Comprehensive Psychiatry 48 (2007) 145 154

www.elsevier.com/locate/comppsych

The interface between borderline personality disorder and bipolar

spectrum disorders
Joel Parisa,4, John Gundersonb, Igor Weinbergb
a

Department of Psychiatry, Institute of Community and Family Psychiatry, SMBD-Jewish General Hospital, McGill University, Montreal, Quebec,
Canada H3T 1E4
b
Department of Psychiatry, McLean Hospital, Harvard University, Boston, MA 02478, USA

Abstract
Objective: This review examines whether borderline personality disorder (BPD) should be considered part of the bipolar spectrum.
Methods: A literature review examined studies of co-occurrence, phenomenology, family prevalence, medication response, longitudinal
course, and etiology.
Results: Borderline personality disorder and bipolar disorder co-occur, but their relationship is not consistent or specific. There are overlaps
but important differences in phenomenology and in medication response. Family studies suggest clear distinctions, and it is unusual for BPD
to evolve into bipolar disorder. Research is insufficient to establish whether these disorders have a common etiology.
Conclusions: Existing data fail to support the conclusion that BPD and bipolar disorders exist on a spectrum but allows for the possibility of
partially overlapping etiologies.
D 2007 Elsevier Inc. All rights reserved.

1. Introduction
It has been persistently suggested that borderline
personality disorder (BPD) could be an atypical form of
mood disorder [1-3]. Originally, because of frequent
comorbidity [4,5], the focus was on whether BPD is a
variant of major depression (MDD) [6,7]. However, a
significant body of research has established important
differences between BPD and MDD: in phenomenology,
family prevalence, medication response, pathogenesis
[8-11], and, most recently, in their influence on each others
course [12]. The suggestion that BPD might be an atypical
form of mood disorder has now shifted from MDD to
bipolar disorder [13,14].
The concept of a bipolar spectrum expands the
diagnostic construct to include a wider range of syndromes [13-19]. In addition to bipolar I and bipolar II,
spectrum disorders would include bipolar III (antidepressant-induced hypomania), and bipolar IV (ultrarapidcycling bipolar disorder) [19]. These subtypes might also

4 Corresponding author.
E-mail address: joel.paris@mcgill.ca (J. Paris).
0010-440X/$ see front matter D 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.comppsych.2006.10.001

supercede cyclothymic disorder, which is heterogeneous in

phenomenology, family history, biologic correlates, and
treatment [20]. It is now being suggested that a bipolar
spectrum exists, including many cases of unipolar depression, anxiety disorders, substance abuse, eating disorders,
as well as many personality disorders, most notably
BPD [14,18,21,22].
The purpose of the present article is to critically evaluate
the relationship between BPD and bipolar I disorder, as
well as the proposed bipolar spectrum, notably bipolar II.
We will examine 4 hypotheses regarding this relationship:
(1) BPD is an atypical form (ie, phenotypic variant) of
bipolar disorder; (2) bipolar disorder is a phenotypic variant
of BPD; (3) BPD and bipolar disorder are independent
disorders; and (4) BPD and bipolar disorder have overlapping etiologies. To examine these hypotheses, we review
findings concerning co-occurrence, phenomenology, family
prevalence, medication response, longitudinal course, and
etiology. Medline and PsycInfo searches using the combined search terms borderline personality disorder and
bipolar disorder elicited 147 published articles since
1966; this review focuses on empirical studies and theoretical articles shedding light on the relationship between
these disorders.

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J. Paris et al. / Comprehensive Psychiatry 48 (2007) 145154

2. Co-occurrence
High levels of bipolar disorders in BPD patients would
support hypothesis 1, whereas high levels of BPD in bipolar
patients would support hypothesis 2, and either could
support hypothesis 4. If most cases remain distinct,
hypothesis 3 would be supported.
Table 1 shows that in 8 studies of 1006 BPD patients
where rates of bipolar I were measured, the range was from
5.6% to 16.1% (median, 9.2%) [23-30]. In 6 studies of
436 BPD patients in which rates of bipolar II were reported,
the range was 8% to 19% (median, 10.7%) [5,25,28-31],
whereas 1 study found 22% with cyclothymia [32]. In the
most methodologically rigorous study, 12% of patients with
BPD met criteria for bipolar I, and another 8% met criteria
for bipolar II [30]. Still, illustrating how (applying the
concept of a broad spectrum and using untested measures)
much higher levels of co-occurrence can be found, a study
of 16 BPD inpatients reported that 2 had bipolar I; 3 had
bipolar II; and another 8 could be rediagnosed with bipolar
III, bipolar IV, or cyclothymia [29].
Table 2 shows that in 12 studies with 830 bipolar I
patients, between 0.5 and 30% (median, 10.7%) were found

