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Schizophrenia Bulletin
doi:10.1093/schbul/sbu175
© The Author 2014. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved.
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Schizotypy From a Developmental Perspective
MartinDebbané*,1−3 and NeusBarrantes-Vidal4–7
1Developmental Clinical Psychology Research Unit, Faculty of Psychology and Educational Sciences, University of Geneva, Geneva,
Switzerland; 2Ofce Médico-Pédagogique Research Unit, Department of Psychiatry, University of Geneva School of Medicine, Geneva,
Switzerland; 3Research Department of Clinical, Educational and Health Psychology, University College London, London, UK;
4Departament de Psicologia Clínica i de la Salut, Universitat Autònoma de Barcelona, Barcelona, Spain; 5Sant Pere Claver – Fundació
Sanitària, Barcelona, Spain; 6Instituto de Salud Carlos III, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM),
Madrid, Spain; 7Department of Psychology, University of North Carolina at Greensboro, Greensboro, NC
*To whom correspondence should be addressed; Developmental Clinical Psychology Research Unit, Faculty of Psychology and
Educational Sciences, University of Geneva, 40 Boulevard du Pont d’Arve, 1205 Geneva, Switzerland; tel:+ 41-22-379-9418,
Fax: +41-22-379-9359, e-mail: martin.debbane@unige.ch
The schizotypy construct focuses attention on the liability
to develop schizophrenia-spectrum disorders, yet tradition-
ally, the schizotypy models have put more emphasis on
stress-vulnerability interactions rather than developmental
dynamics of emerging risk for psychopathology. Indeed,
developmental accounts of this emerging personality trait
have rarely been explicitly formulated. In this position
article, we wish to convey some of the basic developmen-
tal tenets of schizotypy, and how they can inform high-risk
research. Firstly, we tackle the state vs trait issue to outline
the possible relationship between high-risk states and trait
schizotypy. Second, we review the evidence suggesting that
the consolidation of schizotypy, encompassing its 3 main
dimensions, could be considered as a developmental media-
tor between very early risk factors and transition into high-
risk states. Importantly, developmental dynamics between
endophenotypes, as well as transactional and epigenetics
mechanisms should enter modern conceptualizations of
schizotypy. Finally, we present a developmental psycho-
pathology perspective of schizotypy sensitive to both the
multinality and equinality of schizophrenia-spectrum
disorders. We conclude that schizotypy represents a crucial
construct in a fully-developmental study of schizophrenia-
spectrum disorders.
Key words: high-risk/psychosis/schizophrenia/personality/
developmental/psychopathology
Introduction
Researchers interested in schizotypy generally seek to
examine a personality trait conferring liability to develop
schizophrenia.1 However, 50years after schizotypy’s rst
formal denition as a liability trait,2 which implicitly
designates a developmental dimension to schizophrenia,
we note that the eld of schizotypy research has seldom
explicitly formulated a developmental framework to con-
duct investigations on this putatively stable, continuous
trait signaling increased probability to the unfolding of
schizophrenia-spectrum disorders. Instead, developmen-
tal research has proceeded to focus on the risk of con-
version to schizophrenia,3 by employing a high-risk state
approach, focusing on transient, time-dependent shifts
in functioning, or exacerbation of subclinical symptoms.
Today, prodromal syndromes4 and basic symptoms5 rep-
resent the key preventive identication targets of the high-
risk state approach. Epidemiological research further
contributed by investigating selective schizotypal experi-
ences during childhood and adolescence, mostly from the
positive dimension, and examining their association to
the unfolding of psychotic disorders during adulthood.6,7
Such psychotic-like experiences (PLEs) have been found
to carry predictive value for the future development of
schizophrenia spectrum disorders, although their speci-
city is rather low (see Debbané etal in this supplemental
issue).
With regards to transition to schizophrenia, early pre-
vention research has focused on identifying specic at-
risk states that could discriminate between converters and
nonconverters before the onset of the pathology. Although
the early identication procedures are making signicant
progress,8 these state indicators tend to lose their predic-
tive power when evaluated more than 36months before
putative onset of the disorder. On the other hand, the
pioneering longitudinal Chapman studies have illustrated
how schizotypy traits too can yield predictive power, and
this over the decades of adolescence and young adult-
hood.9,10 These studies and others support dimensional
Schizophrenia Bulletin Advance Access published December 29, 2014
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M. Debbané and N. Barrantes-Vidal
claims that schizotypy traits are etiologically connected
to the schizophrenia-spectrum, and contain informative
value to dene populations at risk for these disorders.
However, as it would be expected, schizotypy traits mea-
sured in nonclinical populations yield lower predictive
power than clinical state indicators typically assessed in
help-seeking individuals. This has sometimes been inter-
preted as schizotypy being a poor risk indicator, with
lower sensitivity and specicity to high-risk states. Also,
the developmental mechanisms linking schizotypy to
clinical expression in the schizophrenia-spectrum remain
to be examined longitudinally.
