Psychiatr Q (2012) 83:281–292

DOI 10.1007/s11126-011-9198-7

ORIGINAL PAPER

Borderline Personality Disorder and Depression:

An Update

Maria Luca • Antonina Luca • Carmela Calandra

Published online: 22 October 2011

Ó Springer Science+Business Media, LLC 2011

Abstract To review the literature related to recent temperamental and biological findings
on borderline personality disorder (BPD) and major depression, the close link between the
two disorders, and the latest therapeutical findings on BPD, focusing on the conditions of
co-morbidity between depression and BPD. The National Institutes of Health’s PubMed
database was used to identify indexed studies on BPD, depression and the co-morbidity
between the two. Only studies published between 2000 and 2011 were assessed. Similar
temperamental features have been demonstrated in BPD and depression. The strong link
between the two disorders seems to be widely recognized by scientific community. Psy-
chotherapy and new antipsychotics are the topics of current major interest of research. The
therapeutic targets in the case of co-morbidity are BPD features associated with depressive
symptoms, thus influencing prognosis. A global assessment is, in fact, fundamental for a
successful therapy for the treatment of the several aspects of a complex psychopathological
phenomenon.

Keywords Borderline personality disorder
Depression
Temperament

Neurobiology
Treatment

M. Luca
C. Calandra (&)

Department of Medical and Surgery Specialties, Psychiatry Unit of the University Hospital
‘‘Policlinico-Vittorio Emanuele’’ of Catania (Sicily), Via S. Sofia 78, 95100 Catania (Sicily), Italy
e-mail: c.calandra@unict.it
M. Luca
e-mail: lucmaria@tiscali.it

A. Luca
Department of Neuroscience, University Hospital ‘‘Policlinico-Vittorio Emanuele’’ of Catania (Sicily),
Catania, Italy
e-mail: antolucaster@gmail.com

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Introduction

Borderline personality disorder (BPD) is a severe psychiatric illness with a lifetime

prevalence of 5.9% [1]. Nine criteria are described in the Diagnostic and Statistical Manual
of Mental Disorders Text Revision (DSM-IV TR), five of which are needed for the
diagnosis: (1) efforts to avoid real or imagined abandonment; (2) unstable and intense
interpersonal relationships; (3) markedly and persistently unstable self-image or sense of
self; (4) impulsivity in at least two areas that are potentially self-damaging; (5) recurrent
suicidal behavior, gestures, or threats, or self-mutilating behavior; (6) affective instability
due to a marked reactivity of mood; (7) chronic feelings of emptiness; (8) inappropriate
intense anger or difficulty in controlling anger; (9) transient stress-related paranoid ideation
or severe dissociative symptoms [2].
Borderline personality disorder is, therefore, characterized by hyper-reactivity to vari-
ous emotional stimuli [3] and instability in almost all functioning areas, from affectivity to
impulse control and self-image.
In addition, elevated rates of suicide attempts have been found in patients with BPD [4].
Patients with BPD are frequently self-damaging and present a considerable suicide risk.
The instability that characterizes this disorder (excluding self-injury) has been strongly
associated with suicidal behaviors [5, 6].
When approaching a depressed patient, it is important, therefore, to consider even
borderline personality traits, such as impulsivity, that have a strong independent impact on
suicidality [7]; on the other hand, certain depressive aspects could be related to borderline
personality traits: depressive rumination has been found to be associated with borderline
personality traits, such as inconsistent sense of self and referred unstable relationships [8].
In everyday practice, the several nuances of a clinical case have to be ‘‘captured’’ by the
clinician so as to choose a self-centred treatment. Empirically-derived categories of per-
sonality disorders symptoms, worth pondering over, may highlight interpersonal dys-
functions that the DSM-IV-TR categories fail to elicit [9].
It has to be considered that there is a strong co-morbidity between BPD and depression,
worsened by the earlier onset of depression in BPD patients and by an increased risk of
suicide and drug abuse. In general, BPD, in fact, is frequently associated with common
mental disorders [10, 11].
A very rich field of research, that has recently been conducted on BPD and depression,
is about temperamental features, some of which are shared by the two disorders.
Behavioral inhibition and, more specifically, the temperament dimension of harm
avoidance (HA) has been found to be associated with depression. In literature, high HA has
been frequently related to current depressive symptoms and to depressive trait [12]. This
data has been confirmed in a study [13] using the Turkish version of the temperament and
character inventory (TCI) [14]: Compared to healthy controls, depressed patients presented
higher scores in HA and lower scores in self-directedness.
High HA and low self-directedness have also been observed in BPD patients [10],
besides high novelty seeking and low cooperativeness [15].
In BPD, experiential avoidance is linked to self-harm behavior. Indeed, BPD severity
relate to a higher self-harm frequency and a greater experiential avoidance [16].
Regarding depression, HA is a mediator of treatment response to serotoninergic anti-
depressants [17].
The association between BPD and depression does not only have a theoretical value, but
also several practical implications.

