© Springer Science+Business Media New York 2015
Lois W. Choi-Kain and John G. Gunderson (eds.)Borderline Personality and Mood Disorders10.1007/978-1-4939-1314-5_1414. Conclusion: Integration and Synthesis
(1)
Department of Psychiatry, Harvard Medical School, 115 Mill Street, Belmont, MA 02478, USA
(2)
McLean Hospital, 115 Mill Street, M/S 312, Belmont, MA 02478, USA
The relationship between mood disorders and borderline personality disorder (BPD) has long been controversial, fueling fierce debates about psychiatric diagnosis and treatment [1–3]. This controversy has spurred the development of a significant body of research, which allows us to ground our hypotheses and claims primarily in evidence rather than polemics. This book is an effort to review, synthesize, and evaluate the current evidence on the relationship between mood and borderline personality disorders. We hope to promote more objective and tentative conclusions that inform more effective clinical care of and continued research on the interaction between these commonly encountered disorders.
The adversarial nature of the original debates between the mood and personality disorder worlds arose from territorial agendas, revolving around efforts to establish the legitimacy of these respective disorders in an era where the criteria for most psychiatric diagnoses known today were in early stages of empirical validation. In the context of these diagnostic turf wars, much of the language and tone of the debate between mood and personality disorder experts was competitive and undercutting. The chapters contributed by Paris as well as Ghaemi and Barroilhet represent the evolution of this debate. Paris argues that the trend towards biological reductionism has caused neurobiological understandings and psychopharmacologic treatments to edge out psychoanalytic concepts and psychotherapeutic interventions. This shift has pushed mental health clinicians to prefer simpler conceptualizations of psychiatric presentations in terms of mood disorders as opposed to more complex formulations in terms of personality disorders. Ghaemi and Barroilhet make a similar distinction with different implications. They argue that bipolar disorder is more of an illness or disease than BPD because it is almost completely genetic in etiology. Both Paris and Ghaemi and Barroilhet distinguish BPD as a complex clinical picture which develops primarily from psychosocial influences. Both chapters focus their criticism more at the way in which the diagnostic concepts are applied and less at the legitimacy of mood or borderline diagnoses. At the same time, these chapters still embody dichotomizing tendencies that falsely or simplistically separate biologically and psychosocially based disorders and interventions. This dichotomy provides clinicians and researchers with hard edges around which to draw lines between categories of psychiatric illness, providing clarity in the face of clinical complexity. The problem arises when these dichotomizing tendencies position disorders as competitive, suggesting, as Ghaemi and Barroilhet indicate, that the overlap between psychiatric syndromes simply means one represents the other.
This collection of chapters reviews and synthesizes the existing literature to enable mental health professionals to develop a more nuanced and realistic way of interpreting and managing the overlaps and differences between these disorders. While residue of this historic hostility still exists, the current conversation between the mood and personality disorder camps accommodates both recognition that (1) unipolar depression, bipolar disorder, and BPD are valid diagnostic constructs and (2) when considered as part of a mutually exclusive differential diagnosis, the use of these diagnostic categories tends to oversimplify the relationships between the underlying vulnerabilities, phenotypic features, and indicated treatments for patients presenting with complex comorbidity and/or atypical variations of these illnesses. As the chapters by Paris and Ghaemi/Barroilhet suggest, our current use of diagnostic constructs is limited and leads to reductive and simplified clinical management. This tendency contributes to misdiagnosis or ineffective prioritization of one diagnosis over another.
In an attempt to clarify what we now know about the overlaps and distinctions between mood disorders and BPD, the authors in this volume have reviewed the current literature on the clinical and neurobiological profiles, development, and course, as well as psychopharmacologic and psychotherapeutic interventions for these disorders. This review has traced five general conclusions from the current status of knowledge about the relationship between these disorders:
1.
Depression and BPD phenotypically diverge yet are highly comorbid, suggesting overlapping underlying liabilities. Depression and BPD also interact significantly in longitudinal course.
2.
Bipolar disorder and BPD phenotypically overlap yet are infrequently comorbid, suggesting more disparate etiologies. This leads to increased diagnostic confusion and misdiagnosis.
3.
Depression, bipolar disorder, and BPD all involve the interaction between temperamental or trait-like features and acute episodic symptoms or state-like features.
4.
Real-world clinical settings involve patients who may present with symptoms, precursors, and risk factors shared among mood disorders and BPD. Premature diagnostic certainty results in therapeutic overkill with overly specialized intensive treatment mismatched to presentations. Clinical interventions scaled with clinical staging considerations may reduce the tendency towards misdiagnosis and iatrogenic interventions.