to meet criteria for BPD [26,33-38,40,43-46]. In 3 studies

with 137 bipolar II patients, between 12% and 23%
(median, 16%) had BPD [39,41,42], and 1 study of
cyclothymia found 62% [14]. When the rate of BPD in
bipolar II was compared to other categories of personality
disorder, 2 found the rate of co-occurrence highest for BPD
[39,41]; 1 found almost equal rates for BPD and histrionic
personality disorder [26]; 4 found histrionic most common
[36,40,43,46]; and 2 found obsessive-compulsive most
frequent [44,45].
We next combined the results of all studies of bipolar I
and bipolar II samples that compared the co-occurrence rates
of BPD to that associated with other personality disorders.
This involved a total of 11 samples with 683 bipolar I
patients [10,26,35-38,40,41,44-46] and 3 samples with a
total of 91 bipolar II patients [10,39,41]. A random effects
regression analysis with rates of disorders as an outcome
measure, adjusted for clustering within the studies, showed
that the rate of comorbidity for BPD was not significantly
higher in bipolar I (v 2 = 2.5, P N .1) or bipolar II (v 2 = 2.3,
P N .1) than for any other personality disorder.
Most of the reports listed in Tables 1 and 2 suffered
from significant methodological problems. Assessments of

Table 1
Bipolar co-occurrence in BPD patients
Study

BD type

Diagnostic measures

Sample

Number (%) of BPD

patients having BD

Pope et al [23]
McGlashan [24]
Links et al [25]

33
169
88

BD-I
BD-I
BD-I, BD-II
CD

DSM-III, DIB
DSM-III, DIB
SADS
DIB

Inpatients
Inpatients
Consecutive inpatients

SCID
SIDP
SCID
DIB
DIPD
DSM-III
Gunderson criteria for BPD
DSM-III-R
DIB
DSM-III-R
DIB-R
SCID

Outpatients

Outpatients + inpatients

3 (9.1%)
7 (4.1%)
Current:
BD-I: 1 (1.1%)
BD-II: 3 (3.4%)
Lifetime:
BD-I: 5 (5.9%)
BD-II: 8 (9.6%)
CD: 15 (17.9%)
BD-I: 0 (0%)
CD: 7 (15.9%)
BD-I: 0 (0%)
BD-II: 0 (0%)
CD: 0 (0%)
BD-II: 17 (17%)
CD: 7 (7%)
BD-I: 0 (0%)
CD: 10 (22%)
14 (16.1%)

Inpatients

36 (9.5%)

Outpatients
BD-II: 5 (8.5%)
Consecutive inpatients

BD-I: 5 (8.5%)

Alnaes and Torgersen [26]

44

BD-I, CD

Zanarini et al [4]

50

BD-I, BD-II, CD

Akiskal [31]

100

CD, BD-II

Levitt et al [32]

46

CD

Hudziak et al [27]

87

BD-I

Zanarini et al [5]

379

Zimmerman and Mattia [28]

59

Deltito et al [29]

16

McGlashan et al [30]

BD-I, II

BD-II
DIB-R
BD-I, BD-II
SIDP-IV
BD-I, II
175

DIPD
SCID
SCID
SCID-II
SCID
DIPD-IV

Outpatients

Consecutive outpatients
Consecutive (inpatient + outpatient)

Inpatients, outpatients

BD-I: 2 (12.5%)
BD-II: 3 (19.0%)
BD-I: 21 (12%)
BD-II: 14 (8%)

BD-I, bipolar I disorder; BD-II, bipolar II disorder; BD, any bipolar disorder; CD, DSM-III, DSM, Third Edition; DSM-III-R, DSM, Revised Third Edition;
Cyclothymic disorder; SCID, Structured Clinical Interview for DSM-III/IV; DIB, Diagnostic Interview for Borderlines; DIPD, Diagnostic Interview for
Personality Disorders; DIPD-IV, Diagnostic Interview for Personality Disorders for DSM-IV; SADS, Schedule for Affective Disorders and Schizophrenia.

