Journal of Personality Disorders, 27(5), pp.

652–679, 2013
© 2013 The Guilford Press

SCHIZOTYPAL PERSONALITY DISORDER

Eran Chemerinski, MD, Joseph Triebwasser, MD,
Panos Roussos, MD, PhD, and Larry J. Siever, MD

Early phenomenological descriptions of schizophrenia have acknowl-

edged the existence of milder schizophrenia spectrum disorders char-
acterized by the presence of attenuated symptoms typically present in
chronic schizophrenia. The investigation of the schizophrenia spectrum
disorders offers an opportunity to elucidate the pathophysiological
mechanisms giving rise to schizophrenia. Differences and similarities
between subjects with schizotypal personality disorder (SPD), the pro-
totypical schizophrenia personality disorder, and chronic schizophre-
nia have been investigated with genetic, neurochemical, imaging, and
pharmacological techniques. Patients with SPD and the more severely
ill patients with chronic schizophrenia share cognitive, social, and at-
tentional deficits hypothesized to result from common neurodevelop-
mentally based cortical temporal and prefrontal pathology. However,
these deficits are milder in SPD patients due to their capacity to recruit
other related brain regions to compensate for dysfunctional areas. Indi-
viduals with SPD are also less vulnerable to psychosis due to the pres-
ence of protective factors mitigating subcortical DA hyperactivity. Given
the documented close relationship to other schizophrenic disorders,
SPD will be included in the psychosis section of DSM-5 as a schizophre-
nia spectrum disorder as well as in the personality disorder section.

CLINICAL DESCRIPTION/SYMPTOM PICTURE

Individuals with schizotypal personality disorder (SPD) contemplate idio-
syncratic beliefs such as “magical thinking,” or a conviction that the mind
has the ability to change the physical world (Table 1). These beliefs diverge
from the social norms of subjects’ culture and usually exert a significant
impact on their speech and appearance. More prominently, SPD individu-
als exhibit suspiciousness, ideas of reference, and, during periods of de-
creased awareness, perceptual distortions such as illusions. However,
while pervasive and disturbing to the patient, these psychotic-like symp-
toms do not lead to prolonged functional impairment, multiple hospital-
izations, and long-term exposure to psychotropic medications. On the
other hand, the relatedness of SPD subjects to others is generally poor
and inappropriate. A combination of factors such as constricted affect,
peculiar appearance and speech, and suspiciousness of the intentions of
This article was accepted under the editorship of Paul S. Links.
From James J. Peters VA Medical Center (E. C., J. T., P. R. L. J. S.).
Address correspondence to Larry J. Siever, Bronx VA Medical Center (OOMH), 130 West
Kingsbridge Road, Bronx, NY 10468; E-mail: larry.siever@mssm.edu

652
SCHIZOTYPAL PERSONALITY DISORDER653

Table 1. DSM-IV Diagnostic Criteria for Schizotypal Personality Disorder

(American Psychiatric Association, 1994)
A. A pervasive pattern of social and interpersonal deficits marked by acute discomfort with,
and reduced capacity for, close relationships as well as by cognitive or perceptual
distortions and eccentricities of behavior, beginning by early adulthood and present in a
variety of contexts, as indicated by five (or more) of the following:
1.  Ideas of reference (excluding delusions of reference)
2. Odd beliefs or magical thinking that influences behavior and is inconsistent with
subcultural norms (e.g., superstitiousness, belief in clairvoyance, telepathy or “sixth
sense”; in children or adolescents, bizarre fantasies or preoccupations)
3.  Unusual perceptual experiences, including bodily illusions
4. Odd thinking and speech (e.g., vague, circumstantial, metaphorical, over elaborate, or
stereotyped)
5.  Suspiciousness or paranoid ideation
6.  Inappropriate or constricted affect
7.  Behavior or appearance that is odd, eccentric, or peculiar
8.  Lack of close friends or confidants other than first-degree relatives
9. Excessive social anxiety that does not diminish with familiarity and tends to be
associated with paranoid fears rather than negative judgments about self
B. Does not occur exclusively during the course of Schizophrenia, a Mood Disorder with
Psychotic Features, another Psychotic Disorder, or a Pervasive Developmental Disorder
Note: If criteria are met prior to the onset of schizophrenia, add “premorbid,” e.g., “schizo-
typal personality disorder (premorbid).”

others is responsible for the social deficits in SPD. Additionally, SPD sub-
jects also exhibit deficit-like symptoms, discriminated by factor analyses
as an independent dimension of social deficits, as well as cognitive disor-
ganization (Bergman et al., 1996; Raine, Reynolds, Lencz, & Scerbo, 1994).
The cognitive impairment of SPD is usually milder and more circum-
scribed than that of schizophrenia (Mitropoulou et al., 2005; Siever & Da-
vis, 2004).
The social deficits exhibited by SPD individuals are recognized in a key
DSM-IV (American Psychiatric Association [APA], 1994) criterion for this
disorder: “lack of close friends or confidants other than first-degree rela-
tives” (p. 645). Many different symptoms exhibited by these individuals
(e.g., excessive social anxiety, odd speech, constricted affect, and suspi-
ciousness) contribute to their social deficits. Recent studies hypothesized
that these deficits could result from schizotypal traits such as lack of em-
pathy (Dinn, Harris, Aycicegi, Greene, & Andover, 2002; Henry, Bailey, &
Rendell, 2008; Langdon & Coltheart, 2004; Pickup, 2006) and altered
emotional awareness (Berenbaum et al., 2006). Furthermore, a study by
Mittal et al. (2006) reported that adolescents with SPD exhibit nonverbal
communication deficits such as limited and abnormal gesturing. More-
over, in a more recent study by this same group (Mittal, Kevin, Tessner, &
Walker, 2007), SPD youths used the Internet for social interaction more
frequently than normal controls. The authors hypothesized that these in-
dividuals might prefer the Internet for social interaction because it pro-
vides an environment where communication is less likely to be hampered
by interpersonal deficits. Social deficits, along with cognitive deficits, con-
tribute to the significant poor functioning exhibited by SPD individuals.
Among the DSM-IV personality disorders (PDs), SPD is one of the most
654 CHEMERINSKI ET AL.

