Journal of Personality Disorders, 27(6), pp.

795–805, 2013
© 2013 The Guilford Press

PARANOID PERSONALITY DISORDER

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

Paranoid personality disorder (PPD) is currently included in DSM-IV’s

“odd cluster” or “cluster A.” In the present article, the authors review
available information pertaining to the psychometric properties of PPD,
as derived from the relevant literature and from databases of personal-
ity disorder study groups. There is comparatively little published evi-
dence for the reliability and validity of PPD, and researchers by and
large have tended not to study the disorder, either because of investiga-
tors’ difficulty recruiting individuals with PPD into research studies, or
(as seems more likely) because the trait-paranoia from which many
psychiatric patients suffer has seemed better explained by other DSM-
IV disorders on Axis I and/or Axis II than by PPD. Given the scant em-
pirical evidence on PPD, it seems reasonable to remove it as an inde-
pendent diagnosis from the next edition of DSM, and instead to
encourage clinicians to code trait-paranoia using a dimensional ap-
proach.

CLINICAL DESCRIPTION/SYMPTOM PICTURE

A lifelong tendency of certain nonpsychotic individuals to respond to other
people with habitual and characteristic suspiciousness has been noted by
writers on mental health since at least Kraepelin (1921), and paranoid
personality disorder (PPD) has been present in every edition of the Diag-
nostic and Statistical Manual, including the first. PPD’s acceptance into
the official nomenclature thus predated that of schizotypal personality
disorder (SPD), which was not introduced until DSM-III but since then, as
we shall see, has in large part subsumed PPD in research and clinical
practice.
Since the introduction of DSM-III, in fact, PPD has been among the least
studied of the personality disorders, with relatively few empirical investi-
gations specifically devoted to it in the published literature. Recent de-
scriptive information about PPD is derived largely from broad-based epi-
demiological studies of personality disorders as a whole (e.g., Coid, Yang,
Tyrer, Roberts, & Ullrich, 2006), plus examinations of the cluster A per-

This article was accepted under the editorship of Paul S. Links.

From James J. Peters VA Medical Center (J. T., E. C., P. R., L. J. S.).
Address correspondence to Larry J. Siever, Bronx VA Medical Center (OOMH), 130 W Kings-
bridge Rd., Bronx, NY 10468; E-mail: [email protected]

795
796 TRIEBWASSER ET AL.

sonality disorders and their relationship to schizophrenia (e.g., Kendler,

Myers, Torgersen, Neale, & Reichborn-Kjennerud, 2007), although this
latter group of studies tends to focus on SPD rather than PPD (e.g., Ha-
zlett et al., 2008; Torgersen et al., 2002). There are virtually no published
neurobiological studies devoted exclusively—or even primarily—to PPD,
and there is almost no published somatic or psychotherapeutic treatment
research. This academic neglect has persisted despite evidence that PPD
is fairly common in both clinical (Molinari, Ames, & Essa, 1994) and gen-
eral (Torgersen, Kringlen, & Cramer, 2001) populations; in clinical sam-
ples, it occurs at a rate about average for the DSM personality disorders
(9.7%) (Stuart et al., 1998; Zimmerman, Rothschild, & Chelminski, 2005),
although its prevalence varies considerably (13.9% to 4.2%). Moreover,
PPD is one of the three personality disorders most strongly associated
with reduction in quality of life (Cramer, Torgersen, & Kringlen, 2006;
Grant et al., 2004), and it is associated with decreased functioning as
measured by the Global Assessment of Functioning Scale (GAF) (Crawford
et al., 2005). In a sample of clients at a homeless drop-in center, PPD was
the most prevalent personality disorder diagnosed (Connolly, Cobb-Rich-
ardson, & Ball, 2008).
Two possible reasons for the relative lack of attention paid to PPD ap-
pear salient. First, paranoia itself, especially if it is a dominant tempera-
mental feature, may militate against the individual presenting either for
treatment (Kelly, Casey, Dunn, Ayuso-Mateos, & Dowrick, 2007) or for
inclusion in studies. Hence, individuals in whom paranoia is a key compo-
nent of their problems in living may be precisely those individuals who are
the most difficult to engage in therapy or psychopharmacology or to re-
cruit or retain in research trials. This may be in contradistinction to other
personality-disordered populations, some of whose members either tend
to seek treatment fairly avidly (e.g., many patients with borderline person-
ality disorder [BPD]) or to be brought into treatment by outside forces
(e.g., many patients with antisocial personality disorder [ASPD]). It may
also be that the symptoms of PPD are more ego-syntonic than, for exam-
ple, those of cluster C personality disorder patients, who typically experi-
ence considerable distress because of their anxieties or inhibitions. Be-
cause of their use of accusatory projection, PPD patients may be the most
highly prone of all psychiatric patients to locate the source of their prob-
lems somewhere other than within themselves. Patients with PPD may be
the purest exemplars of the old saying that an Axis I disorder is something
one has, whereas an Axis II disorder is something one is.
Second, it may be that researchers have not examined PPD because of
an underlying ambivalence about the psychometric properties of the diag-
nosis itself, particularly its divergent validity: Dimensional paranoia is a
key feature of several different disorders, including, most obviously, the
psychotic disorders on Axis I. In particular, delusional disorder, which—
like PPD—can encompass nonbizarre paranoia and need not be accompa-
nied by a catastrophic global decline in functioning, may capture much of
PARANOID PERSONALITY DISORDER797