J. Paris et al. / Comprehensive Psychiatry 48 (2007) 145154

147

Table 2
BPD co-occurrence in bipolar disorder patients
Study

BD type

Diagnostic measures

Sample

Number (%) of BD patients

having BPD

Gavria et al [33]

100

BD-I

Outpatients

13 (13%)

Koenigsberg et al [34]

179

BD-I +CD

RDC
Gunderson and Kernberg
criteria for BPD
DSM-III (clinical diagnosis)

Consecutive inpatients
and outpatients

BD-I: 1 (0.5%)

Jackson et al [35]
Pica et al [36]

26
26

BD-I
BD-I or SA(B)

SIDP, SCID
SCID SCID-II

Inpatients
Inpatients

Alnaes and Torgersen [26]

54

BD-I, CD

SCID SCID-II

Consecutive outpatients

BD-I
BD-I or SA(B)
BD-II
BD-I
BD-II
BD-II
BD-I
BD-I
BD-I
BD-I

DSM-III-R, PDQ-R
SCID, SIDP
SCID, SIDP
SCID, SCID-II
SADS-L/C, SCID-II
SCID, SCID-II
SCID, SADS-L/C SCID-II
SCID, SCID-II
SCID, SCID-II
SCID, SADS-L/C
PDE
SCID, SCID-II

Outpatients
Inpatients
Outpatients
Outpatients
Consecutive oupatients
Consecutive outpatients
Primary Care
Consecutive inpatients
Consecutive inpatients
Not specified

CD: 1 (12.5%)
6 (23%)
Patients: 4 (11.5%) Patients
and informants: 8 (23.1.%)
BD-I: 0 (0%)
CD: 14 (35%)
15 (30%)
4 (21%)
11 (23.4%)
43 (47.7%)
5 (12.5%)
6 (12%)
8 (6.2%)
21 (29.6%)
4 (6.7%)
2 (9.1%)

Consecutive outpatients

28 (62.2%)

OConnell et al [37]
Turley et al [38]
Peselow et al [39]
Ucok et al [40]
Vieta et al [41]
Benazzi [42]
Vieta et al [43]
Rossi et al [44]
Brieger et al [45]
George et al [46]
Perugi et al [14]

50
21
47
90
40
50
156
71
60
52
45

CD

SA(B), schizoaffective, bipolar type; SIDP, Structured Interview for DSM-III Personality Disorders; PDE, Personality Disorder Examination; SADS-L/C,
Schedule for Affective Disorders and Schizophrenia, Lifetime version/Change version; RDC, research diagnostic criteria.

bipolar and BPD were rarely independent. Whether patients

were assessed during acute episodes was inconsistent, and
although not evident in existing data, rates of co-occurrence
would be expected to be higher in patients who were not
euthymic. Moreover, 2 studies [36,39] indicate that rates of
co-occurrence could be affected by use of informants.
Finally, because all studies used clinical samples and many
were confined to inpatients, and because inpatient samples
are not necessarily representative of clinical populations,
rates of co-occurrence would be expected to be elevated
over community populations. Indeed, the observed rates
were considerably above community base rates, where
the overall prevalence of bipolar I is 1.6% [47], whereas
the community prevalence of BPD is about 1% [48,49]. The
prevalence of bipolar II needs more systematic study. One
report [50] described an overall prevalence of 3.7% for
bipolar I and bipolar II combined, whereas another that
found the prevalence of bipolar II alone to be 2.8% [51]
used broadened criteria that reduced the requirement of the
Diagnostic and Statistical Manual of Mental Disorders
(DSM), Fourth Edition, Text Revision [52] for hypomania
from 4 to 2 days.
In summary, the existing data show some increased level
of co-occurrence in both directions between BPD and
bipolar disorder, but these elevations are not specific to BPD
vs other personality disorders, whereas in most cases (ie,
75%-90%) the disorders are distinct. A credible estimate of
co-occurrence rates awaits the study of an epidemiologically
valid community sample. As it stands, although elevated

