REVIEW ARTICLE

Borderline Personality Disorder and Bipolar Disorder

What is the Difference and Why Does it Matter?
Joel Paris, MD* and Donald W. Black, MD
Abstract: Borderline personality disorder (BPD) and bipolar disorder (types I
and II) are frequently confused because of their symptomatic overlap. Although
affective instability is a prominent feature of each, the pattern is entirely different.
BPD is characterized by transient mood shifts that occur in response to interpersonal stressors, whereas bipolar disorder is associated with sustained mood
changes. These disorders can be further distinguished by comparing their phenomenology, etiology, family history, biological studies, outcome, and response
to medication. Their distinction is of great clinical importance because misdiagnosis can deprive the patient of potentially effective treatment, whether it is psychotherapy for BPD or medication for bipolar disorder. On the basis of a
comprehensive literature review, guidelines for differential diagnosis are suggested, and priorities for further research are recommended.
Key Words: Borderline personality disorder, bipolar disorders, differential
diagnosis
(J Nerv Ment Dis 2015;203: 37)

ersonality disorders (PDs) are characterized as enduring and inflexible patterns of thought, feelings, and behaviors that impair a
person's psychosocial or vocational functioning (American Psychiatric
Association, 2013). PDs are frequent in the community but especially
common in inpatient and clinic settings (Lenzenweger et al., 2007;
Zimmerman et al., 2005). These conditions are defined in Diagnostic
and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) as
chronic disorders with major effects on mood, behavior, cognition,
and interpersonal relationships. However, because state-dependent
and trait-dependent phenomena can coexist in many mental disorders,
it can be difficult to distinguish PDs from diagnoses associated with
active symptoms.
Much of the literature and research on PDs concern borderline
PD (BPD) classified in International Classification of Diseases 10th
Edition as emotionally unstable personality disorder, a term that better
reflects the underlying pathology (World Health Organization, 1992).
To receive a PD diagnosis in DSM-5, a patient must a) satisfy general
criteria (maladaptive patterns of behavior causing long-term difficulties
in personal relationships and/or social functioning) or b) meet specific
criteria for 1 of the 10 listed PDs, or if none of these criteria are met, a
residual category (unspecified or otherwise specified) can be used.
BPD, one of the most frequently diagnosed PDs, is characterized
by affective instability (AI), impulsive behavior, deliberate self-harm,
and disturbed relationships. Its community prevalence approaches
1%, similar to that of schizophrenia (Lenzenweger et al., 2007). Although one study found rates as high as 5.9% (Grant et al., 2004), this
result may be an overestimate; a later reanalysis of the data set brought
prevalence down to 2% (Trull et al., 2010). BPD generally has an onset

*Department of Psychiatry, Jewish General Hospital and McGill University School of

Medicine Montreal, Quebec, Canada; and Department of Psychiatry, Roy J. and
Lucille A. Carver College of Medicine, University of Iowa.
Send reprint requests to Joel Paris, MD, Institute of Community and Family
Psychiatry, 4333 cote Ste Catherine, Montreal, Quebec, H3T1E4, Canada.
E-mail: joel.paris@mcgill.ca.
Copyright 2015 by Lippincott Williams & Wilkins
ISSN: 0022-3018/15/203010003
DOI: 10.1097/NMD.0000000000000225

in adolescence (Chanen and McCutcheon, 2013) and can be chronic

(Paris, 2003). Recurrent suicidal behavior is a common and often vexing feature of the disorder (Black et al., 2004; Forman et al., 2004).
Having many of these patients being difficult and demanding
contributes to the stigma that many BPD patients experience (Lewis
and Appleby, 1988). It is possible that stigma contributes to a reluctance
to diagnose the disorder: even among clinicians, BPD patients may be
seen as less mentally ill and more attention seeking than other patients
(Black et al., 2011). However, reluctance to diagnose BPD may be
more related to the current emphasis on neuroscience in psychiatry,
which tends to privilege mood symptoms over personality traits (Paris,
2003; Parker, 2011). In any case, if clinicians express less empathy toward these patients and less optimism about their prognosis, these attitudes can also contribute to misdiagnosis, leading to inadequate or
inappropriate treatment.
Stigma may also contribute to the confusion of BPD with bipolar
disorder, with the latter often seen as a preferred diagnosis. Again, bipolar disorder fits better with the current zeitgeist of psychiatry (Paris,
2013). One study using structured assessments reported that 24% of
persons clinically diagnosed with bipolar disorder would actually have
met criteria for BPD but not bipolarity (Zimmerman et al., 2010).

