Journal of Affective Disorders 170 (2015) 3945

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Journal of Affective Disorders

journal homepage: www.elsevier.com/locate/jad

Research report

Signicance of borderline personality-spectrum symptoms among

adolescents with bipolar disorder
Trehani M. Fonseka, Brenda Swampillai, Vanessa Timmins, Antonette Scavone,
Rachel Mitchell, Katelyn A. Collinger, Benjamin I. Goldstein n
Department of Psychiatry, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON, Canada

art ic l e i nf o

a b s t r a c t

Article history:
Received 8 July 2014
Received in revised form
27 July 2014
Accepted 12 August 2014
Available online 3 September 2014

Background: Little is known regarding correlates of borderline personality-spectrum symptoms (BPSS)

among adolescents with bipolar disorder (BP).
Methods: Participants were 90 adolescents, 1319 years of age, who fullled DSM-IV-TR criteria for BP
using semi-structured diagnostic interviews. BPSS status was ascertained using the Life Problems
Inventory which assessed identity confusion, interpersonal problems, impulsivity, and emotional lability.
Analyses compared adolescents with high versus low BPSS based on a median split.
Results: Participants with high, relative to low, BPSS were younger, and had greater current and past
depressive episode severity, greater current hypo/manic episode severity, younger age of depression
onset, and reduced global functioning. High BPSS participants were more likely to have BP-II, and had
higher rates of social phobia, generalized anxiety disorder, conduct disorder, oppositional deant
disorder, homicidal ideation, assault of others, non-suicidal self-injury, suicidal ideation, and physical
abuse. Despite greater illness burden, high BPSS participants reported lower rates of lithium use. The
most robust independent predictors of high BPSS, identied in multivariate analyses, included lifetime
social phobia, non-suicidal self-injury, reduced global functioning, and conduct and/or oppositional
deant disorder.
Limitations: The study design is cross-sectional and cannot determine causality.
Conclusions: High BPSS were associated with greater mood symptom burden and functional impairment.
Presence of high BPSS among BP adolescents may suggest the need to modify clinical monitoring and
treatment practices. Future prospective studies are needed to examine the direction of observed
associations, the effect of treatment on BPSS, and the effect of BPSS as a moderator or predictor of
treatment response.
& 2014 Elsevier B.V. All rights reserved.

Keywords:
Bipolar
Borderline
Personality disorder
Adolescent

1. Introduction
The association between borderline personality disorder (BPD)
and bipolar disorder (BP), particularly BP-II, has been well documented (Benazzi, 2000, 2006; Zimmerman and Morgan, 2013). BPD
is conceptualized as a chronic and persistent personality disorder whereas BP is conceptualized as an episodic mood disorder
(American Psychiatric Association, 2013). However, there is increasing evidence that symptoms of BPD wax and wane and that there are
often substantial inter-episode symptoms in BP (Akiskal et al., 1989;
Morriss, 2002; Zanarini et al., 2005). Some studies argue that BPD
is best reframed as part of the BP spectrum due to symptomatic
and familial genetic overlap between these diagnostic phenotypes.
n
Correspondence to: Centre for Youth Bipolar Disorder, Sunnybrook Health
Sciences Centre, 2075 Bayview Avenue, Room FG53, Toronto, ON, M4N 3M5,
Canada. Tel.: 1 416 480 6100x5328; fax: 1 416 480 6878.
E-mail address: benjamin.goldstein@sunnybrook.ca (B.I. Goldstein).

http://dx.doi.org/10.1016/j.jad.2014.08.046
0165-0327/& 2014 Elsevier B.V. All rights reserved.