levels of co-occurrence could support hypotheses 1, 2, or 4,

distinctions are most frequent, providing stronger support
for Hypothesis 3.
3. Phenomenology
A high overlap of bipolar phenomenology in BPD would
support hypothesis 1, and a high overlap of BPD phenomenology in bipolar disorders would support hypothesis 2,
whereas either could support hypothesis 4. If most
phenomenology remains distinct, that would support hypothesis 3.
Co-occurrence may simply reflect similarities in the way
disorders are defined. This problem is common in the DSM
system, where disorders are categorized on the basis of
symptoms [52]. More general phenotypic dimensions such
as affective instability and impulsivity, which describe
phenomena common to both bipolar disorder and BPD,
may account for diagnostic overlap.
Affective instability, as a criterion for BPD, is defined as
ba marked reactivity of mood (eg, intense episodic
dysphoria, irritability, or anxiety usually lasting a few hours
and only rarely more than a few days)Q [52]. Affective
instability is a partially heritable trait [53] that may be a core
aspect of BPD [54] and is the component of BPD least
likely to change over time [55-57]. Reactivity of affects to
environmental, especially interpersonal, stressors can distinguish BPD from mood disorders [34]. Studies of
personality trait dimensions have shown that both BPD

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J. Paris et al. / Comprehensive Psychiatry 48 (2007) 145154

[58,59] and mood disorders [60,61] have high neuroticism

(related to affective instability) and low conscientiousness;
however, BPD is high on harm avoidance, whereas bipolar
disorder is not [62].
Mood changes in bipolar disorder can be different from
those that characterize BPD. Changes from depression to
elation distinguish bipolar II from BPD, where moods rarely
include elation and are more likely to shift from euthymia to
anger [34,63]. In addition, although mood changes in BPD
are usually reactions to environmental events [34,63],
stressors are less clearly related to the onset of bipolar
episodes [64].
A hypomanic episode, as defined in DSM, Fourth
Edition, Text Revision [52], consists of bpersistently
elevated, expansive, or irritable mood, lasting throughout
at least 4 days.Q These periods of elation are either brief or
absent in BPD [34,63]. Thus, this criterion should readily
distinguish BPD from bipolar II. Problems arise, however,
because assessment of hypomania often depends on
accurate retrospective reporting by patients of whether
mood has in fact been elevated, how long these changes
have lasted, and whether or not they have been stable over a
4-day period. Because clinicians judgments are easily
biased by preconceptions, ratings of hypomania are often
unreliable [17,65]. It would be better if affective lability
could be assessed with reliable laboratory methods, but this
has, so far, proved difficult [66].
Although affective instability is a phenotype of both
BPD and bipolar II, it is problematic to distinguish rapid
mood swings in BPD from the construct of bipolar IV
because both describe virtually the same phenomena.
Although very rapid mood shifts have been observed in
44% of the relatives of patients with bipolar I disorder
[67], their presence in relatives of BPD probands has not
been tested.
Another partially heritable personality phenotype that
patients with BPD and bipolar disorder seem to share is
impulsivity [68,69]. The biologic correlates of BPD are
consistently related to impulsive traits [69,70], and relatives
of BPD patients often have impulse spectrum disorders [11].
Although BPD patients have higher scores on standard
measures of impulsivity than patients with bipolar II [63],
this trait is also found in interepisode bipolar disorder,
particularly when accompanied by substance abuse [71].
However, impulsive actions in bipolar disorder tend to be
more episodic [68], whereas BPD tends to be characterized
by a pattern in which recurrent suicidal gestures and selfinjury are used to reduce distress [72].
Another potential area of overlap concerns interpersonal relationships. BPD patients are characterized by longings for closeness accompanied by fears of rejection,
dependency, and abandonment [6,73,74]. Interpersonal
issues have rarely been examined in bipolar samples.
One study suggested that bipolar II patients demonstrate
higher levels of rejection sensitivity compared to patients
with MDD, but this pattern only characterized 38% of the

subjects, and whether this subgroup also had BPD was

not tested [42].
In summary, although there is overlap between the
phenomenology of BPD and bipolar disorders, there also
are clear distinctions; periods of elevated mood characterize
bipolar disorders, whereas reactivity to interpersonal
stressors characterizes BPD. The data on bipolar I tend to
support hypothesis 3 but, for bipolar II, could be consistent
with any of the other hypotheses.