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The presence of BPD, in fact, has a negative influence on the functioning of depressed
patients [18], on the course, the recurrence [19] and even the risk of relapse of depression
[20].
In BPD patients, there are various predictors that increase the risk of self-injurious
behavior, such as major depression, a history of sexual abuse and the severity of dysphoric
cognitions [21].
It appears useful to review the latest temperamental and biological findings on BPD, on
major depression, and on the close correlation between the two disorders, so as to clarify
the clinical impact of their co-morbidity.
In addition, the most recent findings, regarding BPD therapeutical interventions,
focusing, in particular, on their potential usefulness when treating co-morbidity between
depression and BPD, have been reviewed.

BPD and Depression: Temperamental Evidence and Clinical Impact of Co-Morbidity

Temperament, childhood environment and psychopathology can be considered three

fundamental risk factors for BPD [22].
Severe affective temperament and maladaptive self-schemas have been demonstrated in
BPD [23]; in particular, temperamental symptoms (e.g. chronic anger) have been related
with high neuroticism, and acute symptoms (e.g. substance abuse), with low agreeableness
[24].
On the other hand, neuroticism has been associated with depression and anxiety dis-
orders, while extraversion has been inversely correlated with these two disorders [25].
Impaired recognition of emotions, thoughts and intentions, has been observed in a study
that tested 64 borderline women [26]. Interpersonal problems are, in fact, significant
markers of personality disorders [9]: disturbed relationship characteristics, such as
manipulativeness and regressions, play a significant role in clinical problems [27].
Furthermore, attachment insecurity has been reported in BPD, in correlation with cer-
tain symptoms. High anger has been associated with high domain disorganization; low
anger with preoccupied attachment. These findings could explain the impaired response to
different social domains in patients affected by BPD [28].
In a study [22] published in 2003, BPD was considered as arising from a combination of
childhood abuse and/or neglect, a borderline temperament, and childhood and adolescent
psychopathology (e.g. depression, conduct disorder, drug dependence).
It is easy to imagine, therefore, how BPD could be burdened by a certain familiarity.
Borderline personality disorder, in fact, has been found to be more common among the
relatives of borderline than Axis II comparison probands, as a diagnostic entity or as a
subsyndromal expression [29].
In addition, Barnow S et al. [30] found that children of BPD mothers presented high
scores on the temperament dimension of HA, and considerable rates of emotional and
behavioral problems.
The impact of childhood abuse on borderline personality traits, negative life events and
depression is considerable. Neglect, emotional abuse, as well as, sexual maltreatment have
been demonstrated to predict borderline personality traits and baseline depression [31].
These results confirm the importance of childhood environment and psychopathology
on BPD etiopathogenesis.
The clinical impact of BPD is worsened not only by a high co-morbidity with
depression but also with an early onset of depression, a higher number of depressive