(Akiskal, 2004; Akiskal et al., 1985; Perugi et al., 2003; Smith et al.,
2004). For example, both BPD and BP are associated with emotional
lability, impulsivity, irritability and anger, unstable interpersonal
relationships, feelings of emptiness, and suicidality (Akiskal, 2004;
Bowden and Maier, 2003; Henry et al., 2001; Perugi and Akiskal,
2002). The diagnosis of comorbid BPD in BP is also sensitive to
the cross-sectional presentation of any active mood symptoms at the
time of assessment. For instance, studies have shown that BPD
assessments made during episodes of BP illness lead to a 30%
increase in BPD prevalence rates compared to if the diagnosis is
made during periods of euthymia (Smith et al., 2004). However,
others view BPD as a distinct diagnostic entity (Gunderson, 2009)
because, even within areas of shared symptomology, there are
signicant differences in the phenomenology of BPD as compared
to BP (Feliu-Soler et al., 2013; Zimmerman and Morgan, 2013).
For example, while both BPD and BP patients experience affective
lability, the severity and direction of affective shifts differ between
groups (Henry et al., 2001; Nilsson et al., 2010). Such observations

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T.M. Fonseka et al. / Journal of Affective Disorders 170 (2015) 3945

challenge the conceptualization of BPD as part of the BP spectrum.

However, most agree that patients with the symptoms of BPD are
highly stigmatized and often neglected. For a recent review on the
differential nature of BPD relative to BP, refer to (Bayes et al., 2014).
In many cases, it is not a question of BP or BPD, but rather BP
and BPD, and in such cases there appears to be greater complexity
and symptom burden. Rates of comorbid BPD in adult BP range
from 12% to 30% (Barbato and Hafner, 1998; Benazzi, 2000; Rossi
et al., 2001; Vieta et al., 1999), with BPD occurring in approximately
10% of BP-I and 23% of BP-II patients (Zimmerman and Morgan,
2013). Some studies report BPD as the most common personality
disorder among adult BP patients (OConnell et al., 1991; Peselow
et al., 1995; Vieta et al., 1999). Adult BP patients with comorbid
personality disorders have less favorable outcomes including longer
and more frequent hospitalizations (Barbato and Hafner, 1998;
Dunayevich et al., 2000), increased suicidal ideation and attempts
(Carpiniello et al., 2011; Vieta et al., 1999), greater symptom severity
and functional impairment (Barbato and Hafner, 1998; Carpenter
et al., 1995; George et al., 2003), earlier age of mood symptom onset
(Vieta et al., 1999), greater unemployment (Kay et al., 2002), higher
rates of axis I comorbidity (Kay et al., 2002; Preston et al., 2004),
and worsened long-term outcomes of symptomatic and functional
recovery (Bieling et al., 2003; Dunayevich et al., 2000) compared
to those without personality disorders. This comorbidity has
been further associated with poor pharmacotherapy outcomes as
evidenced by reduced compliance (Colom et al., 2000) and response
to treatment (Barbato and Hafner, 1998), and necessity for polypharmacy (Kay et al., 2002).
Only one study to our knowledge has focused on personality
disorders in BP adolescents. (Kutcher et al., 1990) found that 15%
of BP adolescents had comorbid BPD, and among the total sample,
personality disturbance was associated with greater use of antipsychotics and decreased lithium response. No studies have
specically investigated the effects of BPD in BP youth. This
adolescent BP-BPD relationship is important to investigate given
that maladaptive personality traits often rst appear during
adolescence or early adulthood (Bowden and Maier, 2003), and
can negatively impact long-term patient outcomes (Winograd
et al., 2008).
Given the propensity of comorbid BPD to yield greater symptomatic burden and impairment in BP adults, coupled with a paucity
of data on this topic in adolescent samples, we sought to examine
the demographic and clinical correlates of self-reported borderline
personality-spectrum symptoms (BPSS) among BP adolescents.
Given previous ndings, we hypothesized that high levels of BPSS
would be associated with worsened BP outcomes, as determined
by earlier age of mood symptom onset, and increased symptom

severity, functional impairment, axis I comorbidity, psychiatric

hospitalization, and suicidality.