It thus appears that in developmental high-risk
research, the different phenomena contained in the con-
struct of schizotypy have been split and scattered over dif-
ferent investigation elds, yielding crucial evidence to the
importance of prepsychotic states. By the same token, the
different high-risk approaches are sometimes susceptible
to yield piece-meal accounts that can become difcult to
integrate. Furthermore, states can be predictive of future
pathological development, but their articulation with
schizotypal traits and their own predictive value has been
understudied. The main objective of this position article
will be to articulate the basic elements of a developmen-
tal model of schizotypy, and situate this model within
the current research on high risk for schizophrenia. To
achieve this objective, each of 3 sections seeks to provide
what appear to us as critical elements in the developmen-
tal cascade of schizophrenia-spectrum disorders. The rst
section aims to tackle the issue of the coexistence between
“clinical” or “schizotypy” states and trait schizotypy, and
provide evidence supporting the probable association
between high-risk states and schizotypal traits during
development. In the second section, we highlight how
early schizotypal traits may indeed constitute a develop-
mental mediator between endophenotypes and increased
risk of conversion to adult schizophrenia-spectrum dis-
orders. In the nal section, we present a developmental
psychopathology perspective of schizotypy sensitive to
both the multinality of schizotypal traits (associated to
a number of different psychopathological outcomes), as
well as the equinality of schizophrenia-spectrum disor-
ders (how different developmental interactions may lead
to this class of diagnosis). Together these sections sketch
what could be called a preliminary developmental frame-
work for the schizotypy construct.
State vs Trait Schizotypy?
The rst section aims to deal with the conceptual chal-
lenge arisen by the current coexistence of 2 related yet
differential strands of research. On the one hand, the
“prodromal” or clinical high-risk approach puts by de-
nition a marked emphasis in the detection of at risk men-
tal states, which are very similar to the phenomenology
of overt psychosis even if they differ in dimensions such
as severity, frequency, or insight about their nature. On
the other hand, schizotypy research conducted in the
domain of individual differences refers to it as a stable
personality trait; its operationalization is not conditioned
by the endeavor of detecting “true” at risk individuals for
transitioning to psychosis. At the same time, both refer to
“subclinical” psychosis and index risk for it, so not sur-
prisingly some confusion seems to be present in the litera-
ture in regards to the trait or state nature of schizotypy.
As Claridge and Davis11 pointed out, the dimensional
model of mental disorder takes account of the 2 “uni-
verses of discourse” [as Foulds (1965) put it] that are nec-
essary to comprehensively describe abnormal behavior:
the “trait-like personality” and the “symptom-state ill-
ness” aspects of disorder. Acritical issue is that schizo-
typy (or any other) personality trait has a dual nature,
as it denes both enduring psychological characteristics
that vary along a continuum in the population and, at
the same time, a varying predisposition to psychotic dis-
order. Thus, there is not a clear-cut dissociation between
the domains of personality and illness, between traits and
states, although this is sometimes overlooked as person-
ality tends to be conceived as a highly rigid, nondynamic
construct. At the same time, it is obvious that an individ-
ual with high trait schizotypy, for instance someone who
has usually felt ego-syntonic peculiar body sensations
with good psychosocial functioning, is not the same as an
individual who is experiencing a “schizotypal” or high-
risk mental state characterized by perplexity and distress
over a dismorphophobic concern that changes his/her
usual behavior. Such state reects a temporary uctua-
tion that derives from the personality trait; as Claridge
and Davis11 put it, it denotes the trait “in action.” From
a quasidimensional account, various latent liability mod-
els of schizophrenia have also postulated that the genetic
susceptibility to schizophrenia produces a hypothetic
latent liability trait that can become expressed as nonob-
servable endophenotypic deviances, schizotypy personal-
ity traits and/or clinical states, or schizophrenia spectrum
disorders (see Meehl,12 Holzman’s latent trait model,13,14
and Lenzenweger15). These models thus also intrinsically
assume a developmental life-span perspective and articu-
late the relationship between trait and state manifesta-
tions. However, unlike the so-called fully-dimensional
perspective referred to above, these models consider
that despite there being phenomenological continuity
between traits and symptoms, the latent liability (eg the
genetic susceptibility) is not continuously distributed in
the population, which yields a group of liable individu-
als (a taxon) which is qualitatively different from the rest
(ie structural discontinuity). The investigation of the
structure of schizotypy with taxometric analyses is a con-
vulse topic given its methodological complexity16 and has
raised mixed ndings, with some studies supporting17,18
and others not19–21 the existence of a schizotypy or schizo-
typal personality disordertaxon.
