Approximately, half of the sample exhibited clinically significant levels of autistic traits, and over a third on applying a more conservative cut-off. This is consistent with the single previous study of autistic-like traits conducted in an adult BD sample, in which half of the participants

Contributors

A.A. and J.K. analysed the data and wrote the study. A.A., L.J., K.G.S. and J.K. designed the study. All authors contributed to and have approved the final manuscript.

Acknowledgements

Many thanks to members of the Bipolar Disorder Research Network and all participants.

References (53)

  • K.S. O’Shea et al.

    Neurodevelopmental origins of bipolar disorder: iPSC models

    Mol. Cell Neurosci.

    (2016)
  • D.A. Robertson et al.

    Social dysfunction in schizophrenia: an investigation of the GAF scale’s sensitivity to deficits in social cognition

    Schizophr. Res

    (2013)
  • F. Schurhoff et al.

    Schizotypal dimensions: continuity between schizophrenia and bipolar disorders

    Schizophr. Res

    (2005)
  • A.A. Spek et al.

    Autism and schizophrenia in high functioning adults: behavioural differences and overlap

    Res. Autism Spectr. Disord.

    (2010)
  • J. van Os et al.

    Schizophrenia

    Lancet

    (2009)
  • G. Vannucchi et al.

    Bipolar disorder in adults with Aspergers Syndrome: a systematic review

    J. Affect Disord.

    (2014)
  • H.M. Abdolmaleky et al.

    An update on the epigenetics of psychotic diseases and autism

    Epigenomics

    (2015)
  • A. Abu-Akel et al.

    Perspective-taking abilities in the balance between autism tendencies and psychosis proneness

    Proc. Biol. Sci.

    (2015)
  • A. Abu-Akel et al.

    Autism and psychosis expressions diametrically modulate the right temporoparietal junction

    Soc. Neurosci.

    (2016)
  • A. Abu-Akel et al.

    The bias effect of CNVs conferring risk for both autism and schizophrenia

    npj Schizophrenia

    (2016)
  • A. Abu-Akel et al.

    Autism tendencies and psychosis proneness interactively modulate saliency cost

    Schizophr. Bull

    (2016)
  • A.C. Altamura et al.

    Role of immunological factors in the pathophysiology and diagnosis of bipolar disorder: comparison with schizophrenia

    Psychiatry Clin. Neurosci.

    (2014)
  • A.C. Altamura et al.

    Duration of untreated illness and suicide in bipolar disorder: a naturalistic study

    Eur. Arch. Psychiatry Clin. Neurosci.

    (2010)
  • A. Bateman et al.

    8-year follow-up of patients treated for borderline personality disorder: mentalization-based treatment versus treatment as usual

    Am. J. Psychiatry

    (2008)
  • E. Bora et al.

    Meta-analysis of Theory of Mind (ToM) impairment in bipolar disorder

    Psychol. Med

    (2016)
  • L.S. Carroll et al.

    Genetic overlap between autism, schizophrenia and bipolar disorder

    Genome Med

    (2009)
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