2. Methodology
2.1. Participants
Ninety adolescent participants, 1319 years of age, with a
Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition, Revised (DSM-IV-TR) diagnosis of BP-I, BP-II or operationalized BP Not Otherwise Specied (NOS) were included in the
study. Participants were recruited from a tertiary sub-specialty
outpatient clinic in an academic health sciences center. Operationalized BP-NOS was dened according to the Course and Outcome
of Bipolar Youth (COBY) study criteria (for details see (Birmaher
et al., 2006)). Participants and their parent(s)/guardian(s) provided
written informed consent after reviewing study parameters
with research staff. This study was approved by the local research
ethics board.
2.2. Assessment
Demographic information was collected for all participants
including age, sex, race, and family composition. Psychiatric
diagnoses were determined using the Schedule for Affective
Disorders and Schizophrenia for School-Aged Children, Present
and Lifetime Version (KSADS-PL) (Kaufman et al., 1997), a semistructured diagnostic interview. Bachelor's or Master's-level interviewers completed extensive training under the supervision of the
senior author, who also provided diagnostic consensus on all cases
(B.G). Mood symptom severity was determined with the KSADS
Depression Rating Scale (DRS) (Chambers et al., 1985), and KSADS
Mania Rating Scale (MRS) (Axelson et al., 2003). Age of depressive
and hypo/manic symptom onset was dened as the age when
symptoms rst impaired functioning. Substance use disorders
were dened as alcohol and/or drug abuse and/or dependence.
BPSS were self-reported using the 60-item Life Problems
Inventory (LPI) which assessed symptom severity across four
BPD-related subscales: identity confusion, interpersonal problems,
impulsivity, and emotional lability (Rathus and Miller, 1995) (refer
to Table 1). Participants characterized BPSS over the past six
months using a 5-point likert scale (1 not at all like me to
5 extremely like me). According to Rathus, Wagner, and Miller's
2005 validation study of the LPI (as cited in (Muehlenkamp et al.,
2011)), the LPI was developed and validated using psychiatric
outpatient and community-based adolescent samples. Preliminary

Table 1
Life Problems Inventory (LPI) subscale examples (Rathus and Miller, 1995).
LPI subscale

Item examples

Confusion about self

Im not sure I know who I am or what I want in my life

Other kids my age seem more sure than I am of who they are and what they want
I am so different at different times I sometimes dont know who I really am

Interpersonal chaos

Relationships with people I care about have a lot of ups and downs
Many of my relationships have been full of intense arguments
I have had a lot of break-ups with people Ive been close to

Impulsivity

I usually act quickly, without thinking

If I want to do something, I just do it without thinking of what might happen
Ive spent money on things I didnt need or couldnt afford

Emotional dysregulation

I sometimes get so upset that I want to hurt myself seriously

When I dont get my way, I quickly lose my temper
Once I get upset, it takes me a long time to calm down

T.M. Fonseka et al. / Journal of Affective Disorders 170 (2015) 3945

data support the LPI's internal consistency reliability (alpha

coefcients:0.890.92; subscale alpha coefcients:0.820.90; testretest correlations:0.880.91), and criterion validity with the BPD
subscale of the Structured Clinical Interview for DSM-IV Axis II

41

Personality Disorders (SCID-II) (Muehlenkamp et al., 2011; Rathus

and Miller, 2002). Finally, LPI discriminant validity differentiates
BPD adolescents from depressed patients and healthy controls
(Muehlenkamp et al., 2011).

Table 2
Univariate analyses examining demographic and clinical characteristics associated with BPSS.

Demographics
Age
Sex (%female)
Race (%Caucasian)
Living with both natural parents

High BPSS (n 44)

Low BPSS (n 46)

15.86 7 1.19
33 (75.0%)
37 (84.1%)
23 (52.3%)

16.48 71.68
28 (60.9%)
41 (89.1%)
30 (65.2%)

2/t value

2.01
2.06
0.49
1.56

p-value

pcorrecteda

0.048*
0.152
0.482
0.212

0.134
0.322
0.637
0.362

0.011*
0.036*
0.887
o 0.001*
0.025*
0.022*
0.493
0.258
0.001*
0.139
o 0.001*
0.806