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Schizotypy During Development
There is recent evidence supporting the association
between schizotypy and high-risk states in early adult-
hood and during development.22,23 In a recent longitudi-
nal study spanning over a 30-year interval, Rössler etal24
examined the latent-state and trait structure of subclinical
schizotypal signs (reduced close relationships, odd beliefs,
ideas of reference and suspicious/paranoid ideation) col-
lected over 7 semistructured interviews in subjects aged
20years at the start of the study. They also examined the
latent state and trait structure of subclinical schizophre-
nia nuclear symptoms (thought insertion, thought broad-
casting, thought control and hearing voices), phenomena
that overlap with positive schizotypal experiences. Their
study analyses demonstrate the importance of schizo-
typal traits over 3 decades of development, during which
it consistently accounted for more than half of the vari-
ance of subclinical psychotic expression. Importantly, in
the high-risk age interval for developing schizophrenia,
22–30 years old, latent schizotypal-traits explained sig-
nicantly more variance than its state counterpart. This
study thus supports the hypothesis by which psychotic
expression varies as a function of schizotypal traits, but
that uctuating and occasion-specic states can also con-
tribute to its expression. The results suggest that state
schizotypy explains more variance than its trait counter-
part at 20/21 and 49/50years of age. It is unclear whether
developmental transitions at these ages could contrib-
ute to this nding. Furthermore, the study reveals that
other personality dimensions inuence both trait and
state schizotypy. Low sense of mastery, depressiveness
and poor self-esteem signicantly associated with schizo-
typal signs. Employment distress, intimate relationship
problems and drug-use were found to be the main time-
dependent state inuences to schizotypal expression. In
essence, this report illustrates the multifactorial develop-
ment of psychotic expression, and how schizotypal traits
and states contribute to the unfolding of risk for schizo-
phrenia-spectrum disorders.
Schizotypy: ADevelopmental Vehicle Towards
Emerging Psychopathology
Ever since abandoning the single gene hypothesis of
schizophrenia, many scientists focusing on the genetic
basis of the disease have lead investigations consis-
tent with a polygenetic, endophenotype approach.25
Endophenotypes of schizophrenia, often identied at
the neurophysiological or neurocognitive levels, consist
in measurable variables that cannot be assessed at the
“visible” phenotypic level, whose expression is closely
tied to risk-conferring genes (risk genotype). Individual
measures on these endophenotypes typically reveal
abnormalities in samples of patients diagnosed with
schizophrenia, but also in family members carrying the
genotype underlying the impairments. It is thought that
each endophenotype accounts for a small percentage of
risk to develop schizophrenia, and that put together, an
ensemble of endophenotypes could increase the risk for
an individual to convert to schizophrenia.26
Recent advances in the eld of schizotypy research have
shown that endophenotypes typically linked to schizophre-
nia are also associated with the expression of schizotypy in
nonclinical youth samples, and adults from general popu-
lation samples (for a recent review, see Ettinger et al27). Of
note, this literature has shown that, consistent with the mul-
tidimensional nature of schizotypy (and schizophrenia),
there are differential associations between specic schizo-
typy dimensions and certain endophenotypic deviances.
Importantly from a developmental standpoint, schizotypy
has been found to be associated with endophenotypes and
biomarkers whose dimensions can already be assessed dur-
ing infancy or childhood (eg minor physical anomalies) or
relate to basic functions that typically reach full matura-
tion during childhood neurocognitive development. In a
study examining neurocognitive and neurodevelopmental
correlates of adolescent schizotypy in a sample 270 adoles-
cents, recruited from the regular school system and report-
ing elevated scores on the Chapman schizotypy scales, well
recognized schizophrenia endophenotypes and biomark-
ers were found to correlate with executive functions and
dermatoglyphic abnormalities, respectively.28 Similarly, in
a subsequent study investigating schizotypal symptoms in
adolescents at familial risk for developing schizophrenia,
minor physical anomalies, ne motor dyscoordination
and executive function impairments were associated with
negative schizotypy scores.29 Visual backward masking, for
which adult-like performance is generally acquired by the
beginning of adolescence, represents another schizophre-
nia endophenotype found to be associated with schizotypal
expression in youths.30 More specically, deterioration in
visual backward masking was found to be associated with
schizotypy in a sample of late adolescence/early adulthood
students, specically with cognitive disorganization.31 In a
similar vein, the sensorimotor gating function of prepulse
inhibition, thought to reach adult-like levels around 8years
old,32 has not only been associated with gating decits in
schizophrenia, but has also been shown to be impaired
in nonclinical youths at high genetic risk for developing
schizophrenia.33 This wealth of reports has been collated
in scientic reviews, emphasizing signicant superposition
in endophenotypical impairments when drawing compari-
son between nonclinical youth samples recruited on the
basis of schizotypal expression to samples of individuals
diagnosed with schizophrenia.34 Most importantly per-
haps, the developmental evidence of such associations can
be observed during childhood and adolescence. The grow-
ing number of studies thus makes it difcult to ignore the
commonalities between schizophrenia endophenotypes
and early expression of trait schizotypy (also in subjects
without familial risk), which continue to be observed at the
neurocognitive, neurophysiological, and cerebral levels all
along development.
