Neuroscience and Biobehavioral Reviews 37 (2013) 317–327

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Neuroscience and Biobehavioral Reviews

journal homepage: www.elsevier.com/locate/neubiorev

Review

Evidence of a dimensional relationship between schizotypy and schizophrenia:

A systematic review
M.T. Nelson a,b,c,∗ , M.L. Seal b,d , C. Pantelis c , L.J. Phillips a
a
Melbourne School of Psychological Sciences, The University of Melbourne, Parkville, Victoria, Australia
b
Murdoch Children’s Research Institute, Royal Children’s Hospital, Parkville, Victoria, Australia
c
Melbourne Neuropsychiatry Centre, Department of Psychiatry, The University of Melbourne and Melbourne Health, Parkville, Victoria, Australia
d
Department of Paediatrics, The University of Melbourne, Parkville, Victoria, Australia

a r t i c l e i n f o a b s t r a c t

Article history: The personality dimension of schizotypy is well established, and schizotypal traits can be taken to rep-
Received 20 June 2012 resent a proneness toward developing psychosis. Yet, there are competing theories about the latent
Received in revised form structure of schizotypy. More specifically, there is controversy over the extent to which this propensity
26 December 2012
toward psychosis is present only in a small proportion of the population, or whether it is spread dimen-
Accepted 3 January 2013
sionally throughout the general community. On the basis of accumulating research findings the present
article argues for a fully dimensional model of schizotypy. It describes recent neurobiological, neuropsy-
Keywords:
chological, social and environmental evidence supporting the idea that schizotypy in healthy populations,
Schizotypy
Psychosis
and disorders on the schizophrenia spectrum are fundamentally linked. Directions for further research
Schizophrenia are also considered.
Schizoaffective disorder © 2013 Elsevier Ltd. All rights reserved.
Schizophreniform disorder
Schizotypal personality traits
Fully dimensional model

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317
2. The quasi-dimensional approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 318
3. The fully dimensional approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319
4. Genetic research: family, twin and adoption studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
5. Genetic research: molecular genetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
6. Neuropsychological research: cognitive deficits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321
7. Environmental and social research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 321
8. Biological research: neuroanatomical abnormalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322
9. Methodological considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323
10. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 324

1. Introduction
and Broussard, 2009). These symptoms are usually subsumed
Schizophrenia is a psychiatric disorder characterised by expe- under three main categories. They are; positive symptoms
riences such as hallucinations, delusions, personality changes, including hallucinations and delusions, disorganised symptoms
thought disorder, bizarre behaviour, impaired social interac- including thought disorder and bizarre behaviour; and negative
tion, and difficulties in carrying out daily activities (Compton symptoms including alogia, apathy, and amotivation. Although
these psychotic symptoms are most commonly associated with
schizophrenia, they are also characteristic of other psychotic disor-
∗ Corresponding author at: The Melbourne School of Psychological Sciences, The ders like schizophreniform disorder, schizoaffective disorder, and
University of Melbourne, Parkville, VIC, Australia. Tel.: +61 421812989. delusional disorder. Symptoms of psychosis can also be seen in neu-
E-mail address: nelsonm@unimelb.edu.au (M.T. Nelson). rological disorders such as dementia, and in psychiatric disorders

0149-7634/$ – see front matter © 2013 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.neubiorev.2013.01.004
318 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
that are not generally considered under the rubric of psychotic
disorders, for example severe depression.
Categorical diagnostic categories for mental health difficulties
like schizophrenia are described in current nosological systems,
such as the Diagnostic System of Mental Disorders (DSM-IV-TR; APA,
2000). They are useful in that they help to ensure disorders are
easily identifiable; they serve as a basis for treatment decision-
making; and they aid communication between clinicians (Livesley
and Jackson, 1992; Kraemer et al., 2004).
However, there are also a number of criticisms of the assump-
tion that psychotic disorders are truly categorical phenomena. For
example, there is considerable hetereogenity within diagnostic
categories (Wing and Agrawal, 2003; Beck et al., 2009), and homo-
geneity between them. Furthermore, diagnoses do not necessarily
remain stable across individuals’ lifetimes, and it is often not until
a person has experienced multiple episodes and chronic disability
that a psychotic diagnosis becomes stable and clear-cut (McGorry
et al., 2009). Also, despite numerous studies into the physiologi-
cal correlates of schizophrenia and related disorders, no biological
markers, or endophenotypes have yet been discovered (Beck et al.,
2009). There is no test (biological or otherwise) that will unequiv-
ocally distinguish someone with psychosis, from someone who is
psychologically healthy (Wing and Agrawal, 2003; Wong and van
Tol, 2003; Beck et al., 2009). This is reflected in Heinrichs’ (2005)
review of biological studies, which describes a substantial over-
lap between samples of people with schizophrenia, and samples of
people who are psychologically healthy.
This overlap between clinical and non-clinical samples indicates
that categorical diagnoses such as that of schizophrenia, decided
upon by expert committee consensus rather than by nature, may
obscure the true psychosis phenotype. This could reflect a mis-
representation of latent constructs, and may lead to erroneous
diagnoses, inappropriate treatment, and conflicting research find-
ings. Indeed, there is a growing consensus that dimensional views
of schizophrenia and other psychotic disorders may be a more valid
representation of the population distribution (van Os et al., 2009;
Neuvo et al., 2012).
For similar reasons, traditional (categorical) understandings of
schizotypy have also met with theoretical criticism. Schizotypy
describes a cluster of personality traits that include odd or bizarre
behaviour, strange speech, magical thinking, unusual perceptual
experiences, and social anhedonia. There is some disagreement
regarding the underlying factor structure of schizotypy (Stefanis
et al., 2004; Mason and Claridge, 2006; Fonseca-Pedrero et al.,
2011). However, the prevailing understanding is that it is com-
prised of three identifiable factors, which broadly correspond to
the positive, negative and disorganised dimensions of schizophre-
nia (Wuthrich and Bates, 2006; Fonseca-Pedrero et al., 2011). The
first factor is the ‘cognitive-perceptual factor’, which includes magi-
cal thinking, unusual perceptual experiences, ideas of reference and
paranoia (Raine, 1991, 2006). The second is the ‘interpersonal fac-
tor’, which includes constricted affect, social anxiety, lack of close
personal relationships, and suspiciousness (Raine, 1991, 2006). The
final ‘disorganised factor’ includes odd behaviour and odd speech
(Raine, 1991, 2006).
