VOL 21, NO.
1, 1995
Schizotypal Personality
Disorder in Parents and
the Risk for Schizophrenia
in Siblings
by Kenneth S. Kendler Abstract
and Dermot Walsh
With one exception, previous
studies examining the familial
relationship between schizotypal
personality disorder (SPD) and
schizophrenia have compared
rates of SPD in relatives of pro-
bands with schizophrenia versus
control probands. In the Roscom-
mon Family Study, an epidemio-
logically based family study of
major psychiatric disorders con-
ducted in the west of Ireland,
we used a Cox proportional haz-
ards model to examine the im-
pact of a parental diagnosis of
SPD on the risk for psychiatric
disorders in siblings of probands
with schizophrenia or schizo-
phrenia spectrum disorders. In
siblings of probands with schizo-
phrenia or schizophrenia spec-
trum, a parental diagnosis of
SPD significantly increased the
risk for schizophrenia and schiz-
ophrenia spectrum disorders, but
not for affective illness or anx-
iety disorders. These findings
replicate our previous results
from the Roscommon Family
Study, further supporting the hy-
pothesis that SPD has a substan-
tial familial relationship with
schizophrenia and other schizo-
phrenia spectrum disorders, but
not with affective illness.
Schizophrenia Bulletin; 21(1):
47-52, 1995.
Clinicians have observed for nearly
a century that certain close rela-
tives of patients with schizophre-
nia, although never psychotic, have
odd, eccentric personalities clini-
cally reminiscent of schizophrenia
(Kendler 1985a). Based on inter-
views from the Danish Adoption
Study of schizophrenia, Spitzer et
al. (1979) developed specific crite-
ria for a new diagnostic category
that attempted to describe individ-
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uals with these personality charac-
teristics. This syndrome, termed
schizotypal personality disorder
(SPD), was subsequently included
in DSM-H1 (American Psychiatric
Association 1980) and, with mini-
mal change, in DSM-IH-R (Ameri-
can Psychiatric Association 1987).
We are aware of 10 previous stud-
ies that examined the prevalence
of SPD in relatives of probands
with schizophrenia and matched
control probands. With one ex-
ception (Coryell and Zimmerman
1988), all found substantial evi-
dence for a familial relationship
between schizophrenia and SPD
(Lowing et al. 1983; Kendler et al.
1984; Kendler and Gruenberg 1984;
Baron et al. 1985b; Frangos et al.
1985; Coryell and Zimmerman
1988; Gershon et al. 1988; Onstad
et al. 1991; Parnas et al. 1993).
Results have been less clear in
studies that began with SPD pro-
bands (Torgersen 1983; Baron et al.
1985a; Schulz et al. 1989; Siever
et al. 1990; Battaglia et al. 1991;
Kendler et al. 1993a; Thaker et al.
1993), perhaps because many of
these studies had small sample
sizes (and hence low statistical
power) and used family history
rather than family study methodol-
ogy. However, two recent studies
have reported a significantly el-
evated risk for schizophrenia in
relatives of probands with SPD
(Kendler et al. 1993a; Thaker et
al. 1993).
The Roscommon Family Study is
an epidemiologically based family
study of major mental illness con-
Reprint requests should be sent to
Dr. K.S. Kendler, Dept. of Psychiatry,
Box 980 MCV, Richmond, VA
23298-0710.
48
ducted in a rural county in the
west of Ireland (Kendler et al.
1993a). Compared with relatives of
unscreened controls, we found in
this study a substantially increased
risk for SPD in relatives of pro-
bands with schizophrenia and
other nonaffective psychoses, but
not in relatives of probands with
affective illness (AI) (Kendler et al.
1993b). This traditional analysis,
while particularly powerful, does
not contain all the information
available in this study about the
relationship between SPD and
other psychiatric disorders. Further
information is contained in the re-
lationship between a parental di-
agnosis of SPD and the risk for
schizophrenia spectrum and other
psychiatric disorders in siblings of
probands. While the strategy of
examining the relationship between
parental disorders and risks for ill-
ness in siblings was commonly
used in early family studies of
schizophrenia (e.g., Riidin 1916;
Kallmann 1938), we are aware of
only one recent application. Baron
et al. (1983) found that a parental
diagnosis of SPD significantly in-
creased the risk for both schizo-
phrenia and SPD in siblings of
probands with schizophrenia.