4. Family prevalence
Increased family prevalence for bipolar disorder in BPD
probands would support hypothesis 1. Increased family
prevalence for BPD in bipolar probands would support
hypothesis 2. Elevation of both could support hypothesis
1 or 2, and 4, whereas lack of elevation for either would
support hypothesis 3.
Early reports suggested that BPD and bipolar disorder
tend to run in the same families [75-77]. However, these
studies did not use standardized criteria or reliable
instruments to establish diagnoses. In 7 subsequent studies
[23,78-83], the frequency of bipolar disorder in first-degree
relatives of BPD probands ranged from 0.5% [78] to 4.5%
[79], with a median value of 1.9%. This is roughly
equivalent to the 1.6% lifetime prevalence of bipolar I
found in the general population [47], and these rates are no
higher than those found in relatives of schizophrenics. In
2 studies that compared probands with BPD to those with
bipolar I, rates were not increased [23,78].
Even for bipolar I and bipolar II, family prevalence data
do not fully support a spectrum model [84]. One study
found that although bipolar I and bipolar II had a similar
prevalence in the first-degree relatives of bipolar I
probands, bipolar II was much more prevalent among
first-degree relatives of bipolar II probands [85]. These
observations suggest that bipolar II itself may be heterogeneous. In addition, when a familial relationship to bipolar
I is not established, some patients identified as bipolar II
could also have BPD. No studies to date have examined the
familial relationship of BPD and bipolar II, but given the
overlap in their phenomenology, it might be expected
to exist.
Thus, existing family prevalence data tend to support the
conclusion that bipolar I disorder is unrelated to BPD,
although this conclusion is weakened by reliance on family
history methodology. No study has assessed the relationship
of bipolar II to BPD. The existing data tend to support
hypothesis 3.

5. Response to medication
Similar responses to medication in BPD and bipolar
disorders could support hypotheses 1 or 2 and 4. Responses to mood stabilizers in BPD would favor hypoth-

J. Paris et al. / Comprehensive Psychiatry 48 (2007) 145154

esis 1. Distinct responses to medications would support

hypothesis 3.
bPharmacologic dissectionQ [86] may provide a way to
determine whether disorders fall in the same spectrum,
based on overlapping responses to medications. Clinical
trials using randomized, placebo-control designs have
shown both similarities and differences in response to
medication between BPD and bipolar patients.
Antidepressants, useful in bipolar depression [87], also
show efficacy in BPD, where both tricyclics [88] and
monoamine oxidase (MAOs) inhibitors [89] have empirical
support. Three studies suggest that selective serotonin
reuptake inhibitors (SSRIs) are mainly effective for impulsivity in BPD [90-92], although 2 others found reduced
dysphoric mood [93,94]. Several antidepressants can produce manic symptoms in bipolar I [95,96] and bipolar II
[96], although the validity of this relationship has been
challenged [97]. Although these effects have not been
examined systematically in BPD, they were not observed
when tricyclics were prescribed for 4 years [88].
Given the presence of affective instability in both BPD
and bipolar II, the 2 disorders might be expected to have a
similar response to mood stabilizers [63]. However,
although lithium reduces mood fluctuations in bipolar I
[96,98] and has some efficacy in bipolar II [99], the only
double-blind study in BPD [100] failed to show that lithium
affected mood. Studies of anti-convulsants show effectiveness for controlling mood in bipolar I and bipolar II
[96,98,101,102]; yet, for BPD, these agents have stronger
effects on impulsivity. For example, although carbamazepine helps control mood in rapid cycling bipolar disorder
[96,101], its effects in BPD are largely on impulsive
behaviors [103]. Similarly, controlled studies of valproate
for BPD found only marginal improvement of mood
[104,105], whereas more positive findings appeared in a
BPD sample comorbid for bipolar II [106].
Three studies support the use of low-dose atypical
neuroleptics in the management of impulsivity in BPD
[94,107,108]. Although impulsivity is not the identified
target, the use of these agents to control manic symptoms in
bipolar I patients suggests they may have overlapping
effects [109,110]. Neuroleptics have not been systematically
studied in bipolar II.
Existing research provides no direct comparisons of
responses by bipolar and BPD samples to the same
medication, but available evidence suggests significant
differences. In particular, the profile of pharmacologic
response in BPD and bipolar I appears distinct. Notably,
neither BPD nor bipolar II responds consistently to lithium
with the specificity seen in bipolar I. The overlap of BPD
response to medications seems more evident with bipolar II
than bipolar I.
Conclusions based on response to medications still
require double-blind placebo controlled studies with separate groups of BPD without bipolar disorder, BPD plus
bipolar disorder, and bipolar disorder without BPD. The