0.064
0.119
0.922
0.004*
0.106
0.106
0.637
0.407
0.018*
0.322
0.004*
0.872

Symptom severity and clinical characterization (Domain 1)

BP-I
6 (13.6%)
BP-II
24 (54.5%)
BP-NOS
14 (31.8%)
Depression severity (current episode)
23.747 11.73
Depression severity (past episode)
32.42 76.42
Hypo/mania severity (current episode)
18.45 7 10.56
Hypo/mania severity (past episode)
26.16 79.34
Psychosis
8 (18.2%)
Age of onset of depressive symptoms
11.19 7 3.66
Age of onset of hypo/manic symptoms
13.39 7 2.40
CGAS Score (Current Episode)
48.43 7 7.00
CGAS score (most severe episode)
41.18 75.52

17 (37.0%)
15 (32.6%)
14 (30.4%)
13.91 711.49
28.34 79.89
13.077 11.38
27.63 7 10.82
13 (28.3%)
14.007 2.58
14.317 2.49
56.047 10.32
40.80 78.69

Lifetime Psychiatric Comorbidities (Domain 2)

Panic disorder
Social phobia
Generalized anxiety disorder
Any anxiety
Anorexia nervosa
Bulimia nervosa
Conduct disorder (CD)
Oppositional Deant disorder (ODD)
CD and/or ODD
Attention decit hyperactivity disorder
Substance use disorder

11 (25.0%)
18 (40.9%)
27 (61.4%)
36 (81.8%)
2 (4.5%)
6 (13.6%)
8 (18.2%)
22 (50.0%)
23 (52.3%)
19 (43.2%)
18 (40.9%)

6 (13.0%)
7 (15.6%)
18 (39.1%)
31 (67.4%)
0 (0.0%)
3 (6.5%)
0 (0.0%)
10 (21.7%)
10 (21.7%)
17 (37.0%)
12 (26.1%)

2.10
7.08
4.45
2.46
2.14
1.27
9.18
7.84
9.03
0.36
2.22

0.147
0.008*
0.035*
0.117
0.144
0.261
0.002*
0.005*
0.003*
0.547
0.136

0.322
0.053
0.119
0.310
0.322
0.407
0.027*
0.044*
0.032*
0.647
0.322

Lifetime Safety (Domain 3)

Police contact/arrest
Homicidal ideation
Death threats
Assault of others
Sexual activity
Non-suicidal self injury
Suicidal ideation
Suicide attempt
Physical abuse
Sexual abuse

20 (45.5%)
9 (22.0%)
8 (19.5%)
17 (41.5%)
22 (53.7%)
27 (61.4%)
32 (72.7%)
14 (31.8%)
6 (13.6%)
6 (13.6%)

17 (37.0%)
1 (2.4%)
4 (9.5%)
8 (19.0%)
20 (48.8%)
16 (34.8%)
24 (52.2%)
9 (19.6%)
1 (2.2%)
4 (8.7%)

0.67
7.50
1.67
4.95
0.20
6.37
4.04
1.78
4.12
0.56

0.413
0.006*
0.196
0.026*
0.659
0.012*
0.044*
0.183
0.042*
0.456

0.600
0.045*
0.359
0.106
0.743
0.064
0.130
0.359
0.130
0.620

Lifetime Treatment History

Psychiatric hospitalization
Any psychotropic medication
Second generation antipsychotic
Stimulant
Lamotrigine
SSRI antidepressant
Non-SSRI antidepressant
Lithium
Antimanic anticonvulsantb

20 (45.5%)
30 (68.2%)
21 (47.7%)
5 (11.4%)
2 (4.5%)
16 (36.4%)
6 (13.6%)
4 (9.1%)
5 (11.4%)

24 (52.2%)
34 (73.9%)
26 (56.5%)
10 (21.7%)
4 (8.7%)
11 (23.9%)
7 (15.2%)
12 (26.1%)
5 (10.9%)

