Association between processing speed and subclinical psychotic symptoms in the general population: Focusing on sex differences

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Abstract

Evidence is growing that persons along the schizophrenia spectrum, i.e., those who also display subclinical psychotic symptoms, exhibit deficits across a broad range of neuropsychological domains. Because sex differences in the association between cognitive deficits and psychosis have thus far been mostly neglected, we believe that ours is the first study specifically focused upon those differences when examining the relationship between subclinical psychosis and processing speed. Using a sample of 213 persons from the general population from Zurich, Switzerland, psychotic symptoms were assessed with three different questionnaires including the Schizotypal Personality Questionnaire, an adaptation of the Structured Interview for Assessing Perceptual Anomalies, and the Paranoia Checklist. Processing speed was assessed with the WAIS digit-symbol coding test. Two higher-order psychosis domains were factor-analytically derived from the various psychosis subscales and then subjected to a series of linear regression analyses. The results demonstrate that in both men and women associations between subclinical psychosis domains and processing speed were weak to moderate (β ranging from − 0.18 to − 0.27; all p < 0.05). However, we found no sex-differences in the interrelation of subclinical psychosis and processing speed (ΔR2 < 0.005; p > 0.30). In conclusion, it appears that sex differences in psychosis manifest themselves only at the high end of the continuum (full-blown schizophrenia) and not across the sub-threshold range. The small magnitude of the effects reported herein conforms to the etiopathology of the disorder. Since schizophrenia and related disorders from the spectrum are assumed to be multifactorial diseases, it follows that many etiological components of small effect are involved.

Introduction

Since the writings of Kraepelin (1896), there has been a widespread notion that schizophrenia is associated with cognitive decline. Indeed, individuals with schizophrenia exhibit deficits across a broad range of neuropsychological domains, e.g., working memory, attention and vigilance, executive functioning, and processing speed. Cognitive deficits already can be found in patients with a first episode of schizophrenia (Galderisi et al., 2009, Heydebrand et al., 2004). Today, those deficits are regarded as relatively stable over the course of the illness and independent of the clinical states (Green, 2006).

In their seminal work, Jones et al. (1994) reported developmental disruptions and cognitive impairments in children with later onset of schizophrenia. Various ensuing studies replicated those cognitive deficits prior to the onset of full-blown psychosis (e.g., MacCabe et al., 2008, MacCabe et al., 2013, Metzler et al., 2014, Müller et al., 2013, Reichenberg et al., 2010, Zammit et al., 2004). Broad scientific consensus now exists among experts that poor premorbid cognitive functioning is a risk factor for schizophrenia and other psychotic disorders (Khandaker et al., 2011, MacCabe, 2008).

Interest is growing in understanding these deficits in persons from the whole schizophrenia spectrum, since the notion of an inherent continuum of psychotic disorders provides interesting new insights in the etiopathology of the various categorical disorders from this spectrum (Barrantes-Vidal et al., 2015). As such, impairments in working memory, attention, processing speed, and verbal learning have been found in subjects with schizotypal personality disorder (see review by Siever et al., 2002). Along with the increasing body of evidence for a continuum that encompasses schizotypal personality disorder (Raine, 2006), subclinical psychosis (Rössler et al., 2007, Rössler et al., 2013a) or psychotic experiences (Linscott and van Os, 2013) in the general population, research is needed concerning cognitive capacities at the low end of the schizophrenia spectrum, i.e., sub-threshold psychotic states in non-clinical community samples. Measures that encompass this extended psychosis phenotype – schizotypal personality and subclinical psychosis – have been shown to be negatively related to executive functions (Gooding et al., 1999, Lenzenweger and Korfine, 1994), sustained attention (Chen et al., 1998, Gooding et al., 2006), verbal intelligence (Noguchi et al., 2008), working memory (Gooding and Tallent, 2003, Kelleher et al., 2012), or processing speed (Hengartner et al., 2014, Kelleher et al., 2012).

To date, sex differences have been mostly disregarded within the field despite some evidence of variations between males and females. For example, Welham et al. (2010) found that premorbid fluid and verbal intelligence in childhood and adolescence related to adult non-affective psychosis were slightly lower in males, but not in females. We are unaware of further reports about cognitive deficits that are separated by sex in those phenotypes. Many conclusions about premorbid cognitive functioning in psychosis have been drawn exclusively from male samples (e.g., MacCabe et al., 2013, Müller et al., 2013, Zammit et al., 2004). None of the studies focusing on the extended psychosis phenotype have examined potential sex differences. Therefore, the aim of the research presented here was to fill those gaps by analyzing several established measures of subclinical psychosis in association with processing speed, separating by sex for participants drawn from a representative community sample.

Section snippets

Study design and sampling

This study was conducted as part of the Zurich Program for Sustainable Development of Mental Health Services (ZInEP), a research and mental health care program involving several such services in the canton of Zurich, Switzerland. The Epidemiology Survey, one of nine ZInEP subprojects, comprised four components: 1) telephone screening; 2) comprehensive semi-structured, face-to-face interviews followed by self-report questionnaires; 3) tests in a socio/neuro-physiological laboratory; and 4) a

Results

A total of 14 subjects (6.2%) did not complete all questionnaires or tests in the laboratory. Thus, for the present study we included 213 participants (118 females and 95 males) who finished the questionnaires related to the extended psychosis phenotype and provided complete data from the DSCT. Their ages ranged from 20 to 41 years (mean of 29; standard deviation: 6.6 years). In all, 50 subjects (23%) were married, another 136 (64%) lived in a committed relationship, and 45 subjects (21%) had

Discussion

Cognitive deficits are considered a predominant core symptom underlying the psychopathology of schizophrenia (Elvevag and Goldberg, 2000, Reichenberg and Harvey, 2007). With the present study we provide evidence that some of those deficits are also prevalent in sub-clinical psychosis, which represents the rather low sub-threshold region along the continuum of an extended psychosis phenotype. Our findings are in accord with a growing body of literature showing significant associations among

Role of funding source

ZInEP was supported by a private foundation. Research in the Sociophysiological Laboratory was also funded by the Swiss National Science Foundation (Grant Number 3247B0-122071). The donors/sponsors had no further role in the experimental design; the collection, analysis, and interpretation of data; the writing of this report; or the decision to submit this paper for publication.

Contributors

Wulf Rössler wrote and revised the manuscript and is responsible for ZInEP. Vladeta Ajdacic-Gross and Wulf Rössler designed the ZInEP Epidemiology Survey. Mario Müller, Stephanie Rogers, and Vladeta Ajdacic-Gross contributed significantly to data management and critically revised the manuscript. Wolfram Kawohl and Helene Haker were responsible for the laboratory testing and also critically revised the manuscript. Michael P. Hengartner contributed significantly to data management; conducted the

Conflict of interest

All authors declare no conflicts of interest.

Acknowledgment

We want to thank our sponsors for their unconditional support. We were supported by a private foundation. Research in the Sociophysiological Laboratory was also funded by the Swiss National Science Foundation (Grant Number 3247B0-122071).

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