strongly associated with reduced quality of life in the community (Cramer,

Torgersen, & Kringlen, 2006; Ullrich, Farrington, & Coid, 2007). Crawford
et al. (2005) found SPD individuals to have the third lowest GAFs scores
among the PDs. Additionally, Skodol et al. (2002) found that the impair-
ment at work and in social relationships exhibited by these individuals is
not only more severe than that of patients with other PDs but also that of
patients with major depressive disorder in the absence of PDs.
SPD was classified in the DSM-III as a personality disorder because its
criteria reflect enduring patterns of perceiving, relating to others, and
thinking about the environment and oneself. A contributing factor for the
inclusion of SPD as an independent DSM disorder was the need to define
a prototypical personality disorder that encompassed the attenuated
schizophrenia-like symptoms observed in the relatives of patients with
schizophrenia. Before the conception of SPD, these psychotic-like symp-
toms were part of the diagnostic criteria of schizoid and borderline person-
ality disorders. As a result, the diagnostic criteria of these personality dis-
orders were believed to lack clear boundaries. Studies attempting to
identify symptoms specific and sensitive to SPD have demonstrated that
social withdrawal, odd/eccentric speech and behavior, and suspicious/
paranoid ideation are “core” disturbances in this disorder (McGlashan,
1987; Widiger, Frances, Warner, & Bluhm, 1986).
A considerable amount of concern about the reliability, validity, and in-
ternal consistency of SPD (Lindsay et al., 2007; Livesley, 2002; Widiger,
2000) arose after its incorporation into the DSM-III (APA, 1980). There is a
dearth of data on the internal consistency of SPD. Furthermore, studies
assessing the validity of this diagnosis have relied on a small number of
subjects and inconsistent diagnostic instruments. The consistency re-
ports for SPD from some of these studies have been less than encourag-
ing. For example, a within-category interrelatedness Cronbach’s coeffi-
cient alpha for SPD of 0.52 was found in a study of 38 adult psychiatric
inpatients (Becker et al., 1999). Similar results (coefficient alpha of 0.54)
were found in an earlier retrospective chart review of 37 inpatients (Morey,
1985). Furthermore, a reliability coefficient for SPD of 0.63 was found in a
study examining DSM-IV (APA, 2000) personality disorder diagnoses in
164 subjects (Lindsay et al., 2007). An added criticism of the DSM person-
ality disorders diagnostic criteria is the reported overlap between these
supposedly discrete classifications (Hopwood et al., 2005). This is also
true for SPD, which shows high rates of co-occurrence with other “odd”
cluster personality disorders (Kendler, Myers, Torgersen, Neale, & Reich-
born-Kjennerud, 2007) as well as with personality disorders from other
clusters, especially borderline personality disorder (Cohen et al., 2008;
Grant et al., 2008). SPD also exhibits comorbidity with Axis I disorders.
Since it is an exclusion criterion for schizophrenia, only a few authors
have been able to report a co-occurrence of these two disorders (Adler &
Strakowski, 2003; McGlashan et al., 1986; Sanislow et al., 2009). Other
Axis I disorders found to be comorbid with SPD include major depression
(McGlashan, 1983; Pfohl, Stangl, & Zimmerman, 1984), obsessive-compul-
SCHIZOTYPAL PERSONALITY DISORDER655

sive disorder (Poyurovsky et al., 2008; Shin et al., 2008), and Tourette
disorder (Cavanna, Robertson, & Critchley, 2007).
Schizophrenia-spectrum subjects share common phenomenological fea-
tures emerging from common spectrum-related risk factors (Faraone,
Green, Seidman, & Tsuang, 2001; Siever et al., 2002). Thus, a continuous
or dimensional conceptualization of these disorders might be preferred
(Fossati et al., 2005) to the categorical point of view adopted by the DSM-IV
(APA, 1994). The cognitive deficits and social deterioration exhibited by
SPD subjects are more circumscribed and less severe than in chronic
schizophrenia. Meehl (1962) coined the term schizotaxia to describe the
latent trait or predisposition in schizophrenia-spectrum disorders to ex-
hibit a deviant psychological profile or “schizotypy” that does not reach
the level of the clinical manifestations of schizophrenia. For example, SPD
individuals are protected from the severe cognitive deterioration and so-
cial deficits associated with chronic schizophrenia. This might be ex-
plained by a model that hypothesizes that these individuals possess great-
er frontal reserves and capacity to recruit other related brain regions to
compensate for dysfunctional areas during cognitive demands (Buchs-
baum et al., 2002; Siever & Davis, 2004). SPD individuals are also signifi-
cantly less vulnerable to psychosis than patients with schizophrenia, and
thus they are spared from multiple hospitalizations and long-term expo-
sure to psychotropic medication (Siever & Davis, 2004).
SPD also shares phenomenological features with schizoid and paranoid
personality disorders. For example, individuals with SPD and those with
schizoid personality disorder usually lack close friends or confidants.
However, in contrast to SPD, the social deficits observed in schizoid indi-
viduals are not secondary to cognitive-perceptual distortions or distrust of
others but to a lack of pleasure from casual or intimate relationships. SPD
also shares phenomenological characteristics with paranoid and border-
line personality disorders. For example, individuals with SPD and those
with paranoid personality disorder exhibit a significant degree of suspi-
ciousness. However, while the perceived hidden threatening meanings in-
fluence the behavior of subjects with paranoid personality disorder, this
thought content disorder is held with less conviction by those with SPD.
The overlap initially observed between SPD and borderline personality dis-
order is reduced when psychotic-like symptoms are viewed as transient
and dissociative in borderline PD but more relentless and unaccompanied
by affective instability in SPD (Kavoussi & Siever, 1992). Finally, the social
detachment of SPD overlaps with the social avoidance of avoidant person-
ality disorder, which also has been related to the schizophrenia spectrum
(Fogelson et al., 2007; Kendler et al., 1993b). Thus, the differential diag-
nosis of SPD is often with other personality disorders.