Methods
Sample. Three proband groups
were ascertained in the Roscom-
mon Family Study: (1) schizo-
phrenic—all cases with a diagnosis
of schizophrenia from the Ros-
common County Case Register
(Walsh et al. 1980) (n = 303); (2)
affective—a randomly chosen sub-
sample of 75 percent of the cases
from the case register with a diag-
nosis of major affective disorder
(n = 99); and (3) control—age- and
sex-matched controls chosen from
the county electoral registry (n =
150). We tried to personally inter-
view all probands and, blind to
proband diagnosis, their first-
degree relatives aged 16 and older
residing in Ireland, Northern Ire-
land, and central and eastern Eng-
land. To improve cooperation, the
same interviewer was usually as-
signed to interview all members of
a given family. All available psy-
chiatric hospital records for pro-
bands and relatives were obtained
and abstracted.
An adaptation of the Structured
Clinical Interview for DSM-IU-R
Diagnoses (Spitzer et al. 1987) was
used for the diagnosis of Axis I
conditions; the interview-based as-
sessment for Axis II disorders was
performed with early versions of
the Structured Interview for Schiz-
otypy (SIS; Kendler et al. 1989).
DSM-IH-R criteria were used by
Kenneth S. Kendler or Alan M.
Gruenberg to make blind, best-esti-
mate diagnoses, using all available
information, for probands and rela-
tives for whom personal interviews
and/or hospital records were
available. Interrater reliability
was assessed for 69 cases and
both percentage agreement and
chance-corrected agreement (Cohen
1960) were high: 83 percent and
0.77 ± 0.05, respectively (Kendler
et al. 1993a).
A number of individuals and
families in the Roscommon Family
Study were ascertained more than
once. To obtain the correct risk in
relatives, we used the general pro-
band method, in which all individ-
uals are counted once for each
time they are independently ascer-
tained (Crow 1965). All counts of
relatives in this report refer to
numbers of ascertained relatives.
Using DSM-IH-R diagnoses, we
define the major diagnostic catego-
ries of interest as follows: all non-
SCHIZOPHRENIA BULLETIN
affective psychoses (ANAP)—schiz-
ophrenia, schizoaffective disorder,
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schizophreniform disorder, delu-
sional disorder, and psychosis not
otherwise specified (NOS); schiz-
ophrenia spectrum—ANAP plus
SPD and paranoid personality dis-
order (PPD); AI—major depression,
mixed, manic, and depressed bipo-
lar disorder, and bipolar disorder
NOS; anxiety disorder—generalized
anxiety disorder or panic disorder,
with or without agoraphobia; and
alcoholism—alcohol dependence or
alcohol abuse. Diagnoses were
made at three levels of diagnostic
certainty (Kendler et al. 1993o). In
this article, we report only those
analyses based on the broad crite-
ria of definite, probable, or possi-
ble cases. Schizophrenia spectrum
diagnoses reported here were
based on a hierarchy: schizophre-
nia, schizoaffective disorder, schiz-
ophreniform disorder, delusional
disorder, psychosis NOS, SPD, and
PPD. Diagnoses of AI, anxiety dis-
order, and alcoholism were made
hierarchically, that is, after siblings
with schizophrenia spectrum disor-
ders had been removed from the
analyses (Kendler 1988). We also
repeated these analyses without a
diagnostic hierarchy.
We were able to interview per-
sonally 85.8 percent of all living
and traceable relatives of probands
(n = 1,753). The analyses in this
report were restricted to siblings
from the approximately 50 percent
of proband families that contained
at least one parent and at least
one sibling with a personal inter-
view or hospital record. We focus
on siblings of three groups of pro-
bands that reflect increasingly
broad definitions of schizophrenia-
related disorders: (1) schizophrenia
only (n = 149 from 50 families—
55.7% male, mean age [± standard
deviation] 35.3 ± 9.1 years); (2)
VOL. 21, NO. 1, 1995
ANAP (n = 290 from 88 families—
54.8% male, mean age 35.9 ± 9.3
years), and (3) schizophrenia spec-
trum (n = 307 from 96 families,
53.8% male, mean age 35.8 ± 9.1
years).
Statistical Methods. We used a
Cox proportional hazards model as
operationalized in the PHREG pro-
gram in SAS (SAS Institute 1990)
to examine the impact of one or
more parental diagnoses of SPD
(there was only one family in our
sample in which both parents had
SPD) on the hazard rate for vari-
ous psychiatric disorders in sib-
lings of probands. Age at onset
was not coded for SPD or PPD in
our analyses, because these condi-
tions represented, by definition,
lifelong personality patterns. For
the purpose of the Cox propor-
tional hazards model, however,
these personality disorders were
assigned an age at onset of 18
years. We present the risk ratio
(calculated as e&, where e equals
the natural logarithm and (3 the
regression coefficient estimated
from the Cox regression), which
represents the change in the haz-
ard rate for a given disorder asso-
Table 1. The hazard ratio for psychiatric disorders in siblings, given a diagnosis of
schizotypal personality disorder in parents
Proband diagnosis
Schizophrenia
ANAP
Schizophrenia spectrum
Note.—ANAP = all nonaffective psychoses (see text for definition); AI = affective illness.