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episodes, and even anxious symptoms [32]. Furthermore, the presence of borderline per-
sonality is a strong predictor of major depression and its persistence [33]. Depressive
rumination is significantly correlated, as previously reported, with borderline personality
traits [8]; rumination itself is a mediator between cognitive factors, such as negative
emotionality, and the vulnerability to depression in youth [34].
In literature, the real impact of co-morbid personality disorders (PD) on treatment
outcome for patients with major depressive disorder is not clear. In a recent study [35],
published in 2011, single-level regression showed significantly worse treatment outcome
among patients with co-morbid PD, as compared to patients with no PD. After controlling
the statistical heterogeneity and interdependency, the treatment outcome was no longer
significantly worse for patients with co-morbid PD.
Considering BPD, Skodol AE et al. [33] affirmed that it robustly predicts persistence of
depressive disorder, and it should be taken into consideration when approaching major
depression, since it could influence prognosis and treatment.
The fact that personality plays an important role on the onset of depression is, instead,
supported by the evidence that the presence of a PD can even predict relapse after an
episode of major depressive disorder [20]. A study comparing depressed patients with and
without PD demonstrated how PD influence well-being in depressed patients, having a
negative influence on the scores of scales measuring role limitations due to emotional
problems, social functioning, and general health perceptions [18]. Even stigma experienced
by the patient is not only related to society, but also to the personality features of an
individual [36].
BPD confers a higher risk of recurrence of major depression than other PD, and has a
negative effect on the course of depression [19].
As mentioned above, HA plays a role in the response to medications targeting the
serotoninergic system [12, 17]. Conversely, HA scores can be influenced by a depressive
mood, also correlating it with depression severity [37].

Borderline Personality Disorder and Depression: Neurobiological Evidence

Research on the biological bases of some clinical aspects of BPD is increasing so as to

understand how behavior relates to neurobiology.
There are three domains of functional imaging research about BPD: (1) affective
dysregulation; (2) the complex of dissociation, self-injurious behavior and pain processing;
and (3) social interaction.
Affective dysregulation is a serious problem in BPD because intense emotional reac-
tions can lead to another main problem: self-injurious behavior. A fronto-limbic inhibition
model with a reduced inhibitory drive from the medial prefrontal cortex on limbic regions
has been proposed to explain affective dysregulation [38]. Mu-opioid receptor concen-
trations have been studied in patients with BPD in response to a negative emotional
sadness. Patients showed a deactivation of opioid system in different brain areas, indicating
a dysregulation of regional endogenous opioid function [39].
Considering dissociation, cortical and subcortical areas can be involved in the ‘out-of-
body’ experience. In a study carried out with electrical stimulation, these areas were less
responsive during depersonalization [40].
Pain processing and self-injurious behavior are further interesting topics.
Stress-induced reduction of pain perception is a characteristic feature of BPD whose
mechanisms are still poorly understood. In a study published in 2007, it was found that

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patients with BPD had higher thresholds than the control group in response to identical
heat stimuli. When adjusting the stimulus temperature to the subjective pain level, the pain
induced deactivation in the perigenual anterior cingulate gyrus and in the amygdala in BPD
patients [41].
In another study, while imagining the reactions to a situation triggering self-injurious
behavior, BPD patients showed less activation in the orbitofrontal cortex compared with
the controls. In addition, while imagining the self-injurious act itself, only patients with
BPD showed increased activity in the dorsolateral prefrontal cortex, and a decrease in the
mid-cingulate [42].
In order to evaluate social interaction, 55 BPD subjects were selected to play a mul-
tiround economic exchange game with healthy partners. Healthy subjects showed a linear
relation between anterior insula response, and the magnitude of monetary offer received
from their partner (input) as well as the amount of money repaid to their partner (output).
On the contrary, the activity of the anterior insula of BPD participants was related only to
the output. This could explain the impairment in social gestures of BPD patients [43].
In a recent study [44], published in 2011, it was found that right hippocampal volumes
were significantly inversely correlated with aggressiveness; and dorsolateral prefrontal
cortex grey matter volumes were significantly inversely associated with impulsiveness in
comparison to control subjects.
Co-morbid borderline pathology in major depressive disorder has been associated with
altered activity in parietotemporal and anterior cingulate cortical regions: the regional
glucose uptake in response to fenfluramine (FEN) in depressed subjects with BPD and
depressed patients without Cluster B Axis II disorders was studied by using positron
emission tomography. Patients with co-morbid BPD had greater activity in parietotemporal
cortical regions before and after FEN activation and less relative uptake in the anterior
cingulate cortex (BA 32) at baseline; FEN abolished this difference. Impulsivity and
hostility were respectively positively correlated with fluorodeoxyglucose uptake in supe-
rior and middle frontal cortex and temporal cortical regions [45].
In addition, dopaminergic polymorphism (in particular DRD2 TaqI B1-allele and
A1-allele) has been correlated to borderline personality traits among at-risk young adults
and psychiatric inpatients [46], and a polymorphism in the dopamine transporter has been
demonstrated to be a risk factor for BPD in depressed patients [47], showing that a
neurobiological basis could explain the frequent co-morbidity between the two disorders.