0.41
0.36
0.70
1.74
0.62
1.66
0.05
4.44
0.01

0.524
0.549
0.404
0.187
0.430
0.198
0.831
0.035*
0.941

0.646
0.647
0.600
0.359
0.600
0.359
0.881
0.119
0.959

Family Psychiatric History (1st and 2nd Generation)

Major depressive episode
36 (81.8%)
Hypo/mania
21 (47.7%)
Conduct disorder
2 (4.5%)
Anxiety
24 (54.5%)
Substance use disorder
21 (47.7%)
Suicidal ideation
15 (34.1%)
Suicide attempt
17 (38.6%)

35 (76.1%)
26 (60.5%)
4 (8.7%)
25 (54.3%)
19 (44.2%)
17 (39.5%)
12 (26.1%)

0.44
1.42
0.62
0.00
0.11
0.28
1.62

0.505
0.233
0.430
0.985
0.740
0.599
0.203

0.637
0.386
0.600
0.985
0.817
0.690
0.359

6.43
4.41
0.02
 3.95
 2.29
 2.33
0.69
1.28
3.59
1.50
4.11
 0.25

Values represent number (percent) or mean 7 SD.

n

Value signicant at p o 0.05.

Value corrected for multiple comparisons using false discovery rate.
b
Antimanic anticonvulsant:valproic acid, divalproex, carbamazepine; BPSS:borderline personality-spectrum symptoms; BP-I:bipolar I disorder; BP-II:bipolar II disorder;
BP-NOS:bipolar disorder not otherwise specied; CGAS:Children's Global Assessment Scale; SSRI:selective serotonin reuptake inhibitor.
a

42

T.M. Fonseka et al. / Journal of Affective Disorders 170 (2015) 3945

History of lifetime aggression, suicidality, and sexual activity

were obtained from a Safety Assessment Form. History of lifetime
physical and/or sexual abuse was ascertained using a Medical
History Questionnaire and the KSADS-PL Post-Traumatic Stress
Disorder Screen. Measures of global functioning were clinicianrated using the Children's Global Assessment Scale (CGAS) (Shaffer
et al., 1983). Family psychiatric history was reported for rst
and second generation relatives using the Family History Screen
(Weissman et al., 2000).
2.3. Statistical analysis
Since the LPI does not have established norms or cut-offs, BPSS
status was determined using dichotomized total LPI scores with
subjects at or above the 50th percentile (high BPSS, n 44)
compared against the remainder of the sample (low BPSS,
n 46). Based on the normal distribution pattern of LPI scores in
our sample, a median cut-point was selected over other alternatives to increase statistical power through an almost equal size
of observation between groups. A median cut-point, which has
been used by other studies (Davis and Brekke, 2013; Li et al., 2014;
Sullivan et al., 2012), also prevents any unusual or outlier data
points from biasing statistical results (DeCoster et al., 2009).
Between-group differences were compared using Pearson 2
tests for categorical variables, and Student t-tests for continuous
variables. False discovery rate was used to correct for multiple
comparisons within univariate analyses. Variables signicant from
univariate analyses with an unadjusted p-value of o 0.05 were
analyzed within a logistic regression model performed separately
for each domain (refer to Table 2 for domain and variable
classication), using BPSS status (high vs. low) for total LPI as
the dependent variable. Variables signicant at the p o0.05 level
across all domain analyses were simultaneously analyzed in an
omnibus logistic regression, controlling for participant age. Pearson correlation coefcients examined associations between dimensional scores across total LPI and current CGAS (CGAS-C). Statistical analyses were performed using Statistical Package for the
Social Sciences (SPSS), version 20.0.