Recent reviews summarising research into schizotypy have
examined a range of topics associated with the construct. Examples
include unusual speech associated with schizotypy (Kiang, 2010);
the assessment of schizotypy (Fonseca-Pedrero et al., 2008); affec-
tive traits in schizophrenia and schizotypy (Horan et al., 2008);
schizotypal personality disorder and schizophrenia (Siever and
Davis, 2004); as well as cannabis use, psychosis and schizotypy
(Compton et al., 2007). Much of this research is based on the-
oretical assumptions arising from two competing models of the
distribution of schizotypy in the general population–called the
quasi-dimensional and fully dimensional approaches respectively.
However, these models are often taken at face value, and evi-
dence for them has not recently been critically scrutinised. The
present review sought to resolve this by examining recent empirical
taxometric, neuropsychological, environmental and biological evi-
dence pertaining to a potential dimensional relationship between
schizophrenia and schizotypy in otherwise psychologically healthy
populations. Some methodological issues prevalent in the area will
also be considered, as well as directions for future research.
For the sake of brevity, the present review includes findings
pertaining to schizophrenia and schizotypal personality traits.
However reflecting the aforementioned difficulties, controversies
and complexities inherent in conducting research into categori-
cal psychiatric constructs, we do acknowledge that the findings
herein can be also be common to other clinical phenomena; such
as schizoaffective disorder (e.g. Cheniaux et al., 2008), first-episode
psychosis (e.g. Mesholm-Gately et al., 2009), bipolar disorder
and mania (e.g. Berrettini, 2000; Bramon and Sham, 2001); and
other personality constructs such as psychoticism (e.g. Mason and
Claridge, 2006). It is for this reason, we prefer to use the terms
‘schizotypy’ and ‘schizophrenia’ in a relatively broad sense.
2. The quasi-dimensional approach
The quasi-dimensional approach to schizotypy is based on a
disease model of mental illness. It posits that schizotypy is a per-
sonality organisation specific to a small group of individuals within
the population (approximately 10%), who are labelled ‘schizotypes’
(Rado, 1953; Meehl, 1990; Lenzenweger, 1994; Beauchaine et al.,
2008). They are compared to a larger group (approximately 90%)
who are not at risk. As reviewed by Lenzenweger (2006), the model
can be attributed to Meehl’s (1962) theory; which described a
specific genetic vulnerability towards developing psychosis. This
vulnerability was said to exist in the form of a genetic predispo-
sition, manifesting as a neurointegrative defect called schizotaxia.
According to Meehl (1962), schizotaxia is necessary but not suf-
ficient to cause schizophrenia. Rather than causing schizophrenia
directly, it interacts with environmental influences throughout a
person’s lifetime to determine the degree of decompensation they
experience (Lenzenweger, 2006). From this perspective, genetic
vulnerability towards developing psychotic symptoms is consid-
ered to be ‘taxonic’ (Korfine and Lenzenweger, 1995; Waller et al.,
2006). The approach is quasi-dimensional only because it refers to
levels of expression of a proposed disease process. Otherwise it is
a discontinuous, categorical theory wherein any one individual is
considered to either possess a genetic vulnerability, or they do not.
Support for the quasi-dimensional approach can be found in
studies that employ taxometric analyses (Waller and Meehl, 1998;
Rawlings et al., 2008b). Taxometric analyses are a group of sta-
tistical procedures that are used to determine the underlying
structure of latent constructs. They are able to determine whether
a given construct is categorical (taxonic), or dimensional. In 2008, a
review of 19 published taxometric studies pertaining to schizotypy
reported that fifteen supported a categorical model (Rawlings et al.,
2008b). Furthermore the taxonic base rate estimates in these stud-
ies, ranging between 0.03 and 0.13, appeared to support Meehl’s
(1990) postulation that 10% of the population are schizotypes
(Rawlings et al., 2008b).
Yet there are criticisms of the quasi-dimensional model, and
some of these focus particularly on the sampling methods used
when conducting taxometric analyses (Rawlings et al., 2008b). For
instance, taxometric studies have often used either clinical samples
with insufficient power for the purposes of taxometrics, or they
have used large student samples, which may not be representa-
tive of the general population (Rawlings et al., 2008b). Additionally,
studies often investigate only one aspect of schizotypy, using only
 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
one taxometric procedure (Rawlings et al., 2008b). Lastly and most
importantly, Rawlings et al. (2008b) have argued that evidence
from taxometric analyses which support both a categorical view-
point and a base rate in the range of 10%, may actually arise as an
artefact of positively skewed sample distributions (Rawlings et al.,
2008b). Their own taxometric study attempted to address these
criticisms by using more than one taxometric procedure, a large
diverse adult sample, multiple measures of schizotypy, and by tak-
ing skew into account. Its findings supported a dimensional rather
than a categorical latent structure (Rawlings et al., 2008b).
Another criticism of the quasi-dimensional approach has been
highlighted by research showing that the anomalous perceptual
experiences associated with schizotypy are much more prevalent
in the general population than the 10% estimate proposed by Meehl
(1990). For example, Verdoux et al. (1998) asked 790 individuals
from primary care services to fill in a self-report measure com-
prising items assessing experiences that resembled hallucinations
and delusions. Examples include: “Do you ever feel as if there
is a conspiracy against you?”, “Do you ever feel as if people are
looking oddly at you?”, and “Do you ever think that people can
communicate telepathically?”. For participants with no history of
psychiatric disorder (n = 462), individual item endorsement varied
from between 5% and 70%, with 46.9% of people believing they
could communicate telepathically, 25.5% believing they had been
persecuted in some way, and 4.8% believing that they could hear
voices conversing (Verdoux et al., 1998). Another study investi-
gated the prevalence of psychotic-like experiences in 2441 young
people (aged 18–23) in Australia (Scott et al., 2008). Individual item
endorsement in this study ranged from between 5.5.% (‘do you ever
feel as if you are a robot or zombie without a will of your own?’)
and 77% (‘do you ever feel as if some people are not what they seem
to be?). Indeed, one estimate from a longitudinal study looking at
mental health in the Dutch adult general population indicated that
the incidence of positive subclinical psychotic experiences in oth-
erwise healthy cohorts is up to 100 times greater than traditional
estimates such as Meehl’s would suggest (Hanssen et al., 2005).