'p < 0.05.
2
p < 0.10.
3
p < 0.01.
ciated with a parental diagnosis of
SPD.
In the analyses of schizophrenia
spectrum disorders in siblings, we
controlled for the presence of
schizophrenia or schizoaffective
disorder in parents. In the analy-
ses examining other disorders in
siblings (AI, anxiety disorder, and
alcoholism), we controlled for the
presence of the same disorder in
parents. All analyses also con-
trolled for the presence or absence
of a personal interview with par-
ents and with siblings.
Since this study represents an
attempt to independently replicate
a previous finding of a familial re-
lationship between SPD and other
schizophrenia spectrum disorders
(Kendler et al. 1993b), one-tailed
tests are used for these compari-
sons. Otherwise, two-tailed tests
are employed. We report p values
greater than 0.05 but less than 0.10
as statistical trends. The morbid
risks for schizophrenia, ANAP,
and schizophrenia spectrum disor-
ders in siblings of probands with
schizophrenia, ANAP, or schizo-
phrenia spectrum with and with-
out a parent with a diagnosis of
SPD are available from the authors
on request.
Sibling diagnosis
Schizophrenia
Schizophrenia ANAP spectrum
4.241 2.492 2.491
3.121 1.992 3.01 3
3.391 2.341 2.963
49
Results
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Risk for Schizophrenia Spectrum
Disorders. The risk for a diag-
nosis of schizophrenia was signif-
icantly increased by a parental
diagnosis of SPD in siblings of
probands with schizophrenia (x2 =
3.09, df = 1, p = 0.04, risk ratio
[RR] = 4.24), ANAP ( x 2 = 3.39, df
= 1, p = 0.03, RR = 3.12), or any
schizophrenia spectrum diagnosis
(X2 = 4.57, df = 1, p = 0.02, RR =
3.39) (table 1). A similar pattern
was seen for a sibling diagnosis of
ANAP or schizophrenia spectrum.
In particular, a parental diagnosis
of SPD increased the risk for a di-
agnosis of schizophrenia spectrum
disorder in siblings of schizophre-
nia spectrum probands by an RR
of 2.96 (x2 = 8.28, df = 1, p =
0.004).
Risk for Other Psychiatric Dis-
orders. In examining siblings
of probands with schizophrenia,
ANAP, or schizophrenia spectrum,
we found no evidence that a pa-
rental diagnosis of SPD increased
sibling risk for AI or anxiety dis-
order (table 1). In siblings of
schizophrenia probands, a parental
Anxiety
AI disorder Alcoholism
0.25 0.00 4.111
0.75 0.69 1.79
0.76 0.67 2.07
50
diagnosis of SPD significantly in-
creased the risk for alcoholism (x2
= 5.39, df = 1, p = 0.02, RR =
4.11). However, as the proband di-
agnosis was widened to include
nonschizophrenic psychotic disor-
ders and schizophrenia spectrum
personality disorders (and statisti-
cal power increased), this effect
diminished in magnitude and was
no longer statistically significant,
even at a trend level. These analy-
ses were repeated without a diag-
nostic hierarchy in siblings, and
similar results were obtained with
one exception. A parental diag-
nosis of SPD now conveyed a sig-
nificantly increased risk for alco-
holism in siblings of probands
with a diagnosis of schizophrenia,
ANAP, or any schizophrenia spec-
trum disorder.
Discussion
The lifetime prevalence of SPD
was significantly increased, com-
pared with the prevalence in rela-
tives of controls, in relatives of
probands with schizophrenia, SPD,
and other nonaffective psychoses,
but not in relatives of probands
with AI (Kendler et al. 1993b). We
drew two major conclusions from
these results: (1) consistent with
the results of previous studies be-
ginning with schizophrenia pro-
bands (Lowing et al. 1983; Kendler
and Gruenberg 1984; Kendler et al.
1984; Baron et al. 1985b; Frangos
et al. 1985; Coryell and Zimmer-
man 1988; Gershon et al. 1988;
Onstad et al. 1991; Parnas et al.
1993), SPD shares familial etiologic
factors with schizophrenia and re-
lated schizophrenia spectrum disor-
ders, and (2) consistent with the
results of some previous studies
(Onstad et al. 1991) but not others
(Squires-Wheeler et al. 1988, 1989),
SPD does not have a substantial
familial relationship with AI.