Overview on BPD Treatment: Multi-Target Approach of Co-Morbidity

Literature provides information about pharmacological treatment, particularly about mood

stabilizers and second-generation antipsychotics; however, there is uncertainty as to their
efficacy for overall severity of BPD [48]. The 2001 American Psychiatric Association
guidelines indicate psychotherapy as a core for the treatment of patients with BPD, with
eventually associated symptom-targeted pharmacotherapy [49].
There are few recent articles evaluating therapy with selective serotonin reuptake
inhibitors (SSRIs) in BPD.
In a randomized, placebo-controlled clinical trial fluvoxamine, compared to placebo,
showed effectiveness on rapid mood shifts in 38 female BPD patients [50]. Bellino S et al.
compared, within a sample of 44 patients, fluoxetine alone versus combined therapy with
fluoxetine and interpersonal psychotherapy. The combined therapy was superior to flu-
oxetine alone in BPD patients, concerning anxiety, quality of life and a few core symptoms

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of the disorder, such as instability and impulsivity [51]. A randomized trial found that
fluoxetine and olanzapine were safe and effective in ameliorating chronic dysphoria
and impulsive aggression. However, olanzapine monotherapy or associated olanzapine-
fluoxetine therapy seemed to be superior to fluoxetine monotherapy in the treatment of
both of these dimensions of borderline psychopathology [52]. In addition, response to
treatment with fluoxetine has been related to the serotonin transporter polymorphism, and
particularly, resistance to fluoxetine has been related to the presence of allele s [53]. This
could explain cases of inefficacious treatment.
Research seems to be more and more interested in new antipsychotics. BPD patients
with psychotic-like, impulsive or suicidal symptoms might benefit from atypical antipsy-
chotics [54].
In a double-blind, placebo-controlled study, 43 women and 9 men treated with aripiprazole
presented significant changes in scores on most scales of the symptom checklist (SCL-90-R),
the Hamilton Depression Rating Scale (HAM-D), the Hamilton Anxiety Rating Scale (HAM-
A), and the State-Trait Anger Expression Inventory after 8 weeks [55].
Olanzapine, instead, in a randomized double-blind placebo-controlled trial, showed a
more rapid time of response compared to placebo but there were no statistically different
improvements on overall symptoms of BPD between placebo and olanzapine [56]. Another
double-blind placebo-controlled study compared the treatment with dialectical behavior
therapy and either olanzapine or placebo. Combined treatment showed an overall
improvement in most symptoms in both groups, but olanzapine was associated with a
statistically significant improvement over placebo in depression, anxiety, and impulsivity/
aggressive behavior [57].
A case report highlights how a moderate dose of clozapine (175 mg/day) has been
successfully used in a severe BPD patient without psychotic symptoms [58].
Among mood stabilizers, according to a retrospective case review, lamotrigine showed
a specific effectiveness on treating affective instability [59], while divalproex, in a versus
placebo study, was superior in treating impulsivity and state aggression symptoms. Fur-
thermore, treatment response was shown to be positively related to the severity of baseline
symptoms [60]. An open label trial demonstrated that therapy with divalproex extended-
release was associated with statistically significant improvement on the Clinical Global
Impression–Improvement scale, the Global Assessment Scale, the Overt Aggression
Scale–Modified irritability subscale, and the Aggression Questionnaire [61].
Concerning psychotherapy, the majority part of research and review articles focus on
dialectical behavior therapy (DBT).
In a study conducted on BPD women, DBT showed positive effects in reducing suicidal
behavior, depressive episodes, anger and non-suicidal self-injury [62]. DBT application on
inpatient units have been reported in a relatively recent review: educating new patients and
prioritizing their treatment management targets are some of the several objectives of
inpatient DBT staff [63]. The clinical management of a BPD patients is, in fact, burdened
by difficulties, and a ‘‘re-educational’’ approach, teaching the patients skilful behavior,
could be useful not only to improve the quality of life of the patients, but also to avoid
conflicting relationships between the patients and the clinicians.
According to a randomized trial published in 2010, DBT is considered to be equal to
general psychiatric management of BPD, including a combination of psychodynamically
informed therapy and symptom-targeted medication management [64]. A systematic
review reports how in certain cases, DBT has been demonstrated to be even superior to the
treatment usually adopted in BPD (e.g. chronically parasuicidal and drug-dependent bor-
derline women) [65].