This high prevalence of anomalous experiences in the general pop-
ulation blurs the line between what may be considered ‘normal’
and ‘abnormal.’ It indicates that schizotypy may not be a discrete,
bounded entity affecting only a small proportion of the population,
as would be consistent with a quasi-dimensional model.
3. The fully dimensional approach
A more recent model of the potential relationship between
schizotypal personality and schizophrenia is the fully dimensional
approach, which is outlined by Claridge and colleagues (Claridge
and Beech, 1995; Claridge and Davis, 2003; Rawlings et al., 2008a).
The fully dimensional approach posits that schizotypy represents
‘natural central nervous system variations’, which in their extreme,
manifest as vulnerability to mental illness (Rawlings et al., 2008a,
p. 1669). The main contention advocated by the fully dimensional
approach is that the latent structure of schizotypy is on a contin-
uum applying to all members of the population. It is considered to
range from low schizotypy and psychological health, to extremely
high schizotypy and potential dysfunction in the form of psychosis
(Fig. 1).
As the fully dimensional approach describes schizotypy as con-
tinuous throughout the general population, it can account for the
high prevalence of anomalous experiences reported by researchers
such as van Os and his colleagues (Verdoux et al., 1998; Johns and
van Os, 2001; van Os et al., 2009). In this way, the fully dimensional
approach appears superior to the quasi-dimensional approach. It
is also consistent with the majority of current theories pertain-
ing to schizophrenia, which tend to describe continuity between
319
Fig. 1. A diagrammatic representation of the proposed model of schizotypy
(Claridge and Beech, 1995).
clinical and non-clinical psychosis populations (Linscott and van
Os, 2010). Further evidence for the dimensional approach is based
on analyses supporting the three factor structure of schizotypy
(cognitive-perceptual, interpersonal and disorganised), which is
analogous to the three factor structure of psychosis (positive, neg-
ative and disorganised; Liddle, 1987; Rossi and Daneluzzo, 2002;
Wuthrich and Bates, 2006). There is also evidence that individ-
uals with psychotic disorders tend to score highly on measures of
schizotypy (Lenzenweger, 1994; Camisa et al., 2005).
However, it should be remembered that not all people with high
levels of schizotypy are necessarily dysfunctional. For example, it
has been shown that individuals scoring highly on measures of
schizotypy can (and do) function well in terms of subjective well-
being (Goulding, 2004). Here, subjective wellbeing can be defined
as a self-rated sense that a person has control over their own life, can
balance and cope with both positive and negative life events, and
can maintain stability (Goulding, 2004). Many people who score
highly on measures of schizotypy also exhibit adaptive strengths
such as creativity, as evidenced by increased involvement in cre-
ative activities including painting and drawing, writing, music,
gardening and web design (Batey and Furnham, 2008; Rawlings
and Locarnini, 2008; Nelson and Rawlings, 2010).
Therefore, similar to the quasi-dimensional approach, the fully
dimensional approach does not assume schizotypal traits are suffi-
cient in and of themselves, to indicate risk for psychopathology
(Rawlings et al., 2008a). Rather, it is only when high levels of
schizotypy are combined with other aetiological risk factors that
an individual may be considered at risk for schizophrenia and
other psychotic disorders. According to this perspective, unless
high schizotypy is combined with other risk factors, it is considered
neutral in regards to psychopathology (Rawlings et al., 2008a).
The fully dimensional approach is also consistent with what is
termed the ‘continuum hypothesis’ of psychosis (Allardyce et al.,
2007). This is the current predominant view, that psychosis is sim-
ilar to chronic physical problems like diabetes and heart disease.
It is considered to have multifactorial aetiology, wherein multi-
ple genes interact both with each other and with the environment
to determine outcome (Allardyce et al., 2007; The International
Schizophrenia Consortium, 2009). These different combinations of
genes and environmental risk factors result in a range of different
phenotypic expressions lying on a continuum from normal through
to clinical psychosis.
Consequently by adopting the fully dimensional theory,
research into schizotypy becomes important because it directly
aids investigation into the aetiology of schizophrenia and other
psychotic disorders. Furthermore, it does so whilst avoiding con-
founds often associated with psychosis research, such as illness
chronicity, medication, and hospitalization. From this perspective,
320 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
it is important to assess not only similarities between various levels
of schizotypy and schizophrenia, but also dissimilarities (Fanous
and Kendler, 2004). For example, it has been proposed that pos-
sible biological endophenotypes common to the two constructs
may represent underlying genetic factors, while findings specific
to schizophrenia may represent environmental factors (Cannon
et al., 2002; Fanous and Kendler, 2004). Further empirical evidence
that psychotic symptoms and schizotypal personality features in
psychologically healthy people lie on a common continuum can
be gleaned from genetic, neuropsychological, environmental, and
biological research.
4. Genetic research: family, twin and adoption studies
A first line of convincing evidence that schizotypy lies on a
continuum with schizophrenia comes from genetic research. Both
Kraeplin (1919/1971) and Bleuler (1911/1950) first observed that
relatives of individuals with schizophrenia appeared notably more
odd and eccentric than people in the general population. Since then,
much behavioural genetic research throughout the 20th and early
21st centuries has indicated that schizotypal traits and psychosis
show some level of genetic inheritance (Kety et al., 1975; Baron
et al., 1983; Kendler et al., 1996; Mata et al., 2003).