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M. Debbané and N. Barrantes-Vidal
Another key area of atypical development associ-
ated with trait schizotypy concern the mentalizing func-
tions, that is those social cognitive operations that enable
oneself to employ knowledge on the mental states of
self and others in order to understand social interac-
tions. Cognitive development studies with adolescents
and young adults show that mentalizing functions con-
tinue to mature during the teenage years and well into
the early 20s.35 At the cerebral level, social cognitive spe-
cialization may indeed rely on more distal and complex
internetwork collaboration, typically rened during ado-
lescent brain maturation and specialization.36 To date, 2
functional neuroimaging studies suggest that schizotypal
expression during adolescence is signicantly associated
with atypical brain activation patterns in social cognitive
tasks requiring efcient self-other discrimination (reality-
monitoring and self-appraisal tasks37,38). Interestingly,
adolescents with different risk etiologies (genetic vs clini-
cal risk) may share neural markers associated with atypi-
cal social cognitive functions. In a recent fMRI study on
perspective-taking, comparable patterns of atypical neu-
ral activation during a 1p-3p perspective-taking task were
observed for both typical adolescents reporting transient
auditory verbal hallucinations and adolescents at ultra-
high risk for schizophrenia because of 22q11.2 deletion
syndrome.39 Together, these studies would suggest that
high schizotypy appears to accompany the different endo-
phenotypical risk markers during early risk for schizo-
phrenia spectrum disorders. In other words, and from a
clinical standpoint, the signicant association between
valid endophenotypes and early high schizotypy may sig-
nify the establishment of early risk progress for subclini-
cal schizotypal youths. This motivates further inquiry
into the potential predictive value of an endophenotype/
schizotypy trait association, at the level of the individ-
ual, for conversion to psychotic spectrum disorders. At
the same time, these ndings also support the validity
of schizotypy as the continuous personality dimension
characterized by a specic neurobiological, cognitive, and
socioaffective organization that is both expressed at the
level of healthy individual differences and underlies the
predisposition to psychosis. Most importantly perhaps,
the consolidation of schizotypy may confer a “devel-
opmental vehicle” towards psychopathology. In such a
developmental account, a number of endophenotypes
would consistently inuence the emerging organization
of personality, and each partly consolidating schizotypy.
Then, towards middle childhood and through adoles-
cence, signicant metacognitive, interpersonal and social
experiences may be preferred and consistently selected
by the individual as a result of schizotypy (selective
appraisals of perceptual aberrations, overt eccentricity
in speech and behavior, decreasing social contact, etc.),
thereby initiating developmental transactional inu-
ences that may augment the risk for psychopathology. As
such, schizotypy may be conceived as a developmental
vehicle between early endophenotypes and biomarkers,
to selective transactional processes, towards adult risk for
psychopathology.
To illustrate the underlying developmental interac-
tions that position schizotypy as a developmental vehicle,
we provide a gure based on the traditional account of
schizotypy (Meehl) as framed by Lenzenweger,40 and
sketch the additional developmental interactions setting
the “vehicle” of schizotypy in motion during develop-
ment. Although implicitly developmental in nature, the
traditional model is typically illustrated in linear fashion
(see left side), starting from the genetic component (the
“schizogene” in Meehl’s original formulation), through
the schizotaxic underlying level, toward the manifest
expression of schizotypy. The model accounts for social
learning opportunities as well as psychosocial stress
factors and polygenetic potentiators (PGP) that may
inuence the development of schizotypy, and admits to
interactions between schizotypy and these stressors dur-
ing maturation. The traditional model could be made
more explicitly developmental, by including 3 possible
developmental dynamics within the framework (see right
side of gure1): (1) Firstly, developmental research sug-
gests the utility of assessing multiple endophenotypes
in predicting onset of illness.1 Indeed cooccuring endo-
phenotypes may signal higher risk to develop clinically
relevant symptoms, in part, through interactions during
development that would potentiate the genetic loading
of risk for schizophrenia. These interactions are repre-
sented in red in gure1, and may partly underlie recently
evidenced interactions between schizotypy dimensions
during adolescence.41 (2) Transactional processes during
development could be captured by emphasizing possible
relationships between schizotypy and both psychosocial
learning and stress. Transactional models suggest that
individual characteristics such as traits are not only inu-
enced by contextual dimensions, but themselves contrib-
ute to shaping the context. These processes are captured in
the blue arrows in gure1. Arelevant example for schizo-
typy research could be gathered from the transactional
model of social withdrawal.42 (3) Finally, most environ-
mental risk factors identied in relation to schizophrenia
can also potentially trigger epigenetic effects.43 Therefore,
the strictly unidirectional relationship between risk genes
and psychosis could also include epigenetic mechanisms
as potential mediators of gene expression, as captured by
the green arrows in gure1.