the symptomatology that might otherwise have been ascribed to PPD.

Moreover, the hypervigilance symptoms of posttraumatic stress disorder
(PTSD), along with the associated PTSD feature of “constantly feeling
threatened,” are highly similar to, and indeed can be indistinguishable
from, paranoia. Among the personality disorders, SPD includes paranoia
among its DSM-IV criteria, and BPD’s DSM-IV symptoms include “tran-
sient, stress-related paranoid ideation.” The excessive competitiveness of
a patient with narcissistic personality disorder (NPD)—reflected in the
DSM-IV criterion, “is often envious of others or believes that others are
envious of him or her”—can degenerate into suspicions that some other
person is trying to undermine the patient, or into pathological jealousy,
with its attendant exaggerated or inaccurate accusations. These tenden-
cies to assign either blame or malign intentions to others, although stem-
ming from narcissism, may overlap with paranoia. Thus, although comor-
bidity is the rule, not the exception, in mental disorders, it may be that in
the case of PPD, there frequently is a sense among clinicians and research-
ers that even if a patient meets criteria for the diagnosis, the pertinent
signs and symptoms are better accounted for by another diagnosis(es), for
which the individual also meets criteria, and which provide(s) a more in-
clusive or compelling formulation of the individual’s difficulties.
Zimmerman, Chelminski, and Young (2008), in one of the few published
epidemiological studies of personality disorders that included data about
subjects with only one personality disorder, did find at least some cases of
“isolated” PPD, although it is unclear whether these individuals also had
Axis I pathology that might have explained the paranoid symptoms. Clear-
ly the frequency with which PPD is the sole or best explanation for pa-
tients’ paranoia bears further exploration, as does the question of wheth-
er, in the presence of another paranoia-associated disorder, the coexistence
of PPD provides useful additional information, for example, about impair-
ment, prognosis or treatment response.
PPD is often described as being on a continuum with schizophrenia and
other cluster A personality disorders, the so-called “schizophrenia-spec-
trum” disorders (SSDs) (Kendler, Neale, & Walsh, 1995; Siever & Davis,
2004), although—as noted above—paranoia as a dimension exists in other
disorders (e.g., PTSD, BPD) as well. However, some research has support-
ed the concept of PPD as a separate disorder with its own clinical, epide-
miological, and neurobiological profile. A comparison of patients with PPD
and schizoid personality disorder (ScPD), for example, found that the
ScPD group tended to be hospitalized younger and to have had more treat-
ment prior to hospitalization, and showed greater morbidity afterward
(Fulton & Winokur, 1993). In another study, core beliefs of patients with
six personality disorders, including PPD, were found to distinguish among
individuals with the different disorders (Arntz et al., 2004). In research
volunteers, PPD criteria, but not SPD or ScPD criteria, were found to be
significantly associated with aggressive behavior (Berman, Fallon, & Coc-
caro, 1998). A diagnostic assessment of cohorts of young people who had
798 TRIEBWASSER ET AL.