For example, it has been clearly established from family, twin,
and adoption studies that schizophrenia is heritable (McCue et al.,
1983; Cannon et al., 1998; McClellan et al., 2007). Similarly, there
is growing evidence that heightened schizotypy can also be expe-
rienced by multiple generations of the one family. For instance,
Hanssen et al. (2006) gave three measures of schizotypy to 272
individuals from 82 families. All three measures showed family-
specific variation for both positive and negative traits. However,
only one measure showed family-specific variation for the nega-
tive trait once variation due to the positive trait was controlled for,
indicating that the positive dimension of schizotypy (anomalous
experiences) specifically varied with family membership. Interest-
ingly, these results were obtained in families that were not selected
on the basis of a pre-existing diagnosis of any psychiatric disorder,
providing evidence for dimensional variation within the general
population as well as heritability (Hanssen et al., 2006).
Further evidence of the dimensional and heritable nature of
schizotypy within psychologically healthy populations comes from
Kendler et al. (1991) who administered four measures of schizotypy
(including self-report and interview) to 29 monozygotic and dizy-
gotic twin pairs. Distributions of schizotypy in this sample were
normal, indicating dimensionality rather than taxonicity, which
would have been represented by a bimodal distribution (Kendler
et al., 1991). Comparison of correlations between monozygotic and
dizygotic pairs in this sample also indicated that both positive
and negative schizotypal traits showed family-specific variation
(Kendler et al., 1991).
It is acknowledged, of course, that evidence showing schizotypy
runs in families, and separate evidence showing that schzophrenia
runs in families does not mean that the two phenomena are nec-
essarily associated. Yet, there is also research indicating that both
schizotypy and schizophrenia occur in the same families, which
suggests they may be heritable together (Kety et al., 1975; Baron
et al., 1983; Kendler et al., 1989, 1996; Mata et al., 2003).
One example is a study by Kremen et al. (1998) wherein 44
controls and 40 biological relatives of people with schizophrenia
completed the Schizotypal Personality Questionnaire (SPQ; Raine,
1991). Relatives had higher scores on the Cognitive-Perceptual
(positive) Factor than controls. Similar results using the same mea-
sure were reported in a smaller study of 13 participants with a
family history of psychosis, 38 participants with a family history
of substance use disorder, and 51 control participants (Yaralian
et al., 2000). Also in a more recent study, 263 relatives of people
with psychosis completed three measures of schizotypy – including
two self-report measures and a semi-structured interview (Mata
et al., 2003). In this investigation, it was the positive symptoms
of psychosis, as reported by the patients, which were related to
schizotypy in their relatives. A cluster of symptoms reported by
the patients (delusions, hallucinations and thought disturbance)
was positively correlated with outcomes from all three measures of
schizotypy in relatives, including both positive and negative traits.
Two other family studies have reported mixed findings as
to heritability between schizotypy and schizophrenia. Kendler
et al. (1996) found no differences in levels of schizotypy between
relatives of patients with psychotic illnesses, and relatives of con-
trols. Furthermore, Appels et al. (2004) reported that parents
of schizophrenia patients actually had lower scores on the SPQ
Cognitive-Perceptual Factor than control participants. However,
the authors of both of these studies account for their somewhat
anomalous findings by highlighting the problems of conducting
research into schizotypy using self-report measures (Kendler et al.,
1996; Appels et al., 2004). Appels et al. (2004) also reasoned that
including both parents (mothers and fathers) of schizophrenia
patients in their analysis may have resulted in a loss of power. It
is more likely that only one parent passes on a genetic risk of psy-
chosis, not necessarily both parents (Appels et al., 2004). Indeed,
Appels et al. (2004) then conducted an alternative investigation,
wherein parents of an individual with schizophrenia who reported
a family history of schizophrenia spectrum disorder in earlier gen-
erations (i.e. their own parents or earlier) reported higher levels of
both positive and negative schizotypal traits than parents with no
family history.
Further to the above family-based research, there have been
some investigations that have used a twin design to assess a pos-
sible genetic relationship between schizotypy and schizophrenia.
Self-reported experiences of perceptual aberration and social anhe-
donia in particular were found to be at least partly inherited in
a study of 98 monozygotic and 59 same sex dizygotic twin pairs
(MacDonald et al., 2001). Another study with 105 monzygotic and
90 dizygotic twins described common family specific variation
between psychosis and schizotypy as measured by the Oxford-
Liverpool Inventory of Feelings and Experiences (O-LIFE; Mason
et al., 1995; Jang et al., 2005).
5. Genetic research: molecular genetics
In summary, considerable evidence from family, adoption, and
twin studies indicates that psychotic disorders and schizotypy in
healthy populations share common genetic underpinnings. Yet
although these family, twin and adoption studies are informative
in terms of describing heritability, they cannot identify specific
chromosomal regions giving rise to any one phenotype (Fanous
et al., 2007). Around 25 years ago, Gottesman, McGuffin and Farmer
(1987) remarked that the results of behavioural genetic studies
gave only clues to the genetic basis of schizophrenia, and that
molecular genetics would provide clear answers. However despite
years of molecular genetic research, no single gene, or even a clear
number of possible genes have been identified for schizophrenia,
nor for psychosis more broadly (Allardyce et al., 2007; Tandon et al.,
2008), despite large samples in recent studies (Ripke et al., 2011).
Indeed, there are no genes proposed to be related to schizophre-
nia that are not controversial or subject to conflicting findings.
For instance, in a recent review and meta-analysis of the genetic
research into schizophrenia, it was estimated that there have
been in excess of 1000 genetic association studies exhibiting
largely inconsistent results (Allen et al., 2008). This review found
that across 118 different meta-analyses, there were nominally
 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
significant effects in 24 variants of 16 different genes – namely,
APOE, COMT, DAO, DRD1, DRD2, DRD4, DTNBP1, GABRB2, GRIN2B,
HP, IL1B, MTHFR, PLXNA2, SLC6A4, TP53, and TPH1 (Allen et al.,
2008).