In sum, when considering endophenotype research
from the perspective of developmental schizotypy, 3 criti-
cal observations come into consideration. Firstly, many
of the endophenotypes associated with schizophrenia
concern dimensions and functions already established
during childhood. In other words, some endopheno-
types of schizophrenia are fully manifest long before the
rst signs of the at-risk states make their way into the
clinical picture. Secondly, endophenotypes associated to
Page 5 of 10
Schizotypy During Development
patients with schizophrenia and their family members are
also associated with psychometrically dened measures
of schizotypy in nonclinical youth samples. In a recent
review, Ettinger et al27 provide some of the overlapping
behavioral and neurobiological domains of impairment
between schizophrenia and schizotypy, suggesting some
continuity at the endophenotypic level between schizo-
typy and full-blown schizophrenia. Finally, social cogni-
tive impairments associated with schizophrenia also relate
to schizotypal expression during adolescence.37–39 When
this triad of observations is considered conjointly with
the predictive value of schizotypy for the development of
schizophrenia spectrum disorders, it positions this risk
trait as a potent transactional agent, a developmental
vehicle linking early endophenotypes to growing pro-
pensity of developing psychopathology. In other words,
schizotypy might constitute a measurable intermediate
mediator in the developmental cascade of schizophrenic
disorders.
From a developmental psychopathology standpoint,
developmental mediators along the trajectory of disor-
ders usually appearing during adulthood represent key
targets in longitudinal investigations. Such investiga-
tions are designed to more readily assess the intermediate
points in development that appear to link early risk fac-
tors to adulthood symptom expression. The developmen-
tal psychopathology of borderline personality disorder
(BPD) provides good examples of such conceptualiza-
tions. Most conceptual accounts of developing BPD will
assess childhood constitutional factors (familial anteced-
ents, motor development, temperament) early environ-
ment characteristics (trauma, attachment, life stress), as
well as middle childhood/early adolescence factors (self-
regulation instability, self-representation disturbance,
interpersonal difculties, etc.) as nonspecic risk factors
potentially contributing to the slow unfolding of patho-
logical manifestations at the phenotypic level (early sub-
clinical symptoms), and opening increased probability of
adult BPD psychopathology.44 Agood example of such a
longitudinal, developmental psychopathology approach
to BPD is provided by Carlson etal44, who prospectively
assessed developmental antecedents in 162 rst-born chil-
dren of mothers at high parenting risk because of pov-
erty. The authors rst analyzed the correlation patterns
between early risk factors and adult borderline symp-
toms. They found that early childhood maternal hostil-
ity and maternal life stress, as well as middle childhood/
adolescent self-representations best accounted for adult
borderline personality symptoms at age 28years. In the
following analysis, the authors examined which middle
childhood/early adolescence variable potentially played a
mediating role in development between early risk factors
and later adult BPD symptoms. They observed that mid-
dle childhood/early adolescent self-representations sig-
nicantly mediated the developmental pathway between
childhood attachment disorganization and adult BPD
symptoms. In this way, the authors underlined a pos-
sible developmental cascade linking early disorganized
Fig.1. Meehl’s traditional schizotypy model (based on Lenzenweger40), and modications to account for developmental interactions
propelling schizotypal manifestation into potential clinical risk states. The red, blue and green arrows specify potential developmental
dynamics to consider when examining schizotypy from a developmental perspective. Red arrows: putative developmental interactions.
Blue arrows: putative transactional interactions. Green arrows: putative epigenetic interactions. PGP, polygenic potentiators; Endoph.,
endophenotype.
Page 6 of 10
M. Debbané and N. Barrantes-Vidal
attachment and middle childhood/early adolescence
self-representations towards adult BPD symptoms. Such
prospective designs also suggest that developmental
mediators are construed during development through
successive transactions between the individual’s endoge-
nous vulnerabilities and environmental risk factors work-
ing towards psychopathological outcomes.