PHENOMENOLOGY
Because AI is a major symptom of BPD, some experts have considered this disorder to be a bipolar variant characterized by ultra-rapid
cycling (Akiskal, 2003). Others have conceptualized BPD as a separate
category characterized by unstable mood (Tyrer, 2009). This review
will suggest that both these conclusions are mistaken. Although few
studies have directly compared BPD and bipolar disorder, those that
have done so suggest that they are separate and unique (Paris et al.,
2007; Zimmerman and Morgan, 2013).
The underlying problem is that psychiatry continues to struggle
to understand the endophenotypes behind mental illness (Gottesman
and Gould, 2003). In their absence, specialists have had to rely on phenomenological similarities to classify disorders. This is one of the main
reasons for the uncertain validity of current diagnostic systems (Paris,
2013). Moreover, because of overlapping criteria sets, disorders often
seem comorbid with each other or are frequently confused (Black
and Grant, 2014).
The difference between AI and bipolarity is an example of this
problem. AI is defined in DSM-5 (p. 663) as a marked reactivity of
mood (e.g., intense episodic dysphoria, irritability, or anxiety usually
lasting a few hours and only rarely more than a few days). According
to one influential theory, AI is responsible for the emotion dysregulation underlying BPD, a core trait that is exaggerated by failures of psychological validation (Linehan, 1993).
Research confirms that AI is heritable (Livesley et al., 1998), and
it is the trait least likely to change over time (Paris, 2003). Ecological
momentary assessment methods show that AI is triggered by interpersonal stressors and that BPD patients have unusually high reactivity
to conflictual interactions (Russell-Archambault et al., 2007). Research
also shows that mood shifts in BPD usually move from euthymia to anger, not from depression to elation, as in bipolar disorder. Mood swings
in bipolar disorder tend to be more spontaneous and less responsive to
environmental cues (Koenigsberg, 2010).

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The Journal of Nervous and Mental Disease Volume 203, Number 1, January 2015

Paris and Black

The time course of mood swings is crucial. A hypomanic episode, as defined in DSM-5 (p. 132), consists of persistently elevated,
expansive, or irritable mood, lasting throughout at least 4 days. Applying this definition, hypomania occurs only in a minority of patients with
BPD (Paris et al., 2007). Moreover, because assessment depends on accurate retrospective reporting by patients, the diagnosis of hypomania
can be unreliable without corroborating data from family members or
other informants (Dunner and Tay, 1993).
Some investigators have suggested that most forms of mood instability should be considered to fall within a bipolar spectrum (Angst
and Gamma, 2002). If mood shifts that occur on an hourly basis are
seen a subclinical form of bipolarity, then BPD would easily fall within
such a spectrum. One survey that applied these criteria found that 40%
of all patients at several sites have a bipolar spectrum disorder (Akiskal
et al., 2006). If this construct is valid, then bipolarity is very common
indeed. Bipolar disorder types I and II have a combined prevalence of
2%, but that figure doubles when subclinical cases are included
(Merikangas et al., 2007). DSM-5 also allows for a diagnosis of unspecified bipolar disorder that can be used to describe patients in the
spectrum, even when mood swings do not meet criteria for hypomania.
The bipolar spectrum concept has also been extended to behaviorally disturbed children who present with AI and impulsivity.
Follow-up of cohorts into adolescence (Birmaher et al., 2006; Geller
et al., 2008) has shown that these traits remain stable, but they tend
not to evolve into classical mania (although the authors of both studies
interpreted continued AI as a form of mania or hypomania). Concern
about overuse of the bipolar diagnosis in children prompted the DSM5 to include a new diagnosis, disruptive mood dysregulation disorder,
thought to better describe the recurrent temper outbursts and irritability
seen in this group.
Impulsivity, a heritable trait, is another central feature of BPD
(Crowell et al., 2009). These patients display a wide range of impulsive
behaviors, including repeated self-harm and multiple suicide attempts
(Zanarini et al., 1998). Although impulsive behaviors are also common
in bipolar disorders, they are more episodic than pervasive (Koenigsberg,
2010). BPD patients also have a very wide range of cognitive symptoms,
including micropsychotic phenomena (auditory hallucinations, depersonalization, or paranoid ideas), occurring in more than half of all cases
(Zanarini et al., 1990).
Another major domain of psychopathology in BPD is problems
in interpersonal relationships, characterized by rapid attachment, anxious dependency, and fear of abandonment (Gunderson and LyonsRuth, 2008), features that may not be a result of AI or impulsivity.
Patients with BPD also struggle with an identity disturbance, leading
them to question who they are and what their beliefs and core values
are (Jorgensen, 2006). Although bipolar patients also have difficult interpersonal relationships (Coryell et al., 1993), they do not usually have
these characteristics. Although both disorders show psychosocial
morbidity, there are more deficits in BPD patients (Zimmerman and
Morgan, 2013).
The proposal that BPD is a mood disorder assumes that all other
symptoms of this disorder are secondary to AI. However, that possibility does not explain why AI, impulsive behaviors, interpersonal conflicts, and micropsychotic symptoms co-occur in the same patients.
Nor does it explain why the diagnosis of BPD as a single construct
has been found to be both coherent and heritable (Reichborn-Kjennerud
et al., 2013). To understand why BPD may not fall within the spectrum,
one needs to see the construct as complex and multidimensional, based
on the co-occurrence of symptoms in several domains of psychopathology (Paris, 2007).