PREMORBID BACKGROUND
Findings of risk factors in the development of SPD have been inconsistent.
Berenbaum, Valera, and Kerns (2003) found childhood abuse to be associ-
656 CHEMERINSKI ET AL.

ated with both higher rates of self-reported schizotypy and clinician-

assessed symptoms of SPD. Conversely, Battle et al. (2004) failed to repli-
cate these findings in a study that compared SPD subjects with a de-
pressed control group. Interestingly, abuse has been associated with in-
creased dopamine and homovanillic acid levels (Glaser, 2000; Raine,
2006). Moreover, because abuse appears to be somewhat more associated
with cognitive-perceptual schizotypy features, it could partly account for
the hypothesized link between these schizotypal features and increased
dopamine (Siever et al., 1993).
Another related controversial issue in SPD is the existence of this and
other personality disorders in childhood. In the UCLA Follow-Up Study of
Childhood-Onset Schizophrenia Spectrum Disorders, Asarnow (2005)
provided a modified diagnosis of SPD to 12 children and assessed them for
up to 7 years following the initial intake. The author reported that the
most common clinical outcome for these children was continuing SPD,
supporting the hypothesis of continuity between childhood and later SPD.

LABORATORY STUDIES
Proposed biomarkers of SPD include abnormal results of specific struc-
tural, psychophysiological, and neurocognitive tasks. As described below,
these impairments are indicative of frontal and fronto-parietal-temporal
circuits dysfunction (or heteromodal association cortex) in the brain (Me-
sulam, 1998).

NEUROCOGNITIVE PERFORMANCE

The use of comprehensive neuropsychological batteries has recently per-

mitted the identification of specific neurocognitive impairments among
SPD individuals, compared to healthy control subjects (Mitropoulou et al.,
2002, 2005; Voglmaier, Seidman, Salisbury, & McCarley, 1997; Voglmaier
et al., 2005). Conversely, due to shared neurodevelopmental pathway ab-
normalities, the cognitive deficits observed in these individuals appear to
be similar, although less severe, than the ones observed in schizophrenia
(Kawasaki et al., 2004; Kurachi, 2003; Matsui et al., 2007; Mitropoulou et
al., 2002; Raine & Lencz, 1995; Siever & Davis, 2004; Suzuki et al., 2005;
Trestman et al., 1995; Voglmaier et al., 1997). On the other hand, while
these impairments are severely manifested across numerous cognitive
functions in schizophrenia, the dysfunctions observed in SPD are circum-
scribed to specific cognitive areas such as working memory and episodic
memory (Cadenhead, Perry, Shafer, & Braff, 1999; Lees Roitman et al.,
1997; Lenzenweger & Gold, 2000; Mitropoulou et al., 2005; Moritz &
Mass, 1997; Siever & Davis, 2004; Voglmaier et al., 1997, 2000). SPD in-
dividuals have been found to perform poorly on executive function tasks
such as the Wisconsin Card Sorting Test (Braff & Freedman, 2002; Difo-
rio, Walker, & Kestler, 2000; Trestman et al 1995; Voglmaier et al., 1997)
and the Stroop Color Word Interference Test and the Trail Making Test B
SCHIZOTYPAL PERSONALITY DISORDER657

(Mitropoulou et al., 2002; Trestman et al., 1995), as well as tests measur-

ing abstraction (Farmer et al., 2000; Voglmaier et al., 1997). It has been
suggested that poor performance on these tasks may be a result of im-
paired working memory (Gold, Carpenter, Randolph, Goldberg, & Wein-
berger, 1997; Goldman-Rakic, 1999; Mitropoulou et al., 2002; Saykin et
al., 1991). Working memory, a system necessary for the storage and ma-
nipulation of information (Baddeley, 1992), is thought to be subserved by
the dorsolateral prefrontal cortex (DLPFC) dopaminergic system (Barch,
2003; Lewis, Slabosz, Robbins, Barker, & Owen, 2005). Subtle deficits in
this region have been implicated in the neuropathology of clinical SPD
populations (Koenigsberg et al., 2003; Matheson & Langdon, 2008; Raine,
Sheard, Reynolds, & Lencz, 1992; Siever & Davis, 2004). The view that
working memory represents a core deficit of these populations is sup-
ported by results from a recent study by Mitropoulou et al. (2005). In this
study, SPD subjects (n = 82) performed significantly worse than healthy
volunteers (n = 63) and patients with personality disorders unrelated to
the schizophrenia spectrum (n = 44) on tasks of working memory, epi-
sodic memory, and delayed recall such as the Paced Auditory Serial Addi-
tion Test, WMS visual reproduction test, Dot test, and California Verbal
Learning Test. Working memory performance was demonstrated to ac-
count for the group differences. Deficits in tasks used to assess working
memory have been also described in nonclinical populations who exhibit-
ed either negative or positive schizotypy (Gooding & Tallent, 2003; Park,
Holzman, & Lenzenweger, 1995; Park & McTigue, 1997; Tallent & Good-
ing, 1999). Furthermore, in a recent study by Matheson and Langdon
(2008) of 87 university student participants with no known family history
of schizophrenia, impairment in executive working memory tests was as-
sociated with higher levels of both negative and positive schizotypy traits.
Another key area of cognitive impairment in SPD includes selective atten-
tion (Barch et al., 2004; Lees Roitman et al., 1997; Lenzenweger, 2001),
believed to be modulated by frontostriatal circuits, as well as verbal learn-
ing, which is modulated by the temporal cortex. Thus, SPD subjects show
impairment on tasks of initial word list learning and multitrial memory
learning (Bergman et al., 1998; Mitropoulou et al., 2002; Voglmaier et al.,
1997, 2000; Saykin et al., 1991). In a recent study by Dickey et al. (2005),
male (n = 64) and female (n = 40) neuroleptic-naive SPD subjects exhibited
lower vocabulary scores on the WAIS-R compared to healthy comparison
subjects, with male SPD subjects exhibiting more odd speech than female
SPD individuals.