5.
Psychopharmacologic treatment is primary for depression and bipolar disorder and adjunctive for BPD. Psychotherapeutic approaches are primary for BPD and adjunctive for depression and bipolar disorder. A combination of approaches is indicated with comorbid or diagnostically unclear presentations, but further research is needed to determine the effectiveness of combined treatments and step-wise approaches to care.
The remainder of this summary will review and consider the evidence presented in this text supporting each of these conclusions.
Depression and BPD: Superficially Divergent, Fundamentally Overlapping
Depression and BPD are clinically distinct disorders with divergent treatment strategies but appear to stem from shared underlying vulnerabilities. Depression is one of psychiatry’s most prevalent disorders with heterogeneous variations that respond to a diversity of treatments. BPD is a specific and severe clinical syndrome, which was distinguished initially, per Choi-Kain and Rodriguez-Villa’s historical review, by its lack of or negative response to typical treatments which were generally effective for a range of common mental disorders. A number of chapters (Goodman et al.; Yalch, Hopwood, and Zanarini; Silk) in this book highlight differences in clinical features of MDD and BPD. Silk and Goodman et al. characterize depressive features of individuals with BPD in terms of dysphoria, emptiness, loneliness, and fears of abandonment. In addition, core features of impulsivity and interpersonal sensitivity in BPD distinguish it from MDD. The severity of mood symptoms and degree of functional impairment in individuals with BPD exceeds that found in those with MDD. The limited response of BPD symptoms to antidepressants also suggests a significant clinical difference between MDD and BPD. These differences suggest that these disorders are distinct and not just reflections of each other.
At the same time, comorbidity between MDD and BPD is significant. A vast majority of BPD samples, that is, 70–80 % [4, 5], report comorbidity with MDD. Conversely 50–85 % of outpatients with MDD have personality disorders, of which BPD is the most prevalent [6]. Furthermore, family studies have established a significant risk for MDD in relatives of probands with BPD [7–9]. Although there are clear differences in clinical phenomenology and biological features which can differentiate these two diagnostic entities as noted in Goodman and collaborators’ chapter (i.e., brain region involvement, neurohormonal indices, and sleep architecture), the high rate of co-occurrence and familiality implies the existence of shared underlying liabilities between the two disorders. These underlying liabilities increase the likelihood of not only developing either MDD or BPD but also of developing both disorders comorbidly. In the last decade, research on broader underlying familial internalizing and externalizing dimensions of psychopathology has confirmed overlaps in latent liability factors that explained the co-occurrence of disorders [10–12]. Studies have indicated that BPD is associated with both internalizing and externalizing factors, which explains its complex comorbidity pattern [13, 14].
Skodol summarizes the literature on the longitudinal interactions between MDD and BPD in Chap. 10. His summary illustrates that the co-occurrence of BPD and MDD is associated with both slowed remission and increased relapse in both disorders, thereby contributing to a greater chronicity in each. The reciprocal interactions between the two disorders suggest there may be shared underlying factors that contribute to the persistence and recurrence of acute symptoms in both disorders. Additionally, Yalch, Hopwood, and Zanarini report that as MDD severity increases, its overlap with BPD increases.
While many possible explanations for the interaction between MDD and BPD have been proposed (see chapter by Goodman et al.), the current state of knowledge seems to support the following hypotheses: (1) MDD and BPD are manifestations of the same phenomenon, (2) MDD and BPD share common vulnerabilities, and (3) MDD and BPD share common biological features which foster each other’s development [15, 16]. These hypotheses are not mutually exclusive. In order to refine our understanding of the complex relationship between the two disorders, it is necessary to first identify the shared liabilities and biological features.
Throughout this book, several authors have reported on the role of personality traits or temperamental endowments, such as negative affectivity, emotional dysregulation, and interpersonal hypersensitivity in the development of both mood and borderline personality disorders. Goodman et al. describe several biological characteristics including amygdala hyperreactivity, subgenual ACC volume changes, and deficient serotinergic function that are thought to underpin the emotional dysregulation seen in both MDD and BPD. Genetic findings point to serotonin, tryptophan hydroxylase, and monoamine oxidase systems as potential sources of the shared vulnerability towards altered processing of social and emotional information. Future research is needed to clarify the biological factors that may underlie the relationship between emotional and relational characteristics contributing to liability for both disorders.