ETIOLOGY
There are insufficient data to define a precise etiology for either
BPD or bipolar disorder. This is not unexpected, given that psychiatry
has thus far been unable to determine an etiology for most mental
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disorders. Behavioral genetic studies have shown that almost all mental
disorders have a significant heritable component (Jang, 2005). The precise nature of the biological vulnerability to bipolar disorders and BPD
is unknown. Moreover, no consistent biomarkers are associated with either disorder; although some authors (e.g., Bassett, 2012) have claimed
that there could be biomarkers common to both patient groups, the evidence is insufficient to reach that conclusion. In BPD, although repetitive suicide attempts have sometimes been linked to alleles related to
serotonergic function (New et al., 2008), these associations do not provide an explanation for the complex psychopathology associated
with BPD.
Neuroimaging research in BPD also finds multiple abnormalities but little specificity. Structural and functional changes in the prefrontal cortex, amygdala, hippocampus, and other subcortical sites
have been reported (Schmahl and Bremner, 2006). There have been
no direct comparisons of these findings with samples diagnosed with
classical bipolar disorders. However, neuroimaging can be used to examine responses to standardized stimuli such as human faces, and
one study found that BPD patients have a lower threshold of amygdala
reactivity to angry faces (Donegan et al., 2003), whereas another found
that AI, in response to emotional stimuli, is slow to extinguish
(Koenigsberg et al., 2014).
A distinction between BPD and bipolar disorder is also supported by family studies. The most common disorders in the firstdegree relatives of people with BPD are depression and antisocial PD
(White et al., 2003), whereas the frequency of bipolar disorder in
first-degree relatives of BPD patients is similar to its lifetime prevalence
in the general population (Paris et al., 2007). The claim that first-degree
relatives of BPD patients are more likely to have bipolar spectrum disorders, even when classic bipolar disorders are absent (Akiskal, 2003),
begs the question as to whether these syndromes are true forms
of bipolarity.
Psychosocial risk factors play an important role in the etiology of
BPD, and this profile also helps differentiate the disorder from bipolar
disorder. Retrospective and prospective studies have each documented
high rates of childhood adversity, including abuse, neglect, and insecure
attachments (Zanarini, 2000). Although these risk factors are not present in all patients, childhood abuse has been associated with a more
severe prognosis (Soloff et al., 2002). There is also evidence for childhood adversities in bipolar disorder (Leverich and Post, 2006), but they
are much less frequent. Direct comparisons between the etiological factors associated with both disorders remain, however, rare in the literature. The evidence suggests that, whereas bipolar disorder has a very
strong heritability (Craddock and Sklar, 2013), BPD fits better with
a biopsychosocial model that takes account of genetic predispositions, adverse life events, and social stressors (Gunderson and
Lyons-Ruth, 2008).