3. Results
3.1. Univariate Analyses
Participants were 90 English-speaking males (n 29) and
females (n 61), 1319 years of age (mean age: 16.18 71.5 years),
of various ethnicities, with a DSM-IV-TR diagnosis of BP-I (n 23),
BP-II (n 39), or BP-NOS (n 28). Results from univariate analyses
are summarized in Table 2. High BPSS participants were younger
(t(81) 2.01, p 0.048), and more likely to have a diagnosis of BP-II
(54.5% vs. 32.6%, p 0.036), in addition to a reduced likelihood of
BP-I (13.6% vs. 37.0%, p 0.011), as compared to low BPSS participants. High BPSS participants showed higher rates of lifetime
psychiatric comorbidity across all examined diagnoses, with signicant differences emerging for social phobia (40.9% vs. 15.6%,
p 0.008), generalized anxiety disorder (GAD) (61.4% vs. 39.1%,
p 0.035), conduct disorder (CD) (18.2% vs. 0.0%, p 0.002), and
oppositional deant disorder (ODD) (50.0% vs. 21.7%, p 0.005).
All lifetime safety-related variables were elevated in the high
BPSS group, with signicant differences emerging for homicidal
ideation (22.0% vs. 2.4%, p 0.006), assault of others (41.5% vs.
19.0%, p 0.026), non-suicidal self injury (NSSI) (61.4% vs. 34.8%,
p 0.012), suicidal ideation (72.7% vs. 52.2%, p 0.044), and physical abuse (13.6% vs. 2.2%, p 0.042).
High BPSS were associated with worsened clinical course, as
evidenced by greater current (t(85)  3.95, p o0.001) and past

(t(74) 2.29, p 0.025) depressive episode severity, current

hypo/manic episode severity (t(88)  2.33, p 0.022), younger
age of depressive symptom onset (t(62) 3.59, p 0.001), and
reduced current global functioning (t(79) 4.11, p o0.001). Despite
these worsened outcomes, high BPSS participants were less likely
to report lifetime use of lithium (9.1% vs. 26.1%, p 0.035). After
applying a correction for multiple comparisons, the following
outcomes remained signicant: CD (p 0.027), ODD (p 0.044),
homicidal ideation (p 0.045), current depression severity (p
0.004), age of depression onset (p 0.018), and current global
functioning (p 0.004). No between-group differences were observed for family psychiatric history. There was a signicant
negative correlation between total LPI and CGAS-C scores (r
 0.39, p o0.001) indicating a decline in global functioning with
increasing BPSS.
Exploratory analyses across each LPI subscale (identity confusion, interpersonal problems, impulsivity, emotional lability)
revealed a similar overall pattern of ndings as observed within
total LPI univariate analyses (data not shown). In particular,
analysis of the identity confusion subscale, which isolates a
symptomatic construct specic to BPD over BP, revealed that BP
participants who endorse high levels of confusion about the self
have the same general outcomes as presented here for total LPI
analyses, in addition to a greater likelihood of panic disorder, and
reduced likelihood of lifetime psychosis. These results suggest that
overall study ndings are indeed informative of a true synergy
between BP and BPSS on worsened clinical trajectories in adolescent patients, rather than being a mere artifact of more severe BP
symptomology.
3.2. Multivariate analyses
Variables signicant from total LPI univariate analyses at the
unadjusted p o0.05 level were analyzed within logistic regression
models performed separately for each domain: (Domain 1) symptom severity and clinical characterization, (Domain 2) lifetime
psychiatric comorbidities, and (Domain 3) lifetime safety-related
variables. Demographics, lifetime treatment history, and family
psychiatric history domains were not analyzed due to a predominance of non-signicant ndings. However, lithium use was
included in Domain 1 as the only medication that was associated
with BPSS. Due to a zero frequency distribution in the low BPSS
group for CD, CD and ODD were analyzed together as a single
variable (CD and/or ODD). To minimize redundancy, only the BP-I
variable was entered into the regression while the BP-II variable
was excluded.
Variables signicant at the p o0.05 level from each domain
analysis (refer to Table 3) were simultaneously analyzed in an
omnibus logistic regression, where participant age was a forced

Table 3
Domain-specic multivariable predictors of high BPSS.
OR

95% CI

Symptom Severity and Clinical Characterization

BP-I
0.09 0.010.58
Age of Onset of Depressive Symptoms 0.73 0.531.00
CGAS Score (Current Episode)
0.78 0.690.90

Wald

p-value

6.40
3.89
12.91

0.011
0.048
o 0.001

Lifetime Psychiatric Comorbidities

Social Phobia
CD and/or ODD

3.57
4.99

1.1910.74
1.8213.67

5.12
9.74

0.023
0.002

Lifetime Safety
Non-Suicidal Self Injury

2.79

1.057.47

4.19

0.041

BP-I:bipolar I disorder; CGAS:Children's Global Assessment Scale; CD:conduct

disorder; ODD:oppositional deant disorder, OR:odds ratio, CI:condence interval.