a parent with schizophrenia, a parent with a nonschizophrenia psychiat-

ric illness, or no parents with a psychiatric illness found that offspring of
parents with schizophrenia were at risk for SPD but not for PPD (Hans,
Auerbach, Styr, & Marcus, 2004). Rates of the cluster A disorders in pop-
ulations with alcohol dependence may also differ: One study found that
PPD was present in 10% of a sample with alcoholism, while ScPD was
present in only 3.3% (Echeburúa, de Medina, & Aizpiri, 2005). With re-
spect to experimental laboratory parameters, auditory mismatch negativ-
ity to frequency deviance has been shown to differentiate between PPD
patients and those with SPD and ASPD (Liu et al., 2007).
An analysis of data from our research group, which for decades has
studied a large sample of personality-disordered individuals, shows a fair-
ly high frequency of PPD but almost no cases of PPD unaccompanied by at
least one other diagnosis, most frequently SPD, that also has paranoia as
a criterion or associated feature. Out of a sample of 914 medication-free,
nonhospitalized personality-disordered individuals recruited from the New
York metropolitan area, more than one-fourth (249/914) met full criteria
for PPD. Out of these 249, however, fewer than one-third (71/249) did not
meet criteria for another SSD, and out of those 71, only 13 did not have
any active Axis I pathology. PTSD and social phobia, both of which include
fearfulness and avoidance of others that might overlap phenotypically
with paranoia, were frequent Axis I co-morbidities. Out of the 13 individu-
als with PPD uncomplicated by another SSD or an Axis I disorder, more
than three-fourths (10/13) met full criteria for BPD, and 2 had substan-
tial, although subthreshold, BPD traits. Our one remaining subject who
met full criteria for PPD without Axis 1 pathology, BPD, or another SSD
suffered from marked ASPD, with a long history of criminal behavior and
a history of having tortured animals for enjoyment, as well as NPD.
Available published and unpublished data thus demonstrate the exis-
tence of individuals who meet DSM-IV criteria for PPD, but the disorder’s
independent occurrence as a distinct entity remains in question.

PREMORBID BACKGROUND
Negative childhood experiences have been found to be strongly correlated
with PPD in adulthood. In a sample of adult personality-disordered indi-
viduals, for example, PPD was associated with childhood physical, sexual,
and emotional abuse more strongly than was any other personality disor-
der (Bierer et al., 2003). Early body-contact trauma, in particular, has
been found to be associated with the later development of severe PTSD
along with several personality disorders, especially PPD (Gómez-Beneyto,
Salazar-Fraile, Martí-Sanjuan, & Gonzalez-Luján, 2006). Dimensional
paranoia in adolescents also seems to be correlated with a history of child-
hood victimization (Lataster et al., 2006).
Among the childhood/adolescent traits that might be posited to harbin-
ger the later emergence of PPD, social anhedonia, but not perceptual aber-
PARANOID PERSONALITY DISORDER799

ration or magical ideation, has been found to presage the disorder (Kwap-
il, 1998). A comparatively high prevalence (8.3%) of PPD was found in a
30-year follow-up study of patients with traumatic brain injuries (Kopo-
nen et al., 2002).
It appears, then, that trauma, both physical and emotional, predisposes
individuals to PPD and/or dimensional paranoia.