NEUROCHEMICAL, FUNCTIONAL, AND STRUCTURAL STUDIES

It is hypothesized that the severity of the psychotic-like symptoms of SPD

correlates with increased levels of the HVA, a DA metabolite. The plasma
and CSF concentrations of HVA were found to be significantly increased in
SPD subjects compared with controls and other patients with personality
658 CHEMERINSKI ET AL.

disorders (Siever & Davis 2004). Conversely, the plasma levels of HVA
were found to be reduced in SPD subjects who exhibited poor cognitive
performance (Siever et al., 1993) or deficit-like symptoms (Amin et al.,
1995). The administration of the DA agonist amphetamine to these sub-
jects reduces their cognitive deficits (Kirrane et al., 2000). In contrast to
schizophrenia, this improvement is not followed by the appearance of psy-
chosis (Abi-Dargham et al., 1998; Kirrane et al., 2000; Siever et al., 2002).
This might be explained by the fact that striatal DA release, induced either
by amphetamine (Abi-Dargham, Mawlawi, & Lombardo, 2002; Siever et
al., 2002) or by physiological stressors (alpha 2-deoxyglucose infusion;
Mitropoulou et al., 2004) is significantly lower in SPD than that observed
in schizophrenia during illness exacerbation. The reduced DA activity
might be compatible with reduced striatal volume in SPD patients, com-
pared to patients with schizophrenia. The striatal structures reported to
suffer decreased volume in SPD subjects include the caudate (Koo, Levitt,
& McCarley, 2006; Levitt, McCarley, & Dickey, 2002; Levitt et al., 2004)
and the putamen (Shihabuddin et al., 2001). However, in contrast to
schizophrenia, the medial dorsal nucleus of the thalamus has not been
consistently observed to be reduced in these subjects (Byne et al., 2001).
Reductions in thalamic nuclei might be parallel to the reductions in as-
sociated cortical regions (i.e., temporal but not frontal volume reductions).
Other regions that usually are reduced in volume in schizophrenia but not
in SPD include middle temporal regions such as the amygdala and hip-
pocampal complex (Gur et al., 2000; Seidman, Pantelis, & Keshavan,
2003; Takahashi, Suzuki, & Zhou, 2006). Another protective mechanism
that makes SPD patients less vulnerable to psychosis compared to pa-
tients with schizophrenia might result from DA-mediated inhibition of the
putamen, an area rich in D2 receptors, by its ventral area. Conversely,
hyperactivity of subcortical D2 in schizophrenia has been associated with
the emergence of psychotic symptoms. Functional imaging studies per-
formed by our group (Shihabuddin et al., 2001) have shown that SPD
subjects show increased metabolic activity in the ventral putamen com-
pared to patients with schizophrenia and healthy volunteers. Additionally,
those SPD subjects with greater activation in this area exhibited fewer
psychotic-like symptoms than those with reduced activation.
The frontal cortex volumetric decreases in SPD subjects do not occur to
the same extent in schizophrenia (Kawasaki et al., 2004; Siever & Davis,
2004; Siever et al., 1990b, 2002; Suzuki et al., 2005). This lack of signifi-
cant frontal volume cortical reduction may account for the significantly
lower cognitive and social deterioration in SPD subjects compared to pa-
tients with schizophrenia. In a recent study of cortical gray/white matter
volumes in a large sample of unmedicated schizophrenia-spectrum pa-
tients (SPD, n = 79; schizophrenia, n = 57) and 148 healthy controls, Ha-
zlett et al. (2008) showed that the frontal cortical volume reduction in SPD
was only about half of that observed in schizophrenia and may not even
distinguish SPD subjects from healthy controls (Buchsbaum et al., 2002;
SCHIZOTYPAL PERSONALITY DISORDER659

Siever, 2000). An additional protective factor that prevents SPD subjects

from suffering significant cognitive deficits is their ability to recruit differ-
ent PFC areas as a compensatory mechanism during cognitive tasks (Siev-
er & Davis, 2004; Trestman et al., 1995). For example, results from a PET
study by Buchsbaum at al. (2002) showed that SPD patients exhibited
less activity than healthy individuals in the precentral gyrus and increased
activity of the middle frontal gyrus. In an fMRI study of working memory,
SPD subjects showed greater frontal pole (BA10) activation (presumably
compensatory) than healthy controls (Koenigsberg et al., 2005).

PSYCHOPHYSIOLOGICAL STUDIES

Individuals with schizophrenia-spectrum personality disorder have defi-

cits in information processing that might result from difficulty in inhibit-
ing trivial internal and external stimuli. This inhibitory phenomenon can
be examined by psychophysiological paradigms. Abnormalities in these
paradigms might help define an inhibitory endophenotype.
Prepulse inhibition (PPI) represents the ability of the higher brain cen-
ters to filter sensory information (Braff & Geyer, 1990; Davis, Gendelman,
Tischler, & Gendelman, 1982; Dawson, Schell, Swerdlow, & Filion, 1997;
Geyer & Braff, 1987; Graham, 1975). Besides schizophrenia, reduced PPI
was found to be present in SPD subjects and in asymptomatic first-degree
relatives of schizophrenia patients (Cadenhead et al., 1993, 2000a, 2002;
Evans, Gray, & Snowden, 2005; Kumari, Das, Zachariah, Ettinger, &
Sharma, 2005). In SPD, PPI is associated with a general schizotypy score
reflecting a general “proneness to psychosis” or vulnerability (Abel, Jolley,
Hemsley, & Geyer, 2004).
Eye-tracking impairments, hypothesized to be genetic vulnerability
markers for schizophrenia (Boudet, Bocca, & Chabot, 2005), were found
to be present in SPD but not other personality disorders (Siever et al.,
1989, 1990a). These impairments have also been associated with high
degree of schizotypy in nonclinical populations such as adult healthy vol-
unteers (Lenzenweger & O’Driscoll, 2006), college students (Siever, Coursey,
Alterman, Buchsbaum, & Murphy, 1984), and military conscripts aged
18–25 (Smyrnis et al., 2007a). A study by Holahan and O’Driscoll (2005)
found that a significantly larger percentage of schizotypy individuals with
positive-like symptoms than controls showed elevated antisaccade error
rates on standard antisaccade tasks. Conversely, the percentage of schizo-
typy participants with negative-like symptoms who exhibited elevated an-
tisaccade error rates did not differ from that of control subjects. These
findings have not been replicated by other authors. In a study comparing
29 SPD, 17 schizophrenia, and 25 normal subjects, Brenner, McDowell,
Cadenhead, and Clementz (2001) reported that SPD subjects were more
similar to normal than to schizophrenia subjects on antisaccade and de-
layed response variables.
Several authors have found P300 amplitude to be reduced in SPD sub-
660 CHEMERINSKI ET AL.