To recapitulate, research on schizotypy has provided
some signicant clues into its developmental involvement
as a distal risk marker for schizophrenia. During devel-
opment, it is both related to early acquired endopheno-
types and developing social cognitive functioning. As it is
also correlated to later onset of psychopathology, it may
be considered as a key developmental mediator along
the risk trajectory. Yet, the developmental mechanisms
by which this risk is maintained and or exacerbated still
require further research. Critical developmental interac-
tions between schizotypal dimensions, as reviewed in the
next section, may start revealing some of these develop-
mental mechanisms bringing distal trait schizotypy closer
to proximal state schizotypy.
Critical Interactions in the Developmental Course of
Schizotypy
A typical criticism of a developmental schizotypy
approach in the eld of high risk for psychosis resides in
the low sensitivity and specicity provided by an assess-
ment of schizotypy, often taking place a decade or more
before signicant preclinical and clinical psychotic states
manifest themselves. Taking example from the Dunedin
prospective sample, which followed 1007 individuals from
birth to 38years of age, a summary evaluation of positive
schizotypy (clinician-rated psychotic symptoms of hallu-
cinations and delusions) at age 11years signicantly pre-
dicts later adult development of schizophrenia-spectrum
disorders. It was observed that a signicant proportion
of identied 11-year-olds with signicant positive schizo-
typy (n=13), developed schizophrenia by age 38 (3 out of
13 (23 %)). However, it was also found that the total pro-
portion of unidentied cases with weak positive schizo-
typy at age 11 developed schizophrenia by age 38 that
developed schizophrenia was substantial (24 out of 776
(3%), which represent 24 cases out of the total 27 cases
identied with the disorder (89%)).45 These prospective
ndings suggest poor sensitivity when solely examining
positive schizotypal experiences in youths. Furthermore,
specicity analyses of the adult sample having reported
signicant childhood positive schizotypy suggested that
these individuals were at higher risk of meeting diagnosed
criteria not only for schizophrenia, but also for posttrau-
matic stress disorder and attempt/complete suicide by age
38 in comparison to the rest of the sample.
From a developmental psychopathology approach of
schizotypy, 3 observations may be offered with regards
to the sensitivity/specicity critique. Firstly, when taking
early positive schizotypy as the main variable, it is not
surprising to observe multiple developmental nalities.
In fact, multinality represents one of the founding prin-
ciples of developmental psychopathology.46 From this
perspective, early positive symptoms act similarly as any
other risk factor, such as trauma for example, associated
with various developmental trajectories. Indeed, trauma
has not only been associated with increased risk for the
development of schizophrenia,47 but also to increased
risk for the development of internalizing disorders48 and
BPD.49 The mechanisms by which early and enduring
traumata induce deleterious effects appear to be related to
the developing hypothalamo-pituary-adrenal (HPA) axis,
a key axis in the regulation of developmental stressors,
involved in neurobiological accounts of these psychiat-
ric disorders.50 In a hypothetically similar fashion, stable
positive schizotypy may reinforce atypical regulation in
the mesolimbic dopaminergic system depending upon
transactions with high risk environments (eg bullying),
genotype and the constellation of other critical personal-
ity dimensions such as negative affect, thereby consoli-
dating increased risk during childhood and adolescence.51
Asecond observation, critical to a developmental schizo-
typy perspective, is that most prospective research fails
to examine the multifactorial nature of schizotypy, even
if there is general agreement in the eld that, at minima,
schizotypal traits rest on a triad of relatively stable mani-
festations encompassing positive schizotypy (unusual
perceptual experiences in cognitive-perceptual phenom-
ena), negative schizotypy (at affect, social withdrawal,
anhedonia in the interpersonal domain), and disorgani-
zation schizotypy (odd and eccentric speech and behav-
ior as behavioral proxies). However, most research often
bypasses the signicant and equally predictive value
of the negative schizotypy dimension (see Debbané,
Schultze-Lutter etal, this issue). In reality, the sensitiv-
ity/specicity critique cannot be conrmed nor denied
until prospective cohorts evaluated on all 3 schizotypal
dimensions are followed longitudinally past the critical
age interval of schizophreniaonset.
This observation links directly with a third comment,
which is that sparse but signicant preliminary longitu-
dinal data on developing schizotypy support the impor-
tance of assessing schizotypy in its multifactorial nature.
At least 3 reports suggest that during adolescent develop-
ment, crucial interactions between positive, negative and
disorganized schizotypy take place to both sustain/exac-
erbate schizotypal expression, and augment the risk for
signicant psychotic outbreaks.