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In addition, a double-blind placebo-controlled trial demonstrated that adding fluoxetine

to a DBT did not provide any additional benefits [66].
Among the few studies suggesting other kinds of psychotherapeutic approaches, in an
overview published in 2009, a mentalization-based treatment was recommended [67].
In the case of co-morbidity between depression and BPD, a pharmacotherapy combined
with an interpersonal psychotherapy should be considered; indeed, this has been demon-
strated to be more effective than an antidepressant therapy alone, both in treating symp-
toms of major depression and in improving the dimensions of the quality of life and
interpersonal functioning [68]. Combined fluoxetine and interpersonal therapy versus
combined fluoxetine and cognitive therapy have been compared and have both been found
efficacious [69].
A considerable problem regarding BPD treatment is that of drug-resistance.
In a context of enhancing knowledge, Jan Prasko et al. have found the association
between SSRIs and bright light therapy to be effective in depressed drug-resistant BPD
patients [70].

Materials and Methods

Research Strategy

A literature research, using the U.S. National Library of Medicine’s PubMed database, was
conducted to identify recent articles on temperamental and biological findings on BPD and
major depression, and on the close link between the two disorders; to review the latest
therapeutical findings on BPD, focusing on the conditions of co-morbidity between
depression and BPD.
Only articles published between 2000 and 2011 were selected. The following terms
were included in the search: ‘‘prevalence of BPD’’, ‘‘BPD/BPD and depression’’, ‘‘therapy
of BPD/therapy of depression co-morbid BPD’’, ‘‘psychotherapy in depression co-morbid
BPD’’, ‘‘attachment in BPD’’, ‘‘neuroimaging in BPD and depression’’.
We also selected interesting bibliographic references from identified articles excluding
those published before 2000. Due to the small number of studies, no methodological or
quality exclusion criteria were applied. For example, the overview on BPD treatment
includes randomized, double-blind/single-blind, placebo-controlled trials as well as open
trials and a single case report.

Results and Discussion

Considering in particular HA, similar temperamental features have been demonstrated both
in depression and in BPD [12, 13, 22]—two severe psychiatric disorders presenting high
rates of co-morbidity [19].
It has been demonstrated that BPD features of impulsivity and aggressiveness have a
biological structural base [44]; co-morbid BPD in depressed patients is associated with
altered activity in parietotemporal and anterior cingulated regions [45].
The strong link between BPD and depression seems to be widely recognized by
the scientific community.
The presence of BPD has a negative impact on the prevalence, the persistence [33], the
course, the recurrence [19] and even the risk of relapse of depression [20]. In addition, the