149

existing data largely support hypothesis 3, but there is some

overlap of response between BPD and bipolar II to mood
stabilizers, allowing for hypotheses 1, 2, and 4.
6. Longitudinal course
If BPD evolves into bipolar disorder, this would support
hypothesis 1. If bipolar disorder evolves into BPD, this
would support hypothesis 2. If both occur, hypothesis
4 would be supported. If the overall course of the 2 disorders
remains distinct, hypothesis 3 would be supported.
The idea that BPD evolves into bipolar disorder comes
from 2 early studies. In the first, after 200 broadly defined
BPD patients for 15 years, 4% developed bipolar I, whereas
another 2% developed bipolar II [111]. In the second, a
chart review study of 100 consecutive outpatients diagnosed at baseline with BPD and followed up for 6 to
36 months, 15% developed bipolar I or bipolar II, whereas
another 8% developed mixed states [31]. Since then,
however, a series of follow-back studies using improved
diagnostic methodology have failed to confirm this
evolution, either after 5 [23], 15 [24], or 27 years [56].
Prospective studies have the advantage of being able to
assess patients at baseline. In one such study, among 81 BPD
patients, there was 1 new onset for bipolar I, 4 for bipolar II,
and 4 for cyclothymic disorder on 7-year follow-up [112].
Two prospective follow-up studies of adolescents with BPD
did not describe an evolution to bipolar disorder [113,114].
Recently, a prospective study that followed adult BPD
patients for 4 to 6 years found that only 2 of 290 patients
evolved into bipolar disorder [55]. This study also showed
that most patients (73.5%) show remission from BPD and
then rarely have relapses (5.9% of those remitted). Similar
findings have emerged from an even larger prospective
study, which found a 56% remission within 2 years [115]. In
a recent report from the same cohort, the frequency of new
onsets after 4 years was 5.5% for bipolar I and 2.3% for
bipolar II [116]. Although these findings point to a modest
association between BPD and bipolar disorders, they also
show that BPD has a course quite unlike that of bipolar
disorder, which rarely shows remission within 2 years [117].
Thus, the outcome of BPD seems to be significantly better
than in either bipolar I or bipolar II.
A parallel question concerns whether bipolar patients
can develop BPD. Recent prospective follow-up studies of
bipolar I [118] and bipolar II [119,120] failed to examine
this question. Two longitudinal community studies of
adolescents [121,122] found that hypomania at baseline
predicted later borderline symptoms, although subjects did
not qualify for a clinical diagnosis of BPD.
In summary, the overall course of BPD appears to be
different from bipolar disorders. Neither BPD nor bipolar I
disorder appear to evolve into the other frequently,
although this issue requires further examination. When
BPD patients do develop bipolar disorders over time, it is
not clear whether these rates are elevated compared to

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patients with other diagnoses. These data tend to support