jects (Kimble, Lyons, & O’Donnell, 2000; Klein, Berg, Rockstroh, & Andre-
sen, 1999; Mannan, Hiramatsu, Hokama, & Ohta, 2001; Niznikiewicz et
al., 2000; Trestman et al., 1996). However, reports of delayed P300 latency
in these subjects have been less consistent (Kutcher, Blackwood, Gaskell,
Muir, & St. Clair, 1989; Mannan et al., 2001; Nuchpongsai, Arkaki, Lang-
man, & Ogura, 1999; Trestman et al., 1996). Additionally, reduced audi-
tory P300 amplitudes and delayed P300 latencies were exhibited by non-
clinical populations with higher scores on the Schizotypal Personality
Questionnaire (SPQ; Gassab et al., 2006).
P50 ERP assesses attention and information processing (Cadenhead,
Light, Geyer, & Braff, 2000b). Impaired P50 wave suppression has been
identified as a vulnerability marker for the sensory gating deficits observed
not only in patients with schizophrenia and their first-degree relatives,
but also in SPD subjects (Cadenhead et al., 2000b; Cadenhead, Light,
Geyer, McDowell, & Braff, 2002; Clementz, Geyer, & Braff, 1998; Patter-
son et al., 2008; Siegel, Waldo, Mizner, Adler, & Freedman, 1984; Waldo et
al., 1991, 2000). Additionally, Croft, Lee, Bertolot, and Gruzelier (2001)
found that healthy volunteers with higher schizotypal characteristics ex-
hibited poorer P50 suppression.
Certain variations of Catechol-O-methyltransferase (COMT), a candi-
date gene for the modulation of PFC-mediated cognitive tasks performance
(Tunbridge, Bannerman, Sharp, & Harrison, 2004), are hypothesized to
play a role in the phenomenology of SPD. This gene is believed to play a
crucial role in memory function by its regulatory action on the DA level of
the PFC (Tan, Callicott, & Weinberger, 2007). Thus, PFC DA activity is in-
creased when, due to a mutation of the COMT gene, methionine (Met) is
substituted for valine (Val) at codon 108/158 (Bilder et al., 2002; Egan,
Goldberg, & Kolachana, 2001; Joober, Gauthier, & Lal, 2002; Malhotra,
Kestler, & Mazzanti, 2002; Mattay et al., 2003). Conversely, when the Val
in this gene is substituted for Met, DA transmission is reduced due to
greater catabolism of DA in the PFC (Weinberger, Egan, & Bertolino, 2001).
These findings were replicated in other disorders associated with DA ab-
normalities such as Parkinson’s disease (Foltynie, Goldberg, & Lewis,
2004), attention-deficit/hyperactivity disorder (Bellgrove, Domschke, &
Hawi, 2005), and schizophrenia (Glatt, Faraone, & Tsuang, 2003). Recent
studies by our group (Leung, McClure, Siever, Barch, & Harvey, 2007;
Minzenberg, Xu, & Mitropoulou, 2006) demonstrated that SPD subjects
with the Val/Val genotype exhibited worse performance on executive func-
tioning and PFC-dependent memory tasks independent of clinical status.
Additionally, Leung et al. (2007) demonstrated that the tasks that are
most sensitive to COMT variation are those maximally relevant to DA
function such as the AX-CPT and N-back tests. These findings were repli-
cated in a recent study by Smyrnis et al. (2007b) in which those SPD sub-
jects with higher Val loading showed not only worse cognitive performance,
but also more severe negative schizotypy. Additionally, in a study of Greek
conscripts, Stefanis et al. (2007a) showed that carriers of the COMT
SCHIZOTYPAL PERSONALITY DISORDER661

Val(158)Met Val allele are more susceptible to psychosis as a result of

stressful life events than those with the Met/Met genotype.
A recent study that assessed a risk for psychosis haplotype of the Pro-
line Dehydrogenase gene found that healthy individuals who displayed
the markers for the psychosis variant risk factor presented with PPI and
verbal memory deficits as well as higher anxiety and schizotypal personal-
ity traits (Roussos, Giakoumaki, & Bitsios, 2009). Stefanis et al. (2007b,
2008) showed in two different studies that common variants in G-protein
signaling 4 (RGS4) and D-amino acid oxidase (DAAO) genes were associ-
ated with negative schizotypal personality traits among a large cohort of
young healthy individuals, while dysbindin (DTNBP1) variants were asso-
ciated with positive and paranoid schizotypy scores. Finally, preliminary
results from our group using the custom Consortium on the Genetics of
Schizophrenia (COGS) 1,536-SNP chip showed that polymorphisms in
ERBB4, NRG1, and genes involved in glutamate, dopamine, GABA, and
serotonin receptors signaling, as well as cell signal transduction, were
highly associated with categorical clinical diagnosis (SPD vs. healthy con-
trols) and dimensional quantitative phenotypes of SPD, including cogni-
tive impairment, interpersonal deficits, and paranoia (Siever & Roussos,
unpublished data).

EPIDEMIOLOGICAL AND FAMILY STUDIES

Community studies of SPD have reported rates ranging from 0.6% in Nor-
wegian samples (Torgersen, 2009; Torgersen, Kringlen, & Cramer, 2001)
to 4.6% of a U.S. community sample (Johnson, Smailes, Cohen, Brown, &
Bernstein, 2000). The prevalence of this disorder in clinical settings has
also been found to be infrequent (1.9%) (Stuart et al., 1998; Zimmerman,
Rothchild, & Chelminski, 2005). SPD appears to be more prevalent in
males (Downhill et al., 2000). Furthermore, male SPD subjects exhibit
higher scores on measures of negative schizotypy while females score
higher than males on positive schizotypy (Fossati, Raine, Carretta, Leo-
nardi, & Maffei, 2003). It is worth examining if the higher self-reported
rates of schizotypy in Asian Americans and African Americans (e.g.,
Chmielewski, Fernandes, Yee, & Miller, 1995) reflect a relative lack of cul-
tural sensitivity of the DSM diagnostic or, conversely, could be explained
by culture-specific environmental stressor–genotype interaction (Raine,
2006).
A genetic basis for SPD is supported by reports of increased incidence of
this personality disorder in relatives of SPD probands (Siever, Bernstein,
& Silverman, 1996). However, genetic studies of this disorder have consis-
tently demonstrated a strong shared genetic liability with schizophrenia
and other schizophrenia-spectrum diagnoses (Baron, Gruen, Asnis, &
Kane, 1983; Baron, Gruen, Asnis, & Lord, 1985; Battaglia, Bernardeschi,
Franchini, Bellodi, & Smeraldi, 1995; Battaglia et al., 1991; Cadenhead &
Braff, 2002; Kendler & Gruenberg, 1984; Kendler et al., 1993b, Kendler,
662 CHEMERINSKI ET AL.