First, in a group of 34 nonpsychotic help-seeking ado-
lescents assessed longitudinally on trait schizotypy, the
schizotypy dimensions as measured by the Schizotypal
Personality Questionnaire (SPQ),52 were found to be sig-
nicantly associated over a 3-year period. Stability of
schizotypy trait could be observed for the negative and
disorganization dimension, but positive schizotypy scores
Page 7 of 10
Schizotypy During Development
signicantly declined over the study interval. In terms of
developmental interactions between schizotypal dimen-
sions, baseline negative schizotypy was found to signi-
cantly predict positive schizotypy 3 years later, through
its mediating relationship with baseline disorganization.41
In other words, withdrawal and blunted emotion during
adolescence, when associated with disorganized speech
and behavior, can potentially predict the maintenance or
exacerbation of cognitive-perceptual anomalous percep-
tions. Importantly, these results were corrected for any
inuences regarding internalizing and externalizing prob-
lems in these help-seeking adolescents. In a larger study
of similar nature, involving 3021 youths aged 14–24years
at baseline examined for schizotypy using the Composite
International Diagnostic System (CIDI), 10-year longi-
tudinal analysis of psychotic-like positive, negative, and
disorganization experiences were associated with men-
tal health help-seeking incidence over the study interval.
First, on the basis of the assessment interview, psychotic-
like symptoms were clustered into a positive symptom
cluster and a negative/disorganized symptom cluster.
The critical outcome variable consisted in measuring
help-seeking behavior in relation to symptoms. During
the study interval, between 37–39% of those participants
with signicant positive symptom-cluster called upon
professional help in relation to their symptoms. Help-
seeking signicantly augmented by 16.2% for those indi-
viduals with both the positive and negative/disorganized
symptoms clusters. Taken together, these 2 studies sug-
gest that the different dimensions of schizotypy signi-
cantly interact during adolescence to sustain/exacerbate
and perhaps increase the need for professional help in
relation to symptom expression.
A follow-up question regarding potentially pathogenic
developmental interactions concerns their actual links
to the emergence of categorically dened schizophrenia-
spectrum disorders. To the best of our knowledge, there
exists only one study testing this hypothesis.10 In 1 study
testing this hypothesis, ve-hundred and three 19-year-
old college students followed over a 10-year period.
Asignicant interaction was found between the positive
and negative schizotypy dimension, specically in deter-
mining long-term paranoid personality features. Atrend
like but nonsignicant interaction was also found for the
development of any psychotic disorders. We note that the
disorganization dimension was not evaluated here. This
dimension appears to be critical in other studies exam-
ining signicant longitudinal change and help-seeking
behavior in relation to schizotypy.41,53 Future longitudi-
nal studies, encompassing all 3 dimensions of schizotypy,
are needed to investigate the clinical relevance of such
interactions. To date however, the data available do sug-
gest that mechanisms of natural progression, and perhaps
mechanisms of change in schizotypal expression might
involve maladaptive dimensional interactions between
negative, disorganization and positive schizotypy. These
interactions must be critically studied if promising early
identication strategies are to evolve towards empirically-
based and equally promising early intervention strategies.
By embracing principles of developmental psycho-
pathology such as multinality, the developmental
schizotypy approach gains sensitivity to distal dynamic
interactions that take place during development and
effectively play a signicant role in the transition to high-
risk states. This leads to a model that is closer to the
kinds of accelerated developmental dynamics observed
such high-risk states. Clinically, interactions between the
schizotypal dimensions, for example between cognitive
disorganization and positive schizotypy, may also occur
during development.41 Anecdotally, clinical material often
supplies examples of such interactions, as illustrated in
the following case example of Fred, a 16-year-old adoles-
cent consulting in our outpatient psychiatric service, who
reports the following sequence when prompted about
hisPLEs:
Fred: … I’ve always been quite reserved, feeling more com-
fortable when alone, and that people in general couldn’t
really understand me…
… Ithink things started when sometimes, Iwould hear a
kind of music, but Ididn’t know where it was coming from.
Iinspected our house to see if any of the TV or the radio
devices was switched on, but they weren’t… This lasted for
a few months.
… so Ithought it might be due to cannabis, Ithen decided
to stop smoking joints. For more than 3months Istopped,
but the music continued, and also there started to be voices…
… at rst they were kind, but then they were very mean
voices. They were accusing me of all sorts of names, Ithink
they wanted to punish me for the mean things Idid as a
child…
… Then there was this vision Ihad in my room, like an old
man whose face was full of scars…
… The next day… no maybe a week before… hmmm
or was it a weak after… I’m not sure… Iwas in store and
Iwas sure that a couple, a man and a women then ordering
a sandwich, were actually spying on me. They were suspi-
cious; they thought Iwas following them. They were talking
to each other with a low voice, sometimes looking at me over
their shoulder. Then this other man came in the store, and
he had thick scars on his face. Ithen thought the couple had
done that to him, like they did to the old man Isaw in my
room, and they might do it to me. Ithought Iwas caught
and couldn’t get out….