T.M. Fonseka et al. / Journal of Affective Disorders 170 (2015) 3945

covariate. Six variables were included: age of depression onset,

BP-I, current CGAS, social phobia, CD and/or ODD, and NSSI. Of
the six variables entered into the model, the following four
remained signicant: lifetime social phobia (OR 18.26, CI: 2.15154.94, p 0.008), NSSI (OR 7.24, CI: 1.12-0.46.95, p 0.038),
CGAS-C (OR 0.82, CI: 0.74-0.92, p 0.001), and CD and/or ODD
(OR 9.35, CI: 1.49-58.58, p 0.017).

4. Discussion
In this sample of adolescents with BP, univariate analyses revealed
that high BPSS were associated with younger age, earlier age of
depression onset, greater mood symptom severity, increased rates
of axis I comorbidity in the areas of anxiety and disruptive behavior
disorders, greater risk-related behaviors in the areas of aggression,
suicidality and abuse, and greater functional impairment. Despite this
clinical prole, high BPSS participants did not report greater exposure
to psychotropic medication, and in fact had less exposure to lithium.
However, after applying a correction for multiple comparisons, only
those associations involving disruptive behavior disorders, homicidal
ideation, depression severity and age of onset, and global functioning
remained signicant. Exploratory analyses across each LPI subscale
revealed a similar overall pattern of ndings, including the identity
confusion subscale which assessed a BPD-specic construct that had
minimal symptomatic overlap with BP. Multivariate analyses identied lifetime social phobia, lifetime CD and/or ODD, NSSI, and reduced global functioning as the most robust independent predictors of
high BPSS.
However, this study design is not without limitations. First, the
use of cross-sectional and retrospective clinical assessments is
subject to potential recall bias. In the absence of longitudinal data,
inferences of causality for signicant associations cannot be
determined. For example, mood symptoms may have impacted
self-reported BPSS or the converse may be true. Second, since the
LPI is based on self-report, incorporating a parent-report and/or
diagnostic interview for BPD may have yielded different ndings.
Third, dichotomization of total LPI scores may have resulted in a
loss of analytic power and a reduction in effect size estimates
(DeCoster et al., 2009). Despite being one of the larger samples of
BP adolescents, this study was not powered to detect differences
with small effect sizes, particularly in multivariate analyses.
Despite these limitations, our ndings contribute to the nascent
literature on the signicance of BPSS among BP adolescents, a topic
of signicant clinical and scientic importance. As documented in
other studies, high BPSS in our sample were associated with BP-II
(Benazzi, 2000, 2006; Skodol et al., 1999), and younger participant
age (Grant et al., 2008). Preston and colleagues (Preston et al., 2004)
reported BPD to be signicantly more common among BP females
compared to males. We found a numerically, but not statistically
signicantly, higher frequency of females in the high BPSS group.
High BPSS in our sample were associated with increased psychiatric comorbidity in the areas of anxiety and disruptive behavior
disorders, and greater mood symptom severity. Similar clinical
correlates have been observed among BP adults with personality
disorders (Garno et al., 2005; George et al., 2003), and independent
BPD samples (Lenzenweger et al., 2007; Lewinsohn et al., 1997;
Skodol et al., 1999; Zanarini et al., 1998; Zimmerman and Mattia,
1999), with additional work suggesting that rates of axis I comorbidity decline in response to BPD remission (Zanarini et al., 2004).
Despite these ndings, high BPSS participants had lower rates of
lithium use. Reasons for this are uncertain but may be due to
concerns about lethality of lithium in overdose or treatment biases
driven by the salience of BPSS. For example, since BPD patients are
highly stigmatized as exceedingly disruptive and unresponsive to
treatment (Nehls, 1998), clinicians may negatively perceive and be