McGuire, Gruenberg, & Walsh, 1995a, Kendler, Neale, & Walsh, 1995b;
Kety, Rosenthal, Wender, Schulsinger, & Jacobsen, 1975; Siever, 2005).
Additional support for a common genetic substrate for these disorders
was provided by adoption and family studies (Frangos, Athanassenas, Tsi-
tourides, Katsanou, & Alexandrakou, 1985; Gershon et al., 1988; Kendler,
1985, 1988; Kendler, Gruenberg, & Strauss,, 1981; Kendler et al., 1993a;
Kendler, Gruenberg, & Kinney, 1994; Lichtermann, Karbe, & Maier, 2000;
Tienari, Wynne, & Läksy, 2003) as well as linkage methods (Fanous et al.,
2007). The genetic relationship to schizophrenia appears to be closer when
certain features of the factor structure of SPD are considered. For exam-
ple, several authors have suggested that social and cognitive deficits (i.e.,
deficit-like traits) underlie the core pathology across the spectrum and,
compared to positive psychotic-like SPD symptoms, are associated with a
closer genetic relationship to schizophrenia (Gunderson, Wynne, & Läksy,
1983; Ingraham & Kety, 2000; Kendler, 1985; Torgersen, Onstad, Skre,
Edvardsen, & Kringlen, 1993; Webb & Levinson, 1993). Furthermore, re-
sults from a twin study by Kendler et al. (1991) suggest that positive and
negative symptoms of SPD might represent two relatively independent
heritable dimensions. Thus, in SPD and other disorders of the schizophre-
nia spectrum, a set of genetic factors manifested as social and cognitive
deficits (“spectrum phenotype”) might be transmitted independently from
another distinct genetic factor set related to psychosis (“psychotic pheno-
type”) (Siever & Davis, 2004).

FOLLOW-UP STUDIES
Like other personality disorders, SPD is conceptualized in the DSM as a
lifelong disorder with an early adulthood onset and a stable course. The
outcome of SPD subjects has been described as falling between that of
patients with schizophrenia and that of patients with other personality
disorders (McGlashan, 1986). Additionally, phenomenological descrip-
tions of SPD have recognized that many of the symptoms present in this
disorder, such as social deficits, odd speech/behavior, and magical ide-
ation, are also observed in prodromal phases of schizophrenia (Bedwell &
Donnelly, 2005). These behavioral abnormalities might provide further
understanding of the relationship between schizophrenia and the schizo-
phrenia-spectrum personality disorders. However, the study of these
symptoms is complicated by the fact that a significant number of individ-
uals displaying schizotypal psychopathology later go on to develop schizo-
phrenia. Reports of this proportion vary greatly. While Fenton and Mc-
Glashan (1989) found that 17% of a sample of SPD individuals later
received diagnosis of schizophrenia, Walker, Kestler, Bollini, and Hoch-
man (2004) estimated that up to 40% of SPD adolescents follow this pro-
gression. By definition, these adolescents do not have the enduring symp-
tomatology characteristic of SPD as they go on to develop psychosis. These
adolescents also tend to have more prominent ideas of reference and in-
SCHIZOTYPAL PERSONALITY DISORDER663

vestment in fixed paranoid ideas than those who are diagnosed with SPD
in the adult years. Conversely, it is unclear whether more typical SPD in-
dividuals rarely go on to develop schizophrenia, although longitudinal ob-
servations suggest they do not (Shea et al., 2004). A prospective study of
SPD adolescents reported that up to 40%–50% of them later developed
this disorder (Yung et al., 2003). Additionally, findings from retrospective
studies of schizophrenia patients suggest that a significant number of
them might have exhibited schizoid and schizotypal traits before the onset
of illness (Fish, 1986; Foerster, Lewis, Owen, & Murray, 1991; Hogg, Jack-
son, Rudd, & Edwards, 1990; Peralta, Cuesta, & de Leon, 1991). Con-
versely, in a series of studies of the rates of SPD traits in high-risk popula-
tions of the New York High-Risk Project, Squires-Wheeler and colleagues
(Squires-Wheeler, Skodol, Bassett, & Erlenmeyer-Kimling, 1989; Squires-
Wheeler, Skodol, & Erlenmeyer-Kimling, 1992; Squires-Wheeler, Skodol,
Friedman, & Erlenmeyer-Kimling, 1988) failed to find specificity of SPD
premorbid traits to schizophrenia. Furthermore, Olin et al. (1997) found
that the childhood personality of individuals later diagnosed with SPD was
significantly different from that of children who later developed schizo-
phrenia. Thus, while high rates of schizophrenia patients exhibit premor-
bid behavioral disturbances, there is currently no conclusive evidence as
to whether a schizophrenia-spectrum personality disorder is a necessary
transitional stage occurring before the development of this disorder (Siev-
er & Davis, 2004). On the other hand, more recent reports have suggested
that in SPD individuals, the symptom features of this disorder actually
abate with age (Fossati et al., 2003; Mata, Mataix-Cols, & Peralta, 2005,
McGlashan et al., 2005). Grilo et al. (2004) theorized that dimensional
measures in SPD are more stable than categorical ones after finding that
61% of 78 subjects showed remission of DSM-IV SPD symptoms within 2
years. More recently, Skodol et al. (2007) studied 520 patients with differ-
ent personality disorders who were repeatedly evaluated over 4 years and
found that higher rates of remission from SPD were significantly associ-
ated with positive achievement experiences and positive interpersonal re-
lationships during childhood or adolescence. Raine (2006) hypothesized
that certain neurodevelopmental processes such as increased myelination
of white matter as well as social circumstances such as marriage may
ameliorate SPD symptoms.
Results from a study by Ullrich et al. (2007) suggest that SPD subjects
exhibit poor life success in the community. Specifically, compared to sub-
jects with other personality disorders, SPD subjects displayed low scores
in factors representing “status and wealth” and “successful intimate rela-
tionships.” However, when analyzing the results of these studies, it is
worth considering that those SPD subjects assessed in a clinical setting
might show worse social adjustment and global functioning than higher
functioning SPD individuals living in the community. Furthermore, a sig-
nificant number of young individuals meeting criteria for SPD in cross-
sectional studies might actually be in the prodromal stage of schizophre-
nia (Seeber & Cadenhead, 2005).
664 CHEMERINSKI ET AL.