To date there has been limited molecular genetic research into
a potential relationship between schizotypy and schizophrenia
specifically. In a linkage study, Fanous et al. (2007) demonstrated
that a number of genes thought to be related to schizophre-
nia in patients, were also associated with levels of schizotypy in
non-psychotic relatives. Two other studies have indicated a sig-
nificant level of association between schizotypy and the COMT
gene (Avramopoulos et al., 2002), and between schizotypy and the
DTMBP1, NRG1 and DAAO genes (Stefanis et al., 2007). However,
reflecting the conflictual findings in regards to molecular genetic
research and psychosis, another investigation found no clear rela-
tionship between schizotypy and the COMT gene (Ma et al., 2007).
As reviewed by Fanous and Kendler (2004), the following con-
clusions can be drawn from the genetic research on schizotypy
and schizophrenia. First, behavioural genetic research has shown
that both schizophrenia and schizotypy are heritable, and that
schizotypy and psychotic disorders aggregate in families together.
Furthermore, heritability can be broken down into specific traits,
whereby negative psychotic symptoms tend to predict negative
schizotypal traits in relatives, and in particular, positive psychotic
symptoms tend to predict positive schizotypal traits (Fanous et al.,
2001; Fanous and Kendler, 2004). Yet despite the optimism sur-
rounding early molecular genetic research into the genetic causes of
both schizotypy and schizophrenia (Gottesman et al., 1987; Tandon
et al., 2008), findings in this area are still unclear. Further research
is needed before it can be confidently established that there are
shared genetic abnormalities between schizotypy and schizophre-
nia, and even more before we can break these down into specific
traits. This is reflective of the state of genetic research into psychi-
atric disorders more broadly (Meyer-Lindenberg and Weinberger,
2006; Psychiatric GWAS Consortium Coordinating Committee et al.,
2009), and particularly the difficulties of finding genetic common-
alities in inherently heterogeneous populations.
6. Neuropsychological research: cognitive deficits
In another relevant vein of research, it has been consistently
shown that schizophrenia is associated with cognitive deficits
(Tandon et al., 2009). These include generalised cognitive dys-
function (Heinrichs and Zakzanis, 1998; Fioravanti et al., 2005;
Reichenberg and Harvey, 2007; Simonsen et al., 2011), as well as
deficits in verbal IQ (Heinrichs and Zakzanis, 1998; Reichenberg
and Harvey, 2007), working memory (Wood et al., 2003; Haenschel
and Linden, 2011; Simonsen et al., 2011), episodic memory
(Reichenberg and Harvey, 2007), executive functioning (Heinrichs
and Zakzanis, 1998; Fioravanti et al., 2005; Reichenberg and
Harvey, 2007), verbal fluency (Simonsen et al., 2011), processing
speed (Simonsen et al., 2011), and attention (Heinrichs and
Zakzanis, 1998; Fioravanti et al., 2005), amongst others (Heinrichs
and Zakzanis, 1998; Fioravanti et al., 2005; Reichenberg, 2010).
These neurocognitive deficits are more often correlated with neg-
ative and disorganised symptoms than with positive symptoms
(Basso et al., 1998; Pantelis et al., 2001; Galderisi et al., 2009;
Lindsberg et al., 2009).
Heightened schizotypy has also been associated with subtle
cognitive deficits in psychologically healthy people (Moritz et al.,
1999; Noguchi et al., 2008). Specifically, inverse associations have
been found between schizotypy and verbal IQ (Noguchi et al.,
2008), attention (Chen et al., 1997), and working memory (Park
and McTigue, 1997; Schmidt-Hansen and Honey, 2009). Further-
more, at least one paper has explicitly evaluated neurocognitive
321
functioning in both schizotypy and schizophrenia together, on the
basis of a fully dimensional model (Cochrane et al., 2012).
Cochrane et al. (2012) conducted two separate studies. In the
first, it was reported that in 99 psychologically healthy people,
the Interpersonal (negative) Factor of the SPQ was related to
reduced verbal fluency, and the Disorganised Factor was related
to reduced negative priming. In the second study, corresponding
symptom measures from the Scales for the Assessment of Posi-
tive and Negative Symptoms (SAPS and SANS; Andreasen, 1983,
1984) showed similar relationships with verbal fluency and nega-
tive priming in 20 participants with a diagnosis of schizophrenia.
Again, similar to outcomes of research focused on psychosis, rela-
tive cognitive deficits associated with schizotypy appear to relate
to negative (interpersonal) and disorganised traits rather than
positive (cognitive-perceptual) traits (Chen et al., 1997; Park and
McTigue, 1997; Moritz et al., 1999).
One point of departure in neurocognitive findings between
schizotypy and schizophrenia is that effect sizes appear to be larger
in schizophrenia research compared to schizotypy research. Specif-
ically, significant reductions in cognitive variables in people with
schizophrenia are often reported alongside medium to large effect
sizes (e.g. Reichenberg and Harvey, 2007; Simonsen et al., 2011);
whilst effect sizes in studies of schizotypy are often small (e.g. Chen
et al., 1997; Noguchi et al., 2008). This may indicate that cogni-
tive decline is more prominent for people with schizophrenia, and
indeed may be a significant defining feature of clinical psychosis
(Bora et al., 2010).
7. Environmental and social research
Further support for a continuum model of schizotypy and
schizophrenia can be gleaned from research examining environ-
mental and social correlates of the two constructs. Identified
environmental and social risk factors for schizophrenia are wide-
ranging. They include antenatal and birth complications such as
maternal infections (Stober et al., 1997; Brown, 2006; Xiao et al.,
2009), nutritional deficiency (St Clair et al., 2005; Markham and
Koenig, 2011), maternal stress during pregnancy (Markham and
Koenig, 2011), foetal hypoxia (Cannon et al., 2000) and older
parental age at conception (Malaspina et al., 2001; Petersen et al.,
2011). They also include childhood trauma (Lardinois et al., 2011),
migration and minority group membership (Morgan et al., 2010),
urbanicity (Kelly et al., 2010), cannabis use (Richardson, 2010),
parental separation (including death; Morgan et al., 2007), adverse
child rearing (Willinger et al., 2002), and childhood infection
(Rantakallio et al., 1997).
