Schizotypy

New dimensions

Oliver Mason, Gordon Claridge, Oliver Mason, Gordon Claridge

• Publisher: Routledge
• Year: 2015
• ISBN:
  9781317937098
• Edition: 1
• Topic: Psychology
• Subtopic: Clinical Psychology
• Index: Psychology

For several decades there has been an increasing move towards viewing the psychotic illnesses from a dimensional perspective, seeing them as continuous with healthy functioning. The idea, concentrating mostly on schizophrenia, has generated considerable theoretical debate as well as empirical research, conducted under the rubric of 'schizotypy'. This book offers a timely discussion of the most significant themes and developments in this research area.Divided into four key sections which represent current concerns in schizotypy research – Measurement, Brain and Biology; Development and Environment; Consequences and Outcomes; and Future Directions – chapters reflect a broad range of approaches and discuss varied theoretical perspectives on schizotypy. Topics include:

• cognitive and perceptual biases

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• psychometric assessments

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• creativity and schizotypy

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• genetic associations.

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• developmental perspectives

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Schizotypy: New dimensions will appeal to academics, researchers and postgraduate students in the area of psychotic illnesses, as well as professionals including psychiatrists and clinical psychologists who are concerned with the basis of serious mental disorder. The book will inform readers who are new to the topic and will update and expand the knowledge base of those more experienced in the field.

1 The psychometric assessment of schizotypy

Thomas R. Kwapil and Charlotte A. Chun

DOI: 10.4324/9781315858562-1

History of schizotypy

The term ‘schizotypy’ was introduced more than 60 years ago to describe a broad phenotype of schizophrenic-like psychopathology and impairment. However, the concept extends back to the late nineteenth and early twentieth centuries. Kraepelin (1913/1919) and Bleuler (1911/1950) both described schizophrenic-like traits in patients prior to their illness, and in the relatives of patients. Kraepelin suggested these psychotic-like experiences were precursors to dementia praecox, but added that in some cases they represented an arrested form of the illness. Bleuler described that ‘entirely crazy acts in the midst of normal behaviour’ can presage the development of schizophrenia (p. 252). Other scholars have noted that mild forms of schizophrenia frequently appear in the non-psychotic relatives of patients (e.g. Kallman, 1938) and precede the onset of the disorder (e.g. Chapman, 1966), but that they often represent stable forms of pathology that do not advance into psychosis. The twentieth-century descriptive psychopathology tradition described numerous schizophrenic-like conditions such as borderline, ambulatory and pseudoneurotic schizophrenia that captured characteristics of the schizotypy continuum (Kwapil & Barrantes-Vidal, 2012).

Rado (1953) introduced the term ‘schizotype’ to represent the schizophrenic phenotype, indicating a continuum of schizophrenic-like or schizotypic behavioural impairment. Meehl (e.g. 1962) conjectured that a single dominant ‘schizogene’ gave rise to a neurointegrative defect, referred to as ‘schizotaxia’ that was necessary, although not fully sufficient, for the development of schizotypy (and, by extension, schizophrenia). He described schizotypy as the personality organisation that culminated from schizotaxia and left the individual vulnerable to the development of schizophrenia. Meehl (1990) substantially updated his original model by diminishing the role of anhedonia and expanding the contribution of polygenetic potentiators. He suggested that schizotypy was taxonic in nature, adding that approximately 10 per cent of the population was schizotypic and that about 10 per cent of schizotypes decompensated into schizophrenia (corresponding with the 1 per cent lifetime prevalence rate of schizophrenia).

Claridge and colleagues (e.g. Claridge, 1997; Claridge & Beech, 1995) offered an alternative model of schizotypy that built upon dimensional models of personality and psychopathology, and conjectured that schizotypy was fully dimensional in nature and included adaptive manifestations. Claridge’s model indicated that schizotypy resulted from a combination of genetic, environmental and personality variations that were normally distributed in the general population. Thus, Claridge argued that it included the pathological, quasi-dimensional components, but also encompassed healthy manifestations (e.g. creativity).

Meehl and Claridge’s models differed on whether schizotypy was taxonic or fully dimensional in the population. The basis of Meehl’s taxonic model was that a single dominant gene was necessary, albeit not sufficient, for schizotypy and schizophrenia. However, this etiological model has not received support in the literature (e.g. McGue & Gottesman, 1989; Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). More than a dozen studies have employed taxometric analyses to study the structure of schizotypy, primarily using psychometric questionnaires. Many of these studies (e.g. Korfine & Lenzenweger, 1995; Linscott, 2013) have provided at least partial support for a schizotypy taxon (or taxa) with base rates in non-clinical samples generally approximating Meehl’s 10 per cent estimate, although there have been exceptions (Meyer & Keller, 2001; Rawlings, Williams, Haslam, & Claridge, 2008). Widiger (2001) raised concerns that taxonic models were inconsistent with views that psychopathology arose from multifactorial genetic and non-genetic origins. Ultimately, support for any taxonic model requires a compelling etiological basis for discontinuity, not simply results of taxometric analyses (a basis that appears lacking at this point for schizotypy). Additionally, Edmundson and Kwapil (2013) suggested that schizotypy and schizophrenia were markedly heterogeneous in symptom presentation, etiology and treatment response. This heterogeneity raises questions about the extent to which separate etiological processes are occurring, and how many taxa would be represented in our current conceptualisation of schizotypy.