TREATMENT-RELATED STUDIES
The treatment of the psychotic-like symptoms (e.g., ideas of reference,
magical thinking, and suspiciousness) of SPD with antipsychotic medica-
tion is substantiated by the phenomenological similarity of these symp-
toms with the psychosis of chronic schizophrenia. However, in contrast to
patients with schizophrenia, SPD subjects only rarely receive any type of
psychiatric treatment. Initial medication studies of SPD employed first-
generation antipsychotics. These studies suffered from design flaws such
as lack of randomization and inclusion of populations with other person-
ality disorder besides SPD. Despite their shortcomings, these studies were
able to demonstrate a reduction of psychotic-like symptoms of SPD with
first-generation antipsychotics such as thiothixene (Goldberg et al., 1986;
Serban & Siegel, 1984), haloperidol (Hymowitz, Frances, Jacobsberg, Sick-
les, & Hoyt, 1986; Serban & Siegel, 1984; Soloff et al., 1989), and loxapine
(a metabolite of the antidepressant amoxapine with antipsychotic activity;
Jensen & Andersen, 1989) compared to placebo. More recent studies of
the effectiveness of antipsychotic medication for SPD have employed sec-
ond-generation agents. For example, Koenigsberg et al. (2003) showed
that SPD patients randomly assigned to a risperidone treatment group
(n = 14) experienced a significant decline in the positive, negative, and
general score of the Positive and Negative Syndrome Scale (PANSS) com-
pared to those patients on placebo (n = 9). Due to the high levels of soma-
tization in SPD patients, the authors concluded that dosages of risperi-
done of 1 mg/day or less may be best tolerated by these patients. On the
other hand, results from this study failed to demonstrate a reduction of
depressive symptoms of SPD with the use of risperidone. More recently,
this agent was also found to be ineffective in the treatment of the cognitive
deficits of SPD individuals (McClure et al., 2009). In contrast to risperi-
done, a flexible dose of olanzapine (average 9.32 mg/day) utilized in a 26-
week, open-label study by Keshavan, Shad, Soloff, and Schooler (2004) was
associated in 11 SPD patients with significant improvements not only in
psychosis and overall functioning scores, but also in depression. In these
patients, olanzapine was well tolerated but led to significant weight gain.
There is also a lack of reliable evidence showing that in SPD these symp-
toms are improved after the use of antidepressant medication (Herpertz et
al., 2007). For example, an open-label trial of fluoxetine failed to show
significant improvement of mood or psychoticism in SPD patients without
comorbid borderline personality disorder (Markovitz, Calabrese, Schulz, &
Meltzer, 1991).
Early phenomenological descriptions of the schizophrenia spectrum
have recognized that these disorders share similar cognitive deficits. Fur-
thermore, since the DA system has been identified as an important modu-
lator of cognitive processes (Goldman-Rakic, Muly, & Williams, 2000), DA
agonists such as amphetamine have become the main agents for the treat-
ment of these deficits. In addition, a study by Kirrane et al. (2000) showed
that an equal dose of amphetamine resulted in reduction in errors on
SCHIZOTYPAL PERSONALITY DISORDER665

working memory and verbal learning tests in SPD patients but not in oth-
er personality-disordered patients.
Amphetamine acts largely through D1 receptors in the frontal cortex
that are known to modulate visuospatial working memory performance in
primates (Williams & Goldman-Rakic, 1995). Pergolide is a D1/D2 agonist
with preferential activity at D1 receptors (Fici, Wu, VonVoigtlander, &
Sethy, 1997). Initial findings from a recent cognitive enhancement study
by our group showed that, compared to placebo, a 2-week administration
of escalating doses of pergolide led to improved performance of working
memory in SPD subjects without clinical worsening (McClure et al., 2010).
However, recent reports (Schade, Andersohn, & Suissa, 2007; Zanettini,
Antonini, & Gatto, 2007) raised concerns about the possibility of increased
valvular heart disease after the use of pergolide and other ergot-derived
dopamine agonists. Dihydrexidine is another pharmacological compound
with a high ratio of D1/D2 activity. In a recent study by George et al.
(2007), the administration of this compound failed to improve cognitive
deficits of patients with schizophrenia. Nevertheless, this cognitive en-
hancement may be detected more sensitively in SPD populations with less
severe and more readily reversible cognitive deficits than those of schizo-
phrenia. Moreover, in contrast to patients with schizophrenia, SPD sub-
jects do not experience secondary worsening of psychotic-like symptoms
with DA agonists. This might suggest that, despite their common cortical
hypodopaminergia, SPD subjects do not suffer from the subcortical hyper-
dopaminergia present in patients with schizophrenia (Siever & Davis,
2004). In addition to the DA system, Norepinephrine (NE) has been found
to have a significant role in the regulation of working memory and atten-
tion functions of the PFC. In particular, NE increases the “signal/noise”
ratio in the processing of sensory stimuli, enhances long-term memory
consolidation in the amygdala and hippocampus (Ramos & Arnsten,
2007), and modulates cognitive flexibility for insight-based problem solv-
ing (Choi, Novak, Hillier, Votolato, & Beversdorf, 2006). Guanfacine is an
NE agonist agent that, acting on α2a postsynaptic receptors located in the
PFC, has the potential to be an effective option for the treatment of the
cognitive deficits in the schizophrenia-spectrum disorders (Friedman,
Stewart, & Gorman, 2004). In a recent 4-week, placebo-controlled, dou-
ble-blind study of guanfacine, McClure et al. (2007) reported that follow-
ing treatment with this agent, SPD subjects, but not subjects with other
personality disorders, displayed improvement in context processing but
not in verbal and visuospatial episodic memory tasks. This selective im-
provement in cognitive functions suggests that working memory deficits
may in fact underlie the range of cognitive deficits within the spectrum.