LABORATORY STUDIES
There are no published laboratory studies known to us that look solely or
primarily at PPD. Instead, such studies have been done in samples that
include patients with SSDs and/or other personality disorders, which
have included patients with PPD. Most such studies have had SPD as the
predominant Axis II diagnosis (e.g., Hazlett et al., 2008). Nevertheless,
some findings specific to PPD or to trait paranoia have been cited. For ex-
ample, a study in subjects with affective disorders and schizophrenia-
spectrum illnesses as well as healthy controls (HCs) found an association
between the “s” allele and “ss” genotype of the 5-HTTLPR polymorphism
and lower scores on the Minnesota Multiphasic Personality Inventory
paranoia scale (Golimbet et al., 2003).
Cognitive impairment similar to, but usually less severe than, the defi-
cits found in schizophrenia is one of the hallmarks of the prototypical
cluster A disorder, SPD (Siever et al., 2002). No studies known to us have
examined these parameters in PPD itself, but degradations in information
acquisition and processing appear to be a risk factor for dimensional para-
noia. One specific area of exploration has been deafness and hearing loss,
with findings of predisposition to paranoia in both experimental (Zimbar-
do, Andersen, & Kabat, 1981) and real-world (Sánchez Galán, Díez Sán-
chez, Llorca Ramón, & del Cañizo Fernández-Roldán, 2000; van der Werf
et al., 2007) settings. In a study of mismatch negativity to auditory stimu-
li in patients with PPD, SPD, or ASPD and HCs, the PPD group showed
more rapid automatic detection of auditory stimuli and of their change,
but normal inhibition of irrelevant stimuli; whereas the other patient
groups showed normal discrimination of the auditory stimuli (Liu et al.,
2007). Paranoia is, of course, a classic manifestation of early dementia
(Eustace et al., 2002), and it appears to be highly prevalent in the very old
(95 years old), unrelated to intellectual functioning (Ostling, Börjesson-
Hanson, & Skoog, 2007), although paranoia in a slightly younger cohort
(85 years old) was found to be predictive of the subsequent onset of de-
mentia (Ostling & Skoog, 2002).
Of note, some studies demonstrating schizophrenia-like laboratory ab-
normalities in cluster A patients have found these markers only in those
cluster A patients with a family history of schizophrenia (Thaker et al.,
1996, 2000). It is probable, then, that PPD bears a neurobiological rela-
tionship to other SSDs, but the extent and details of this relationship have
not been fully elucidated.
800 TRIEBWASSER ET AL.

EPIDEMIOLOGICAL/FAMILY STUDIES
According to DSM-IV, the prevalence of PPD has been reported to be 2%–
30% in clinical settings, while the prevalence in the general population
has been reported to be 0.5%–2.5%. Since DSM-IV’s publication, the prev-
alence of PPD in clinical populations has been estimated as ranging from
0.1% (Kantojärvi et al., 2004) to 27.6% (Marinangeli et al., 2000), depend-
ing on the diagnostic methods used and the nature of the sample studied.
In general, structured diagnostic methods yield higher prevalence rates
than unstructured clinical assessments. The most convincing estimate of
the prevalence in general psychiatric outpatients is probably that of Zim-
merman and colleagues (2008), who found 4.2% of patients meeting crite-
ria for PPD and 0.7% for whom PPD was the only personality disorder. In
one outcome study of day treatment in personality disorder patients, PPD
was, perhaps surprisingly, one of the three most common disorders (Kar-
terud et al., 2003). In nonclinical samples, prevalence estimates have
ranged from 0.0% (although this figure comes from a study of normal con-
trols, parents, and their children; Moldin, Rice, Erlenmeyer-Kimling, &
Squires-Wheeler, 1994) and 0.4% (in an epidemiological survey of univer-
sity students, assessed through a two-phase sampling process; Lenzenwe-
ger, Loranger, Korfine, & Neff, 1997) to 4.41% (in the National Epidemio-
logic Survey on Alcohol and Related Conditions, a population-based U.S.
study using lay interviewers; Grant et al., 2004). The most convincing
population-based estimates are probably those obtained by Torgersen and
colleagues (Torgersen et al., 2001), who found a weighted prevalence of
2.4% in Oslo, Norway, and Coid and colleagues (2006), who found a
weighted prevalence of 0.7% in the United Kingdom.
The SSDs as a group tend to show strong familial aggregation in some
(Filbey, Holcomb, Nair, Christensen, & Garver, 1999; Parnas et al., 1993;
Siever et al., 1990) but not all (Kendler, Gruenberg, & Kinney, 1994) eval-
uations. This familial aggregation, if it exists, appears not to be caused by
shared environmental effects (Reichborn-Kjennerud, 2008), but may in
part be secondary to a gene–environment interaction (Tienari et al., 2004).
However, as noted above, the research demonstrating familial transmis-
sion of the SSDs has tended to look at these illnesses as a group rather
than at PPD in particular, and has tended to focus on SPD as the proto-
typical SSD and to show the most robust findings in SPD as opposed to
PPD or ScPD (e.g., Asarnow et al., 2001; Kendler et al., 2006; Tienari et
al., 2003), although some evidence of a familial relationship between PPD
and schizophrenia has been found (Kendler et al., 1993; Webb & Levin-
son, 1993). First-degree relatives of Taiwanese probands with schizophre-
nia had a 3.5%–8.5% prevalence of PPD—a higher rate than in the general
population (Chang et al., 2002). However, a study of children and adoles-
cents with one parent with schizophrenia showed no increased incidence
of PPD in the offspring (Hans et al., 2004), while a study that assessed
relatives of German psychiatric inpatients found a lower prevalence of
PARANOID PERSONALITY DISORDER801