RESPONSE TO MEDICATION
Pharmacological dissection has been described as a tool to help
determine whether mental disorders are related (Klein, 1987). This
method points to important differences between BPD and bipolar disorder. A recent Cochrane review (Stoffers et al., 2012) as well as the National Institute for Clinical Excellence (NICE) guidelines for BPD
(Kendall et al., 2010) conclude that antidepressants have limited value
for these patients. Moreover, mood stabilizers are not consistently efficacious. Nonresponse to lithium is of obvious significance, but the evidence for the effectiveness of anticonvulsants, such as lamotrigine, is
also weak (Kendall et al., 2010). This conclusion was clearer in the
NICE guidelines, which excluded several studies that had used a dubious methodology but were included in the Cochrane review. Claims for
the validity of a bipolar spectrum based on response to medication
would require large-scale randomized controlled trials, which have
not been conducted, and there are no studies comparing BPD and bipolar patients receiving the same medication.
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The Journal of Nervous and Mental Disease Volume 203, Number 1, January 2015

BPD and Bipolar Disorder

The most extensively studied group of drugs for BPD are the antipsychotics, which, like antidepressants and anticonvulsants, have sedative effects that can reduce impulsivity when prescribed in low doses
(Kendall et al., 2010). However, these effects are not specific, and pharmacological treatment of BPD has never been shown to lead the core
symptoms of the disorder to remit.

Misdiagnosis of BPD occurs because of a set of mistaken beliefs a) that

the disorder is poorly defined, b) that it has a poor prognosis, and c) that it
does not respond to treatment. As we have seen, none of these conclusions are justified by the research literature.

COURSE AND OUTCOME

Medicine and psychiatry are replete with boundary cases, and

many categories of illness overlap considerably. These problems are
rooted in a lack of knowledge about etiology and in loose diagnostic
definitions. However, as this review has shown, the overlap between
BPD and bipolarity is mainly rooted in signs and symptoms, and there
is convincing evidence that these conditions have a different etiology
and a different pathogenesis. There are, nonetheless, a minority of cases
in which BPD and bipolar II overlap to such an extent that differential
diagnosis is problematic. These patients need to be followed over time
to be sure of the diagnosis.
Parker (2011) has suggested that these two conditions can usually be differentiated by features that point to BPD: absence of a family
history of bipolarity, onset in childhood and adolescence, a preponderance of women in clinical settings, distinctive personality patterns,
emotion dysregulation as opposed to mood episodes, low threshold of
response to stressors, absence of melancholia or hypomania, and nonspecific response to mood stabilizers.
The clinical problem of differential diagnosis is rooted in perceptions of the primacy of mood, whether bipolar or unipolar, and in the
wish to prescribe to control symptoms. This is why PD diagnoses
may also be missed in patients with major depression. One study
(Galione and Zimmerman, 2010) found that many cases with BPD were
not diagnosed but had an earlier age of onset, frequent brief mood episodes, more atypical symptoms, more suicide attempts and anxiety and
substance use disorders, suggesting that the concept of a bipolar spectrum may be more sensitive to PD than to bipolarity itself.
The construct of PD is highly complex, and BPD is a particularly
complicated disorder. Yet, this group of diagnoses does better justice
than bipolar disorder to the clinical features of patients with mood instability, widespread impulsivity, and chronically dysfunctional relationships. Failing to recognize BPD deprives patients with these problems
from the most evidence-based forms of treatment.