IMPLICATIONS FOR THE PROPOSED DSM REVISION OF SPD

Findings from the phenomenological, genetic, psychophysiological, neuro-
chemical, and treatment response studies described here have provided
666 CHEMERINSKI ET AL.

support for the conceptualization of the schizophrenia spectrum as a con-

tinuum of related disorders differing in symptom severity instead of the
more rigid categorical disorders included in the DSM classification. Fur-
thermore, different authors have criticized the categorical approach prev-
alent in the DSM classification criteria as too strict to capture the phe-
nomenological complexities of personality disorders. Presently, a revision
of these criteria is being undertaken by the DSM-5 Personality Disorders
Work Group in order to improve the current classification system. For this
purpose, a more encompassing trait system for the diagnosis of personal-
ity disorders has been proposed. In this system, an initial general criterion
of personality disorder characterizes individuals with chronic personality
dysfunction manifested by impaired sense of self and capacity for close
relationships. A prototypic diagnosis is made only when the individual
matches exclusively the criteria for that diagnosis. SPD is one of the se-
lected prototypical personality disorders to be included in the DSM-5. Pro-
totypical disorders are characterized by core impairments in personality
functioning and different levels of abnormal personality traits or “facets”
grouped in six broad dimensional domains: Negative Emotionality, Intro-
version, Antagonism, Disinhibition, Compulsivity, and Schizotypy. The
proposed traits were selected by experts in personality assessment as rep-
resentative based on existing measures of abnormal personalities. Thus,
the domains that will characterize the DSM-5 schizotypal prototypical dis-
order correlate well with their counterpart DSM-IV-TR criteria. For exam-
ple, the Negative Emotionality domain, which includes traits such as sus-
piciousness and anxiousness, correlates with the following DSM-IV-TR
criteria: suspiciousness or paranoid ideation and excessive social anxiety
that does not diminish with familiarity and tends to the associated with
paranoid fears rather than negative judgments about self. Additionally,
the Introversion domain, which includes traits such as social withdrawal
and restricted affectivity, correlates with the following DSM-IV-TR criteria:
lack of close friends or confidants other than first-degree relatives, and
inappropriate or constricted affect. On the other hand, the Schizotypy do-
main, which includes traits such as eccentricity and unusual beliefs, cor-
relates with the following DSM-IV-TR criteria: odd beliefs or magical think-
ing that influences behavior and is inconsistent with subcultural norms,
and behavior or appearance that is odd, eccentric, or peculiar. Lastly, an
important factor supporting the inclusion of SPD as a prototypical DSM-5
personality disorder is the fact that many of its current criteria have been
validated by external validators (e.g., neurochemical, neuropsychological,
functional, and structural findings). For example, as mentioned in previ-
ous sections, the psychotic-like symptoms of SPD correlate with elevated
levels of the DA metabolite HVA; which may reflect dopamine release,
which is increased in SPD compared to controls. These levels are signifi-
cantly higher in SPD than in other personality disorders and in healthy
control subjects, but lower than in schizophrenia. Moreover, smaller vol-
umes of striatal structures (e.g., caudate and putamen) in SPD compared
SCHIZOTYPAL PERSONALITY DISORDER667

to schizophrenia result in lower striatal DA release mediated by amphet-

amine or physiological stressors in SPD individuals. This has been hy-
pothesized to result in significantly lower vulnerability to psychosis in
these patients, compared to those with schizophrenia. The positive-like
symptoms of SPD have also been found to be correlated with psychophys-
iological findings such as elevated antisaccade error rates and to improve
after the use of antipsychotic medication. Similar to positive-like symp-
toms, the negative-like symptoms and cognitive deficits of SPD have been
assessed with the use of external validators. These are mostly associated
to the fronto-parietal-temporal circuit dysfunction prevalent in this disor-
der. In schizophrenia, frontal cortex volumetric reduction has been shown
to correlate with severity of cognitive and social deterioration. The neuro-
developmental pathway abnormalities shared by SPD and schizophrenia
patients result in their similar cognitive deficit profile. However, several
authors have demonstrated that these deficits are less severe and more
circumscribed to specific cognitive areas in SPD individuals. This has
been hypothesized to be a result of reduced frontal cortical volume in SPD
subjects, which is about half of that observed in patients with schizophre-
nia and not significantly different from healthy controls. While elevated
plasma levels of HVA has been associated in SPD subjects with severity of
positive-like symptoms, the opposite is true when considering their cogni-
tive performance or deficit-like symptoms. In fact, SPD subjects with the
Val/Val genotype of the COMT gene, associated with HVA level reductions
due to greater catabolism of DA in the PFC, normally exhibit worse per­
formance on executive functioning and PFC-dependent memory tasks in-
dependent of clinical status. In summary, the external validation of its
criteria supports the inclusion of SPD as a valid diagnostic entity to be
included in the DSM-5 schizophrenia-spectrum disorders, while being de-
fined and also referenced as a personality disorder with implications for
differential diagnoses with other personality disorders.

CONCLUSIONS
The study of SPD has provided increasing knowledge of the pathophysio-
logical factors that give rise to schizophrenia. The main reason for this
relationship is the shared genetic, phenomenological, and neurobiological
characteristics of these two disorders. Unfortunately, this phenomenologi-
cal overlap has hindered the discovery of reliable diagnostic indicators to
distinguish schizotypy from psychosis. On the other hand, current data
support the existence of a more readily reversible cognitive and social def-
icit and a decreased vulnerability to psychotic exacerbations in SPD com-
pared to schizophrenia. The clinical implication of this phenomenon is
presently recognized by different research groups who evaluate SPD indi-
viduals in studies assessing the nature of the compensatory processes
that provide a buffer against schizophrenia.
Despite its phenomenological overlap with schizophrenia, SPD has been
668CHEMERINSKI ET AL.

recognized as a distinct disorder whose criteria represent the persistent

maladaptive patterns of a personality disorder rather than the overt symp-
tomatic break from reality of a psychotic disorder. Furthermore, several
studies have validated its criteria, prompting the DSM-5 Personality Disor-
ders Work Group to acknowledge SPD among the prototypical personality
disorders in the next edition of this manual. Furthermore, given its well-
documented relationship to chronic schizophrenia and to be congruent
with the proposed ICD-11, SPD will be primarily coded as a schizophre-
nia-spectrum disorder in the psychosis section of DSM-5.

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