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presence of co-morbid BPD increases the risk of self-harm behavior and drug abuse [10],
and influences well-being in depressed patients [18].
Regarding pharmacotherapy, we found few articles about SSRIs: only one considering
mono-therapy, finding positive effects on the specific problem of mood shifts [50].
Our literature research yielded 4 recent original research articles, and a case report on
successful pharmacotherapy with antipsychotics in BPD [52, 55–58].
Two research articles report efficacy of mood stabilizers [60, 61].
The complexity of BPD features can be faced with psychotherapy.
Research is particularly interested in DBT: three research articles state the efficacy of
DBT in BPD [62, 64, 66].
In case of co-morbidity with depression, combined psychotherapy and pharmacotherapy
seem to better solve clinical problems [68, 69].
Taking into consideration what has already been said, the consistency of findings show
that research is more and more interested in new antipsychotics than in SSRIs. Regarding
psychotherapy, DBT seems to be the topic of major literature interest.
A conclusive statement regarding pharmacological management cannot be derived,
each drug being considered for specific symptoms.
More biological data is necessary in order to better understand the organic bases of BPD
and depression, and of their intercorrelation.

Conclusions

What Could be the Future of BPD?

The new findings about biological bases of BPD are giving new ‘‘dignity’’ to the disorder.
There is the proposal, in fact, of including it in the Massachussetts Parity List of
‘‘Biologically-Based’’ disorders in order to increase its insurability as a stand-alone
diagnosis [71].
In DSM-V, the reformulation of PD diagnosis consists in a hybrid dimensional-
categorical model, including not only personality disorder features but also personality
traits, in a broader vision of psychopathological characteristics. Concerning BPD, the work
group is recommending that this disorder should be reformulated as ‘‘The Borderline
Type’’. The clinician should rate the patient’s personality using a 5-point rating scale that
goes from ‘‘very good match’’ to ‘‘no match’’, taking into consideration how many per-
sonality characteristics match or don’t match the symptoms list (www.dsm5.org).

Practical Implications

The future of this disease is still evolving, with different literature contributions and new
therapeutic possibilities. The fact that BPD is less stable than is expected from a PD [72]
represents a further incentive to improve research on the disorder, and on the close link
between BPD and depression, thus optimizing the treatment.
In case of co-morbidity, in fact, therapeutic targets are obviously depressive symptoms,
but so are those BPD features that may influence the prognosis of depression itself, with
particular attention to the problem of self-injurious behavior: in clinical practice, BPD
patients are often suicidal patients [73]. A global assessment is, in fact, fundamental for a
successful therapeutic choice acting on the several aspects of a complex psychopatho-
logical phenomenon. The choice of a correct therapy and the offering, to the patients, of

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effective psychotherapeutic interventions are the goals that will help them to achieve a
social harmonic integration and a better quality of life.

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Author Biographies

Maria Luca, MD was born in Catania, Sicily, in 1987. She attended the University of Catania and
graduated in Medicine in 2010 with honors, presenting a dissertation on schizophrenia and oxidative stress,
resulting from a clinical work played in the Psychiatry Unit of the University Hospital of Catania and a
research work in the Biochemical section of the University of Catania.

Antonina Luca, MD, PhD was born in Catania, Sicily, in 1983. She attended the University of Catania and
graduated in Medicine in 2007 with honors, presenting a dissertation on clinical psychophysiology and
psychodiagnostics. She has a PhD in Neurovegetative Medicine.

Carmela Calandra, MD, Associate Professor of Psychiatry, University of Catania was born in Cerami
(EN), Sicily, Italy, in 1946. She attended the University of Catania and graduated in Medicine in 1970 with
honors presenting a dissertation on therapy with lithium in mood disorders. She specialized in Psychiatry
and Neuropsychiatry. She is a psychotherapist. She is Associate Professor of Psychiatry in the Faculty of
Medicine of Catania and she is the Director of the Psychiatry Unit of the University Hospital of Catania. She
is responsible of the regional Ambulatory of Eating Disorders of Catania.

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