Current conceptualisation of schizotypy

Current conceptualisations indicate that schizotypy is a multidimensional construct that represents the underlying vulnerability to schizophrenia-spectrum psychopathology that is expressed across a broad range of personality, subclinical, and clinical phenomenology (Kwapil & Barrantes-Vidal, 2014). Schizotypy offers a useful and unifying construct – useful in that it has explanatory power for understanding the development, expression, trajectory, risk and resilience, and treatment of schizophrenia-spectrum conditions, as well as for understanding variation in normal behaviour, and unifying because it encompasses a broad spectrum of conditions – schizophrenia, related psychotic disorders, spectrum personality disorders, the prodrome, and subclinical expressions – under a single conceptual framework. Schizotypy allows us to examine the etiological and developmental factors underlying schizophrenia-spectrum psychopathology, while minimizing many of the confounding effects (e.g. hospitalisation, medications, marginalised social status) that complicate the study of patients. There are a number of related terms that are frequently used interchangeably with schizotypy. We suggest that many of these represent specific manifestations along the schizotypy continuum (e.g. schizotypal, prodrome, at-risk mental states) and that care should be used to distinguish such constructs.

Schizotypy and, by extension, schizophrenia are heterogeneous. This heterogeneity occurs at the phenotypic level, as well as at the etiological, developmental and treatment-response levels (Kwapil & Barrantes-Vidal, 2012, 2014). Therefore, treating schizotypy and schizophrenia as homogeneous constructs runs the risk of diminishing our ability to understand the origins, development and expression of these complex conditions. Schizotypy and schizophrenia appear to share a common multidimensional structure. Numerous studies support the view that positive, negative and disorganised dimensions underlie schizophrenia (e.g. Lenzenweger & Dworkin, 1996), and these dimensions have been replicated in non-clinically ascertained schizotypy (e.g. Bentall, Claridge, & Slade, 1989; Kwapil, Barrantes-Vidal, & Silvia, 2008; Raine et al., 1994; Vollema & van den Bosch, 1995).

Measurement of schizotypy

Lenzenweger (1998) discussed the relative strengths and weaknesses of three broad (and by no means mutually exclusive) methods for identifying schizotypy: (a) familial, (b) clinical, and (c) psychometric laboratory index approaches. Of the three methods, the familial is the best known, due in large part to landmark studies of the offspring of schizophrenic patients (e.g. Cannon & Mednick, 1993). The clinical method identifies high-risk individuals based upon schizophrenia-spectrum or prodromal diagnoses, as has been conducted by the North American Prodrome Longitudinal Study (NAPLS) consortium (e.g. Cannon et al., 2008). The final method involves the use of psychometrically sound research instruments designed to identify symptom, trait, neurocognitive and biobehavioural markers of vulnerability. While all three methods have their strengths and limitations, the psychometric questionnaire or screening method provides several notable advantages. First, these measures can be used to screen large numbers of individuals from the general population, rather than selecting participants based upon clinical status or consanguinity. In contrast, family studies provide a somewhat stratified group of at-risk participants, because only a fraction of patients with schizophrenia have a known first-degree relative with the disorder – thus providing a sample that is not wholly representative of future sufferers. Psychometric screening inventories also tend to be relatively non-invasive and inexpensive to administer and score, and thus can be used to screen large numbers of participants at one time. Finally, they can be used in conjunction with other measures of risk, including family studies.

As discussed by Kwapil and Barrantes-Vidal (2014), psychometric assessment of schizotypy has provided a powerful tool for assessing schizophrenic-like symptoms and impairment. Numerous studies have reported that psychometric schizotypy in non-disordered individuals is associated with psychotic-like (Gooding, Tallent, & Matts, 2005), prodromal (e.g. Barrantes-Vidal, Chun, Myin-Germeys, ...

Table of contents

• Cover Page
• Half Title Page
• Series Page
• Title Page
• Copyright Page
• Contents
• Illustrations
• List of Contributors
• Introduction
• I Measurement, brain and biology
• 1 The psychometric assessment of schizotypy
• 2 The role of dopamine in schizotypy
• 3 Genetic associations The basis of schizotypy
• 4 Hemispheric asymmetries in schizotypy
• II Development and environment
• 5 Schizotypy A developmental perspective
• 6 Childhood trauma and schizotypy A systematic review
• 7 Mechanisms mediating the pathway from environmental adversity to psychosis proneness
• 8 Schizotypy and substance use
• 9 Inducing psychotic-like experiences The role of schizotypy
• III Consequences and outcomes
• 10 Dimensional approaches to delusional beliefs
• 11 Schizotypy and psychopathology
• 12 Schizotypy A creative advantage?
• IV Future directions
• 13 Old thoughts: new ideas: future directions
• Index