During development, different dimensions of schizo-
typy are likely to interact together. In the case of Fred,
an adolescent scoring high on negative schizotypy, the
progression of his anomalous perception rst led him to
(rather accurately) question whether they were linked to
cannabis consumption. Then, upon their continuation,
and together with disorganized and hyper associative
thought processes, the quasidelirious content of beliefs
Page 8 of 10
M. Debbané and N. Barrantes-Vidal
made their way into his appraisal and explanations of
what he was going through. It also appeared that con-
fusions in temporality, as well as self-other confusions,
contributed to the process. Other kinds of interactions
between symptoms may occur. Another common devel-
opmental interaction can be observed between an ado-
lescent’s odd speech, or bizarre and eccentric behavior
(disorganizations schizotypy) that can sometimes be
met by uneasiness, sarcasm or even hostility by his peer
group. In school environments where social appraisals
can make or brake adolescents, it is not rare to witness
cognitively disorganized youth being bullied, or pulling
away from social interactions and into social withdrawal
(negative schizotypy). These interpersonal interactions
make it more likely for such adolescents to increase their
time spent in solitude, and away from social feedback that
might balance their growing perception of the hostility of
the environment.
Most clinicians would agree that such interactions
between schizotypal dimensions do occur, and that
emerging high-risk states in youths should be assessed
within this dynamic developmental context. Other devel-
opmental trajectories, such as those observed in youth
populations with “multiple complex developmental dis-
order” represent another potential path to psychotic dis-
orders.54 These considerations are not distant from the
concept of equinality in developmental psychopathol-
ogy (see gure2). Equinality refers to the observation
that potentially different etiological interactions may lead
to the same diagnostic nality. In other words, schizo-
phrenia-spectrum disorders represent a categorical nal-
ity reached through signicantly different developmental
interactions. It thus appears to us that the developmental
schizotypy approach may bear the ingredients to embrace
multinality and equinality, and draw closer to the
clinical complexity of emerging schizophrenia-spectrum
psychopathology.
Conclusion
In this manuscript, we argue that the development of
high trait schizotypy confers an increased liability to
psychotic states which, contingent on endogenous and
exogenous factors, as well as their dynamic transactions
across especially sensitive periods, may ultimately lead
to schizophrenia spectrum disorders. This integrative
view of schizotypy as a liability trait implicitly confers a
developmental dimension to both schizotypy and schizo-
phrenia, and invokes a lifespan, developmental psycho-
pathology framework, to understand the maladaptive
pathways leading to spectrum outcomes.
Currently, most developmental research focuses on
young adults presenting high-risk mental states very close
to clinical psychosis and examines risk for transition to
schizophrenia. However, little is known about the devel-
opmental pathways linking trait schizotypy, high risk
mental states and the progression to clinical expression in
the schizophrenia spectrum. Adevelopmental model of
schizotypy is in a good position to integrate this research.
Importantly, future longitudinal research focusing on
high-risk for psychosis should include schizotypy assess-
ments as a distal risk marker. Accumulating evidence indi-
cates that trait schizotypy (1) is related to and accounts for
the liability to present subclinical psychotic states across
development and (2) is already associated with many of
the endophenotypes established for schizophrenia dur-
ing childhood and adolescence, which suggests that trait
schizotypy could be both an early distal marker to select
populations of interest to conduct longitudinal studies
and, importantly, a measurable developmental media-
tor in the pathway of risk to schizophrenia spectrum
disorders. In this context, epigenetic studies focusing on
schizotypy trait expression are necessary. Finally, prelimi-
nary longitudinal data points out the critical importance
of taking into consideration the multidimensionality of
schizotypy in such developmental framework, as mecha-
nisms of change in schizotypal expression might involve
maladaptive dimensional interactions between negative,
disorganization, and positive schizotypy. Studying these
interactions, the different outcomes of schizotypy traits
depending on the niche of risk and protective factors (ie
multinality) and the various pathways that may conduce
to a schizophrenia spectrum diagnostic entity (ie equi-
nality) are essential to yield empirically based early iden-
tication and intervention strategies.
Funding
Swiss National Science Foundation (100014-135311/1 to
M.D.); Gertrude Von Meissner Foundation (ME 7871);
National Center of Competence in Research (NCCR)
“SYNAPSY - The Synaptic Bases of Mental Diseases”
Fig.2. An illustration of the developmental psychopathology
principles of multinality and equinality.
Page 9 of 10
Schizotypy During Development
nanced by the Swiss National Research Fund (51AU40-
125759). ICREA Acadèmia Research Award (Institució
Catalana de Recerca i Estudis Avançats to N. B.-V.);
the Catalan government (Suport als Grups de Recerca,
2014SGR1070); Spanish Ministerio de Economía y
Competitividad (PSI2011-30321-C02-01); Fundació La
Marató de TV3 (091110).
Acknowledgment
The authors have declared that there are no conicts of
interest in relation to the subject of this study.
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