PPD in families of probands with schizophrenia than of those with unipo-

lar depression (Maier, Lichtermann, Minges, & Heun, 1994).
Research summarized in a prior review (Bernstein, Useda, & Siever,
1995) supports the familial aggregation of PPD with delusional disorder
(Kendler, 1985) as well as with schizophrenia and the cluster A personal-
ity disorders (Kendler et al., 1995).
The heritability of PPD itself has been estimated as .28 in a twin study
using a Norwegian clinical sample (Torgersen et al., 2000), and .21 in a
twin study of dimensional representations of the cluster A personality dis-
orders using a Norwegian population-based sample (Kendler et al., 2006).
In a subsequent examination by Kendler and colleagues of data from the
same population-based sample, this time incorporating self-report infor-
mation collected at a different time-point from the interview information
used in the 2006 paper, found a substantially higher heritability estimate
of .66 (Kendler et al., 2007).
PPD appears, then, to bear genetic and epidemiological relationships to
schizophrenia, although not as strongly as does SPD. Furthermore, it may
be that PPD is especially closely related to delusional disorder, and that
PPD is part of a separate strand of thought disorders, which also includes
delusional disorder and which is marked primarily by delusions rather
than by the broader array of symptoms seen in schizophrenia and SPD.

FOLLOW-UP STUDIES
There is little published research about the outcome of individuals with
PPD. In a follow-up study examining a stratified random community sam-
ple assessed for DSM-III personality disorders and then for psychosocial
functioning 13–18 years later, the inverse relationship between PPD traits
and later GAF scores appeared to be mediated by Axis I comorbidity (Hong
et al., 2005).

TREATMENT-RELATED STUDIES
An outcome study of day treatment programs in personality-disordered
individuals, in which PPD was the most common cluster A diagnosis,
found that cluster A patients showed worse results than other groups
(Karterud et al., 2003). Skills training has been suggested as a useful
treatment modality in this disorder (Stanley, Bundy, & Beberman, 2001).

IMPLICATIONS FOR DSM-5

PPD is primarily defined along a single trait dimension that the data are
strongest for, and lacks the external validating evidence that exists for
SPD. Whether it will be acknowledged as a type or be coded in terms of the
trait of paranoia is not yet resolved. In the proposed DSM-5 system cur-
802TRIEBWASSER ET AL.

rently under review, PPD traits such as suspiciousness, intimacy avoid-

ance, hostility, and unusual beliefs, if sufficiently severe to warrant a
­personality disorder diagnosis, would be subsumed under the new “Per-
sonality Disorder Trait Specified” category.

CONCLUSIONS
We recommend that between now and the publication of DSM-5, efforts be
conducted to provide additional information as to the divergent validity of
the PPD diagnosis; its neurobiological correlates, its relationship to schizo-
phrenia and the other SSDs, and its treatment response characteristics. If
it cannot be demonstrated that a PPD diagnosis provides useful informa-
tion about affected patients’ neurobiology, impairment, prognosis, or
treatment response, then consideration should be given to deleting the
disorder as a separate diagnosis in DSM-5. As an alternative or supple-
ment to PPD, it may be that the dimension or trait of suspiciousness would
be a useful clinical entity to diagnose and study.

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