Similar environmental and social risk factors have been impli-
cated in the development of anomalous experiences associated
with schizotypy. Zammit et al. (2009) report in their longitudinal
study of 6356 children, that ‘PLIKS’ (‘psychotic-like experiences’)
were positively associated with pregnancy and birth complica-
tions. These included maternal infection, maternal diabetes, and
need for resuscitation following birth (Zammit et al., 2009). Addi-
tionally, positive anomalous experiences have been associated
with childhood trauma (Steel et al., 2009; Lovatt et al., 2010),
urbanicity (Scott et al., 2009), and ethnicity and minority group
membership (Sharpley and Peters, 1999; Johns et al., 2002; Morgan
et al., 2009). Parental separation has been associated with symp-
toms of schizotypal personality disorder (SPD), which is said to
lie on the continuum between schizotypy in healthy popula-
tions and full blown psychotic disorders (see Fig. 1; Anglin et al.,
2008). However there does not appear to be any research to date
addressing parental separation and schizotypy in healthy popula-
tions.
322 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
With respect to cannabis use, a large study involving 1049 stu-
dents showed that high levels of cannabis use were associated with
both positive and negative ‘non-clinical psychotic experiences’, as
measured by the Community Assessment of Psychic Experiences
(CAPE) questionnaire (Skinner et al., 2011). Furthermore, the ear-
lier students began their cannabis use, the more likely they were
to report positive experiences (Stefanis et al., 2002; Skinner et al.,
2011). This study along with numerous others, echoes psychosis
research and demonstrates a positive association between schizo-
typy and cannabis use (Barkus and Lewis, 2008; Compton et al.,
2009; Esterberg et al., 2009; Cohen et al., 2011).
In addition, unlike the neurocognitive findings reported above,
it is worth noting that effect sizes for these environmental findings
appear on the whole to be of similar magnitude for both schizo-
typy (Morgan et al., 2010) and psychosis (Morgan et al., 2009).
This may be because most studies investigating environmental
variables in relation to schizotypy have used measurement tools
that assess for positive traits specifically (such as the Psychotic-
Like Experiences Structured Interview and Psychosis Screening
Questionnaire; Bebbington and Nayani, 1995; Horwood et al.,
2008; Morgan et al., 2009; Zammit et al., 2009), rather than all
aspects of schizotypy (as is assessed via the SPQ and O-LIFE). This
might have increased power, as effects did not get ‘washed out’
when averaging across qualitatively different aspects of schizo-
typy.
8. Biological research: neuroanatomical abnormalities
Research has indicated that both schizophrenia and schizotypy
have been associated with a number of similar neuroanatomical
abnormalities. Importantly, several of the key neuroanatomical
findings relating to schizophrenia have also been replicated in
schizotypy research. For instance, neurological soft signs are sub-
tle deficits in areas such as motor coordination, laterality and
sensory-perceptual performance (Obiols et al., 1999). Unlike hard
neurological signs, they do not indicate any specific neurological
disease (Obiols et al., 1999). Higher rates of neurological soft signs
have been identified in people with psychotic disorders compared
to controls (Leask et al., 2002), and they have also been shown
to correlate with schizotypy in non-clinical samples (Bollini et al.,
2007; Kaczorowski et al., 2009; Chan et al., 2010). In two studies,
this relationship with schizotypy appeared to be driven by associa-
tions with interpersonal (negative) and disorganised factors rather
than by associations with the cognitive-perceptual (positive) factor
(Bollini et al., 2007; Kaczorowski et al., 2009). However, two stud-
ies have also found associations between neurological soft signs
and positive aspects of schizotypy (Barkus et al., 2006; Chan et al.,
2010).
Furthermore, people with schizophrenia also have higher levels
of the subtle variations in bone structure, cartilage and soft tis-
sue known as minor physical anomalies (McGrath et al., 2002).
These minor physical anomalies have also been significantly
associated with levels of overall schizotypy, as well as cognitive-
perceptual and interpersonal factors specifically (Bollini et al.,
2007).
In addition, there are wide reports of eye tracking dysfunctions
in relation to schizophrenia (Levy et al., 2010), such as impairments
in smooth pursuit and antisaccade eye movements (Lipton et al.,
1983). Like neurological soft signs and minor physical anomalies,
findings of occulomotor deficits have also been replicated in high
schizotypy groups (O’Driscoll et al., 1998).
More recently, developments in neuroimaging technologies
have identified brain structural, metabolic and functional abnor-
malities in relation to schizophrenia. These technologies include
magnetic resonance imaging (MRI), functional magnetic resonance
imaging (fMRI), diffusion weighted imaging (DWI), magnetic res-
onance spectroscopy (MRS), single-photon computed emission
tomography (SPECT), and positron emission tomography (PET).
There are a multitude of reviews and meta-analyses summarising
the field of neuroimaging and schizophrenia (Ward et al., 1996;
Shenton et al., 2001; Pantelis et al., 2005; Gur et al., 2007; Keshavan
et al., 2008; Fornito et al., 2009; Wood et al., 2011), therefore only
main findings are reported here.
Briefly, structural MRI studies have shown reduced whole-brain
volume and complimentary enlargement of lateral ventricles and
increases in cerebrospinal fluid (Gur et al., 2007; Keshavan et al.,
2008). Affected cortical regions include but are not limited to,
medial temporal lobe areas, most notably the hippocampus and
amygdala (Velakoulis et al., 2006; Gur et al., 2007; Keshavan et al.,
2008). DWI studies report deficits in white matter connectivity
across the whole brain, corpus callosum, cingulum bundle, and
superior longitudinal fasciculus, amongst others (Kubicki et al.,
2007; Kyriakopoulos et al., 2008; Seal et al., 2008; Zalesky et al.,
2011). MRS research seems to have focused on findings of reduc-
tions in N-acetyl aspartate metabolites (Gur et al., 2007). PET
and SPECT research has examined the role of over activation of
dopamine receptors (particularly D2 receptors) in schizophrenia
(Gur et al., 2007; Keshavan et al., 2008). Lastly, fMRI research has
explored decreases in activation of the dorsolateral prefrontal cor-
tex, especially when participants are presented with challenging
cognitive tasks (Berman and Meyer-Lindenberg, 2004; Keshavan
et al., 2008). This tendency is reinforced by outcomes of PET
and SPECT research focusing on the same area (Keshavan et al.,
2008).