43

reluctant to treat BPD patients (Aviram et al., 2006; Sansone and

Sansone, 2013).
BPD patients are at an elevated risk of suicidality and aggression.
Along with increased rates of CD and ODD in our sample, high BPSS
were positively associated with assault of others and homicidal
ideation. Similar ndings have been documented in BPD studies,
with reports of higher rates of BPD in prison populations, often for
perpetration of violent offenses (Latalova and Prasko, 2010; Sansone
and Sansone, 2009). BPD has also been associated with self-injury
and suicidality (Dulit et al., 1994; Gross et al., 2002), with approximately 10% of BPD patients completing suicide (Paris, 2002).
(Zimmerman et al., 2014) found that BPD-BP comorbid samples
were more likely to attempt suicide than BP patients alone. In our
sample, high BPSS was associated with greater NSSI and suicidal
ideation, yet suicide attempt rates, although elevated among high
BPSS participants, did not reach statistical signicance.
In conclusion, the results of our study suggest that BP adolescents
with high BPSS have less favorable clinical and prognostic outcomes in the areas of increased axis I comorbidity, elevated risk
of suicidality and aggression, younger age of mood symptom onset,
greater mood symptom severity, and greater functional impairment.
These ndings are supported by several studies that have concluded
that comorbid personality disorders in BP negatively affect patient
outcomes (Barbato and Hafner, 1998; Bieling et al., 2003; Carpenter
et al., 1995; Carpiniello et al., 2011; Colom et al., 2000; Dunayevich
et al., 2000; George et al., 2003; Kay et al., 2002; Kutcher et al., 1990;
Preston et al., 2004; Vieta et al., 1999; Winograd et al., 2008). Presence of high BPSS among BP adolescents may suggest the need to
modify clinical monitoring and treatment practices. Psychosocial
(Clarkin et al., 2007; Giesen-Bloo et al., 2006) and/or psychotropic
(Ripoll, 2013) treatment may offer benecial effects for BPSS. In
particular, dialectical behavior therapy (DBT), which is routinely used
to treat BPD (Lynch et al., 2007), may be efcacious in comorbid cases
as preliminary ndings suggest benecial effects among BP adolescents (Goldstein et al., 2007). Additional work in neuroimaging has
characterized BPD by dysfunction in various brain regions, particularly fronto-limbic circuits (Ruocco et al., 2013, 2010; Schmahl and
Bremner, 2006), and identied both similar and differential patterns
of fronto-limbic activation between BPD and BP patients (Malhi et al.,
2013). Whether present ndings would extend to full-threshold
BPD is uncertain and this question warrants further investigation.
Although the LPI can neither be used to diagnose BPD or BP, nor to
distinguish between these overlapping disorders, present ndings
suggest that this self-report may have clinically relevant heuristic
value in identifying BP adolescents with high-risk presentations.
Further research in this area is required to more clearly elucidate the
effects of BPSS among BP adolescents. In particular, these compelling
preliminary ndings warrant replication in larger samples using
prospective methodology and employing biological markers.
Role of funding source
The authors would like to thank the grant support from Canadian Institutes of
Health Research, Heart & Stroke Foundation of Ontario, Ontario Mental Health
Foundation, and anonymous philanthropic donations. The content of this paper is
solely the responsibility of the authors and does not necessarily represent the
ofcial views of these organizations. These funding sources were not directly
involved in the study design; collection, analysis and interpretation of data; writing
of the report; or the decision to submit the article for publication.

Conict of interest
We conrm this manuscript describes original work that has not been
published elsewhere and is not under consideration by another journal. We have
no conicts of interest to disclose.

Acknowledgments
The authors would like to thank the participants of this study. We have no
acknowledgments of assistance to disclose.

44

T.M. Fonseka et al. / Journal of Affective Disorders 170 (2015) 3945

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