hypothesis 3.
7. Etiology and pathogenesis
Identification of common factors in the etiology and
pathogenesis for BPD and bipolar disorder would support
hypothesis 4 (as well as 1 or 2). Distinct pathways for each
disorder would support hypothesis 3.
In relation to biologic factors, we lack consistent markers
related to either BPD or bipolar disorder. Behavioral genetic
studies have shown that affective instability and impulsivity
are partially heritable [123,124] and that BPD itself has a
significant genetic component [125]. In molecular genetic
studies, repetitive suicide attempts, a symptom frequently
associated with BPD, has been linked to alleles related to
serotonergic function [126,127]. In research on neurotransmitters, the most consistent finding has been an
association between impulsivity and abnormalities in central
serotonergic functioning [128-130]. These relationships
have not been examined in bipolar spectrum disorders. In
neuroimaging research, BPD and bipolar patients share
broad findings such as decreased volume of the prefrontal
cortex [131,132]. However, although bipolar I and bipolar II
patients have increased or normal volumes of amygdala and
hippocampus [131], BPD patients show a decrease in
volume [132-136]. bipolar I, but not bipolar II, demonstrates
ventricular enlargement [137], which has not been observed
in BPD [130]. Direct comparisons of BPD vs bipolar
spectrum patients are needed.
If it could be shown that either affective instability or
impulsivity phenotypes is associated with a genetic profile
common to BPD and bipolar spectrum disorders, this would
go a long way toward explaining their overlap. Recent
research on the biology of bipolar I disorder using genomewide scans points to alleles at least partially specific to the
disorder [138]. These alleles still need to be studied in the
putative bipolar spectrum disorders or in BPD.
Given the likelihood that BPD is etiologically heterogeneous [7], some cases may demonstrate a common genetic
vulnerability with bipolar disorder, even if an overall
relationship has not yet been demonstrated. This would be
consistent with a report by Stone et al [77].

There is a large literature on the role of psychosocial

factors in the etiology of BPD. Patients with this disorder
report unusually high rates of childhood adversities and
insecure attachment [73,139,140]. Although 1 study found
that patients with bipolar I and bipolar II also report
sexual abuse and neglect, 61% of such cases were
comorbid for a Cluster B personality disorder [141]. Thus
far, no studies have compared the prevalence of childhood
adversity between populations with bipolar disorder and
with BPD.
In summary the etiology of both bipolar disorder and
BPD are still poorly understood, and there is little research
from either biologic or psychosocial perspectives that
adequately tests whether they have overlapping pathogenesis and etiology. The data are insufficient to support
any hypothesis.
8. Conclusions
This review takes place within a historical context in
which the DSM system leads to extensive comorbidity for
most psychiatric disorders. More specifically, both bipolar
disorder [142,143] and BPD [5,7,144] have been found to
have high levels and overlapping types of comorbidity, (ie,
anxiety and substance abuse disorders). Yet, in contrast
with bipolar disorder, the documentation of such comorbidity in BPD has recurrently raised the question as to
whether it should be redefined as a variant of one or
another Axis I disorder.
Our conclusions are summarized in Table 3. After
reviewing the evidence concerning co-occurrence rates,
phenomenological distinctions, pharmacologic responsivity, family prevalence, and longitudinal course, it seems
safe to conclude that the current separation of BPD from
bipolar I, that is, hypothesis 3, is supported. The
association with bipolar II is more complicated. Although
evidence from family prevalence, longitudinal course, and
pharmacologic response is largely nonexistent, the evidence from co-occurrence, phenomenology, and etiology is
inconclusive, preserving the possibility of shared phenotypes (hypothesis 4). More epidemiological, longitudinal,
pharmacologic, family, and genetic research is needed to
answer this question.

Table 3
Summary of conclusions
Co-occurrence
Bipolar I

Increased
co-occurrence;
most cases distinct

Phenomenology

Some overlap but periods

of elevated mood in
bipolar-I vs affective
instability in BPD.
Bipolar II
Increased
Hypomanic episodes in
co-occurrence; several bipolar II, vs affective
points of overlap
instability in BPD
Conclusion Tends to support
Tends to support hypothesis
hypothesis 3
3; other hypotheses possible
for bipolar II

Family prevalence

Longitudinal course

Etiology

Bipolar I not
Lithium and mood stabilizers
frequent in
effective in bipolar I, mainly
families with BPD anti-impulsive effects
in BPD
Not studied
Some overlap in response
to mood stabilizers

Response to medication

Neither disorder
frequently evolves
into the other; BPD
has a better outcome
Infrequent as
outcome of BPD

Insufficient
evidence

Tends to support
hypothesis 3
for bipolar I

Tends to support
hypothesis 3

No
conclusion

Tends to support hypothesis

3; other hypotheses possible
for bipolar II

Insufficient
evidence

J. Paris et al. / Comprehensive Psychiatry 48 (2007) 145154

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