Although there is much neuroimaging research into schizotypal
personality disorder (Dickey et al., 2002; Hazlett et al., 2012), a very
limited number of neuroimaging studies have investigated neu-
roanatomical correlates of schizotypy in psychologically healthy
people. One MRI study reported that schizotypy was associated
with reduced brain volume in prefrontal areas (Raine et al., 1992).
In another investigation, Modinos et al. (2010) gave a self-report
measure of schizotypy to six hundred university students. Thirty-
eight of the highest and lowest scorers subsequently underwent
MRI scans. Differences between groups included significantly larger
volumes in the whole brain, medial posterior congulate cortex and
precuneus for the high schizotypy group (Modinos et al., 2010). This
was the reverse of what is normally seen in psychosis research,
in which there are reductions in volume (Keshavan et al., 2008).
However, the authors concluded that the alterations were consis-
tent with a continuum model. They cite previous research findings
of increases in volume in SPD and first-episode psychosis sam-
ples (Modinos et al., 2010), as opposed to reductions in volume in
chronic schizophrenia samples (Keshavan et al., 2008). Increases
in grey matter in the middle, superior temporal, angular, and
orbitofrontal gyri have also been associated with PLEs (‘psychotic-
like experiences’) in a young adolescent sample (Jacobson et al.,
2010).
In another adolescent sample (aged 12–20), Lagioia et al. (2010)
examined brain networks relating to schizotypy using fMRI. They
report a discontinuity between their findings and those investi-
gating psychosis. However, their study was limited by its small
sample size of only 39 across a relatively large developmental age
range. Then, in our recent DWI study we identified negative corre-
lations between measures of white matter structure and positive
schizotypal traits in seven white matter tracts within frontal and
temporal areas (Nelson et al., 2011). This supports the findings
of Volpe et al. (2008), which showed that ‘psychotic personality
traits’ as measured by the Schizophrenia, Paranoia and Psycho-
pathic Deviate subscales of the Minnesota Multiphasic Personality
Inventory (Greene, 2000), were associated with changes in white
matter structure in the corpus callosum, right arcuate fasciculus,
 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
and frontoparietal fibres (Volpe et al., 2008). Currently, there are
no known investigations of the neurobiological basis of schizotypy
using MRS, PET, or SPECT imaging modalities.
In summary, despite the relative lack of research into a relation-
ship between schizotypy and schizophrenia using neuroimaging
modalities, other biological findings such as those of oculomotor
deficits, MPAs and neurological soft signs indicate there may be
some biological similarity between people who score highly on
measures of schizotypy and people with schizophrenia.
9. Methodological considerations
The above paucity in neuroimaging research is a case in point,
in that further investigation into the relationship between schizo-
typy and schizophrenia is still needed to resolve mixed findings,
particularly in relation to neurobiology and molecular genetics.
Large scale longitudinal and cross-sectional designs are required
that apply the same measures to people in the general popu-
lation, to people with SPD, people at high risk for psychosis,
first episode psychosis and to people with schizophrenia. Again
reflecting the complexity of the field, and reflecting the bur-
geoning unitary psychosis view, which posits that schizophrenia
and bipolar disorder as two representations of a single con-
struct, these investigations could be extended to other psychotic
disorders and affective psychoses. Indeed, as was pointed out
by one reviewer, there is some evidence (to be built upon)
that the unitary psychosis view is also reflected in dimensional
schizotypy research; for example via the four factor overlapping
scales of the O-LIFE (Mason et al., 1995; Mason and Claridge,
2006).
Continuum research of this type is difficult currently, with many
measures designed only for one level of severity on a proposed
schizotypy and psychosis dimension. For example, there are meas-
ures designed to assess the positive symptoms of psychosis, but
not the anomalous experiences associated with schizotypy, and
vice versa. Problems of floor and ceiling effects could be avoided
by designing measurement tools that can account for variation
across the entire continuum. One example of this is the Appraisals
of Anomalous Experiences Interview (AANEX; Brett et al., 2007).
Although lengthy, the AANEX is able to measure experiences ran-
ging from the anomalous, psychotic-like experiences of schizotypy,
to the florid hallucinations and delusions of psychosis.
Another important methodological issue is that thus far, schizo-
typy research has predominantly relied on self-report measures
such as the SPQ and O-LIFE. These questionnaires are short and
easy to administer, however they can be subject to the various
confounds associated with self-report measures, such as social
desirability bias (Moritz et al., 1999; Shean et al., 2007). Therefore
there is a need for wider use of psychometrically sound measure-
ments such as structured and semi-structured interviews. In this
way, the AANEX also meets another need in relation to future
research on schizotypy.
A related issue is the widespread use of statistical techniques
imposing artificial categorical boundaries on what are otherwise
dimensional scales. We refer here to the use of median splits and
similar techniques that dichotomize, or trichotomize samples that
have been administered self-report measures such as the SPQ. They
are used to extract, for example, ‘high schizotypy’ and ‘low schizo-
typy’ groups to be compared in subsequent statistical analyses.
However, they result in a substantial loss of statistical power, and
can therefore lead to mixed and contradictory findings. Interview
measures such as the AANEX, that allow wide variability across the
continuum will avoid floor and ceiling effects, increase power, and
allow investigators to compare ‘apples with apples’ when looking at
similarities and differences between schizotypy and schizophrenia.
323
Another reason that it is difficult to compare studies in this area,
is that although there has been much investigation into under-
lying structure of schizotypy itself (Stefanis et al., 2004; Mason
and Claridge, 2006; Wuthrich and Bates, 2006); further research
is needed to determine the concurrent, discriminant and con-
struct validity of schizotypy and psychosis-related phenomena
together. For instance, terms such as positive and negative schizo-
typy, schizotypal personality, ‘PLIKS’ and ‘PLEs’ (’psychotic-like
experiences’; e.g. Zammit et al., 2009; Kelleher and Cannon, 2011),
subclinical psychotic experiences (e.g. van Os et al., 2009), anoma-
lous experiences (e.g. Brett et al., 2007), cognitive-perceptual,
interpersonal and disorganised personality traits (e.g. Raine, 1991,
2006), SPD-proneness (Chan et al., 2010), and non-clinical dimen-
sions of psychosis (Skinner et al., 2011) are used interchangeably.