We sought to replicate these
findings in an entirely independent
manner in the same sample. To do
this, we examined the pattern of
illness in relatives of schizophrenia
spectrum probands. We predicted
that a diagnosis of SPD in parents
would increase the risk for schizo-
phrenia and schizophrenia spec-
trum disorders in siblings but that
it would not increase the risk for
AI.
Our results are in accord with
our predictions. A parental diag-
nosis of SPD significantly increased
the risk for schizophrenia in sib-
lings of schizophrenia probands.
A similar pattern of findings was
seen if the proband or sibling di-
agnosis was widened to include
ANAP or the total schizophrenia
spectrum.
By contrast, a diagnosis of SPD
in parents did not predict the risk
for AI or anxiety disorders in sib-
lings. Although this result is con-
sistent with the previous results in
this study, as well as those re-
cently reported for relatives of
Norwegian twins with schizophre-
nia and major affective illness
(Onstad et al. 1991), it is inconsist-
ent with the results of two studies
from the New York sample of
high-risk offspring of probands
with schizophrenia and AI
(Squires-Wheeler et al. 1988, 1989).
Our results suggest that SPD re-
flects, with some specificity, famil-
ial vulnerability to schizophrenia
and schizophrenia spectrum
disorders.
Our findings on the relationship
between SPD and alcoholism were
somewhat more ambiguous, but
they were not inconsistent with
our previous finding that relatives
of schizophrenia probands in the
Roscommon Family Study had a
SCHIZOPHRENIA BULLETIN
nonsignificant increased risk for al-
coholism (50% higher than the risk
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of relatives of matched controls;
Kendler et al. 1993c). When diag-
noses were made hierarchically, a
parental diagnosis of SPD con-
veyed a significantly increased risk
for alcoholism only in siblings of
schizophrenia probands. However,
when analyses were conducted
without a diagnostic hierarchy, the
same pattern was seen in siblings
of probands with schizophrenia,
ANAP, or schizophrenia spectrum.
These results suggest that in sib-
lings of schizophrenia spectrum
probands, a parental diagnosis of
SPD predicts a diagnosis of alco-
holism in individuals with a schiz-
ophrenia spectrum diagnosis. Of
the previous studies that have ex-
amined this question, most have
not found evidence for a familial
relationship between schizophrenia
spectrum disorders and alcoholism
(Rimmer and Jacobsen 1977;
Bleuler 1978; Baron et al. 1985b;
Frangos et al. 1985; Kendler 1985b;
Kendler et al. 1985; Gershon et al.
1988), but a few have (Kallmann
1938; Vaziri 1961). Further research
is clearly needed to clarify the
possibility of a modest familial re-
lationship between alcoholism and
schizophrenia and associated
disorders.
These results should be inter-
preted in the context of one po-
tentially significant methodologic
limitation. Interviewers often as-
sessed more than one member of
an individual proband family.
Therefore, although they were
blind to knowledge about proband
diagnosis, they were not always
blind to psychiatric diagnoses in
nonproband relatives. It is possible
that the findings described above
were influenced by interviewer
bias. But we consider this unlikely
for two reasons. First, the inter-
VOL 21, NO. 1, 1995
viewers were repeatedly cautioned
about the importance of assessing
each relative independently. Sec-
ond, all diagnoses reported here
were based on an independent di-
agnostic review of all diagnostic
materials on relatives by a re-
viewer who was blind to informa-
tion on the psychopathologic status
of all other relatives.
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Acknowledgments
This project was supported by
USPHS grant MH-41953 from the
National Institute of Mental Health
and a grant from the Scottish Rite
Benevolent Foundation's Schizo-
phrenia Research Program, U.S.
Northern Masonic Jurisdiction. The
authors gratefully acknowledge the
assistance of our colleagues—Mary
McGuire, M.B.; Alan M. Gruen-
berg, M.D.; Aileen O'Hare, M. Soc.
Sci.; and Mary Spellman, M.B.—
and the staffs of the Roscommon
Family Study, St. Patrick's Hospi-
tal, Castlerea, the Roscommon
Case Register, and the Health Re-
search Board. John Myers, M.S.,
assisted in the statistical analyses.
The Authors
Kenneth S. Kendler, M.D., is
Rachel Brown Banks Distinguished
Professor of Psychiatry and Pro-
fessor of Human Genetics, Medical
College of Virginia, Richmond, VA.
Dermot Walsh, M.B., is Head,
Mental Health Section, The Health
Research Board and is Director, St.
Loman's Hospital, Dublin, Ireland.