One of the principles of psychiatric nosology, first espoused by

Kraepelin (1921) and revived by Robins and Guze (1970), is that valid
diagnoses should be associated with a characteristic course and outcome. An episodic course has always been an essential element in the
diagnosis of bipolar disorder. It has also been established that bipolar
disorder begins early in life but tends not to remit in old age and that episodes tend to continue throughout life (Goodwin and Jamison, 2007).
BPD has a notably distinct course and outcome. Research has
begun to identify childhood precursors that precede the disorder (Sharp
and Tackett, 2014), suggesting that AI and impulsivity are apparent by
late childhood. The disorder is often first diagnosable in adolescence
(Chanen and McCutcheon, 2013) and tends to peak in the young adult
years. Prospective studies have shown that the symptoms of BPD, unlike those of bipolar disorder, diminish with advancing age (Gunderson
et al., 2011; Zanarini et al., 2012). By the age of 40 years, and sometimes much earlier, most patients have greater emotional stability, are
less impulsive, and are less likely to engage in deliberate self-harm or
to make suicide attempts. This outcome is similar to that of other disorders marked by high impulsivity (Paris, 2003), helping to explain why
these patients are seen less frequently in clinical settings during middle
age (Blum et al., 2008a). Prospective studies show that patients often retain a degree of psychosocial dysfunction but are less symptomatic and
have an improved quality of life. In this way, the outcome for BPD is
significantly better than for bipolar disorder, which continues to be
problematic in old age. Moreover, BPD rarely evolves into bipolar disorder over time, and when it does, one should consider whether the
original diagnosis was correct (Paris et al., 2007).

IMPLICATIONS FOR TREATMENT

The misdiagnosis of BPD as a form of bipolar disorder can lead
to inappropriate treatment. Bipolar disorder requires specific pharmacotherapy that is known to be highly effective in well-diagnosed patients (Goodwin and Jamison, 2007). In contrast, medications do not
lead to remissions in patients with BPD (Kendall et al., 2010).
The most evidence-based form of treatment of BPD consists of
psychotherapies specifically designed for these clinical problems. Dialectical behavior therapy (Linehan, 1993) is the best-known treatment,
combining both individual and group-based therapies (17); its efficacy
has been shown in multiple randomized controlled trials (Paris, 2010).
Other methods that have been tested in randomized trials include
mentalization-based treatment (Bateman and Fonagy, 2009), schemafocused therapy Giesen-Bloo et al., 2006), transference-focused psychotherapy (Clarkin et al., 2007), and the briefer group-based Systems
Training for Emotional Predictability and Problem Solving (Blum et al.,
2008b). Although this research is in its early stages and none of these
therapies are effective in all cases, this line of investigation offers a true
breakthrough for patients previously considered to be untreatable.
BPD patients who are misdiagnosed with bipolar disorder may be
denied the option of a referral for treatment with an evidence-based psychotherapy and are likely to receive medications that will not produce a
remission of their condition. They may also be prescribed polypharmacy
when initial pharmacotherapy fails to be effective (Zanarini et al., 2001),
leading to adverse side effects. Misdiagnosis of bipolar disorder as BPD
could deprive patients of effective treatment with mood-stabilizing medication. However, that scenario may not be less common in an era where
diagnoses that lead to pharmacological prescriptions tend to be favored.
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A PRELIMINARY GUIDE TO DIFFERENTIAL DIAGNOSIS

ISSUES FOR FURTHER RESEARCH

1. Differences between BPD and bipolar disorder can best be illuminated by direct comparisons between patients with the two disorders.
Such studies remain unfortunately uncommon. They should be designed to delineate specific etiological factors, precursors, course,
and outcome as well as response to treatment.
2. More research is needed on specialized psychotherapies for BPD. At
present, only dialectical behavior therapy has the multiple replications
needed to provide confidence in its prescription. However, streamlining
and shortening of these therapies are greatly needed. Treatments
that are lengthy and expensive will never meet the large clinical
problem this disorder presents.
3. Funding agencies should support research into BPD at the same level
currently provided for bipolar disorder.
4. Research should address the heterogeneity of both BPD and bipolar
disorder. Each of these disorders has a variable response to treatment,
suggesting that subgroups need to be identified that respond more
specifically to interventions.

DISCLOSURES
Dr. Paris receives royalties from Oxford University Press and
Guilford Press. Dr. Black reports research funding from AstraZeneca,
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The Journal of Nervous and Mental Disease Volume 203, Number 1, January 2015

Paris and Black

the Nellie Ball Trust, and the National Institute on Aging; he also reports royalties from American Psychiatric Publishing, Oxford University Press, and UpToDate.
The authors declare no conflict of interest.

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