It is not clear whether they are measuring the same experiences,
or how they relate to one another. We have assumed that terms
like ‘PLEs’, ‘positive schizotypy,’ and ‘subclinical psychotic expe-
riences’ all refer to the same phenomena. That is, the anomalous
experiences of positive schizotypy which are represented on the
cognitive-perceptual factor of the SPQ. We have similarly assumed
that ‘negative schizotypy’, and the interpersonal factor of the SPQ
are the same construct. Furthermore, we have assumed that the
terms ‘schizotypy’, schizotypal personality’, ‘SPD-proneness’, and
‘non-clinical dimensions of psychosis’ are all subsumed under the
umbrella of schizotypy.
There is certainly evidence that ‘psychotic’ traits and ‘schizoty-
pal’ traits are convergent constructs (Bentall et al., 1989; Claridge
et al., 1996; Stefanis et al., 2002; Kwapil et al., 2008). For instance,
Claridge et al. (1996) assessed the convergence of schizotypal
traits and subclinical hallucinations and delusions in a community
sample of 1095 participants. Factor analysis from this study sug-
gested that subclinical hallucinations and delusions do map onto
the cognitive-perceptual factor of schizotypy. However, more up-
to-date investigation exploring and comparing the psychometric
properties of a range of measures pertaining to schizotypy, anoma-
lous experiences and psychotic symptoms would greatly assist in
further development of the field.
If the above terms are found to be referring the same con-
structs, in our own research and in future research we prefer to
use the following terminology. The term ‘anomalous experiences’
is preferred when referring to PLEs, PLIKs and so forth. The term
‘anomalous experiences’ distances these types of phenomena from
psychotic symptoms, thus avoiding the risk of pathologizing expe-
riences that are considered to lie within the range of normal human
experience. ‘Positive schizotypy’ is preferred when referring to
the tendency to have anomalous experiences, ‘negative schizo-
typy’ is preferred when referring to non-clinical experiences similar
to negative symptoms of psychosis, and ‘disorganised schizotypy’
is preferred when referring to non-clinical experiences similar to
disorganised symptoms of psychosis. We prefer ‘schizotypy’ as
the umbrella term subsuming all of the above. Use of the term
‘schizotypy’ rather than terms such as ‘non-clinical dimensions of
psychosis’ and ‘SPD-proneness’ avoids the loss of its status as a per-
sonality trait, and again avoids pathologizing normal experiences.
Finally, it could well be that all of these methodological issues
mentioned above are contributing to small effect sizes and type II
error in categorical research comparing groups. As has been seen,
some investigations into schizotypy and anomalous experiences
often report much smaller effects sizes than those seen relation to
psychosis. While others – for example those environmental investi-
gations focusing specifically on anomalous experiences rather than
schizotypy as a whole – report findings of similar magnitude to psy-
chosis research. It is not yet possible to conclude whether or not
smaller effects sizes are reflective of low power and extraneous
variables, or whether they reflects a ‘true’ reduction in magnitude
of effect.
324 M.T. Nelson et al. / Neuroscience and Biobehavioral Reviews 37 (2013) 317–327
10. Conclusions
As has been demonstrated, in the last five years there has
been an explosion of research consistently demonstrating simi-
larities between schizotypy and schizophrenia. Indeed, it would
seem that for many findings in relation to schizophrenia, there is
a corresponding finding in relation to schizotypy – although not
always of the same magnitude of effect. This is especially true for
environmental and neurocognitive findings, but is somewhat less
true for biological and molecular genetic findings – where there
is a relative paucity of research. The investigations reviewed in
the present article that report parallel, albeit attenuated, results
between schizotypy and schizophrenia are consistent with a fully
dimensional model, wherein varying levels of schizotypal person-
ality traits throughout the general population lie on a continuum
with schizophrenia spectrum disorders.
It would appear that it is no longer a question of whether or not
the two constructs are related. A more pertinent question would be
what determines whether or not an individual makes the hypothet-
ical transition from high schizotypy to full-blown psychosis? This
transition could happen in a number of different ways. One possible
mechanism might be that as an individual moves along the contin-
uum, their symptoms become linearly more severe. For example, in
relation to cognitive deficits, it might be that impairments become
more numerous, pervasive and severe along an increasing schizo-
typy and psychosis scale.
However, as a fully dimensional model of schizotypy would sug-
gest, it is more likely that the effects of various genetic, biological
and environmental risk factors combine with high schizotypy in
various cumulative, nonlinear and perhaps even idiopathic ways
to determine outcome. Although outside the scope of this article,
valuable intersections could be made here with the burgeoning lit-
erature on ultra high-risk for psychosis groups, which identify the
anomalous psychotic experiences associated with schizotypy as a
risk factor for the development of full-blown psychosis along with a
number of other risk factors such as depression, reduced attention,
and family history of psychosis (Yung et al., 2004).
We propose that the relationship between schizotypy and
psychosis can be viewed as similar to the relationship between neu-
roticism and anxiety disorders. High levels of neuroticism are often
found in people with anxiety disorders, however high neuroticism
is not sufficient in and of itself to indicate the presence of an anx-
iety disorder. The same can be said of schizotypy and psychosis in
that high levels of schizotypy may be associated with psychosis,
and they may be associated with similar variables to psychosis, but
they do not necessarily indicate dysfunction. Just as neuroticism
on its own is insufficient to indicate a specific anxiety disorder,
the value of schizotypy is not found in its use as a screening mea-
sure for specific psychotic disorders. Rather, the value of schizotypy
lies in what it can tell us about normal human experience, and
the possible pathways from psychological health to psychological
dysfunction.
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