In both the depression and BPD research literatures, interpersonal factors have been implicated as central vulnerabilities contributing to risk for developing psychopathology in the context of life stress [17–19]. Interpersonal features, such as attachment insecurity and rejection sensitivity, which have distinguished those with BPD from those without, appear to also be associated with MDD but at lesser degrees [20, 21]. Attachment insecurity and rejection sensitivity may be nonspecific features which confer risk to a number of disorders, but may be more severe and prevalent in individuals with BPD. The degree to which these interpersonal factors contribute to risk for BPD and its comorbidity as well as their relevant underlying biological mechanisms requires further study.
Bipolar Disorder and BPD: Superficially Overlapping, Fundamentally Divergent
Several chapters in this text describe the overlap between bipolar and borderline personality disorders as more limited than the overlap between depression and BPD. All authors in this book agree that bipolar disorder and BPD are distinct disorders which both tend to be delayed in diagnosis and thereby delayed in being adequately treated. Impulsivity is a key feature shared by both disorders, but not considered to be at the core of either. Mood fluctuations are also shared by both disorders, but, as explicated in the chapter by Reich, the affective instability seen in BPD involves more shifts between anger, depression, and anxiety, whereas those seen in bipolar disorder involve more euphoria. Ghaemi and Barroilhet assert that a comparison of these disorders is akin to one of red skies and red apples, suggesting a relationship at a superficial level. Their superficial similarities lead to significant underdiagnosis of BPD with overdiagnosis of bipolar disorder as described by Zimmerman and Morgan in their chapter.
Chapters contributed by Ghaemi and Barroilhet as well as Reich outline important clinical and biological differences between BPD and bipolar disorder. Symptoms of dissociation, parasuicidal behavior, and recurrent deliberate self-harm distinguish borderline patients from bipolar patients. Bipolar patients are more likely to describe euphoric mood, increased goal-directed activity, and psychomotor agitation. Reich reports that the affective instability seen in both disorders stems from different neurobiological bases. Ghaemi and Barroilhet also emphasize the high rates of trauma history in BPD, arguing that environmental factors have a more significant effect on the development of BPD, whereas genetics contribute more strongly to the development of bipolar disorder. The low rate of co-occurrence and lack of influence on each other’s course longitudinally further supports the notion that these are two distinct, unrelated disorders.
Taken together, the authors contributing to this text suggest that borderline personality and bipolar disorder are distinct and unrelated, but their overlaps in symptoms lead to problems of misdiagnosis rather than co-occurrence. Morgan and Zimmerman as well as Ghaemi and Barroilhet suggest using family history and trauma history as clinical indicators. These clinical features may lean practitioners towards either a bipolar or borderline diagnosis. In reality, when clinicians base their diagnostic impressions on self-report, diagnostic clarity remains at times elusive despite the current understanding of differences between these diagnoses.
A specific area of more murky differentiation exists between bipolar type II and borderline personality disorders. As Skodol proposes in his chapter, the overlaps between these disorders in the realm of interpersonal sensitivity, childhood trauma, and recurrent suicidality combined with the relatively weaker associations with family history of bipolar I and more variable treatment response to mood stabilizers point to the possibility that these two disorders may be more related than bipolar type I and borderline personality. The only longitudinal interaction between bipolar disorder and BPD is that type II bipolar disorder slows time to remission of BPD. Skodol suggests that the combination of BPD and bipolar type II may represent a more severe variant of BPD. More research is needed to assess the relative relationship of bipolar II to both BPD and bipolar I.
Temperament, Mood, and Personality: Models for Overlapping and Interactive Concepts
In both the mood and personality disorder literatures, researchers have been investigating the relationship between temperamental endowments, personality features, stressful life events (e.g., trauma), and psychopathology. As described by Lara et al., temperament is conceptualized as an innate disposition that influences basic emotional, behavioral, and cognitive responses. Mood is then expressed from a temperamental basis in response to external or internal stimuli. The position of personality in relation to temperament and mood is variable. Personality traits are similar to temperamental characteristics that are enduring and biologically based. However, like mood, personality is expressed in terms of the interface between temperamental characteristics and environmental exposures. Chapters by Lara et al. as well as Yalch, Hopwood, and Zanarini represent the dimensional and categorical approaches developed to assess and explain the relevance of temperament, mood, and personality to etiology and symptomatic manifestations of these illnesses.
A vast number of assessments and models of temperament and personality have been proposed and validated. Lara et al. present a complex framework combining dimensional and categorical models of temperament and personality, organized in a similar way to the proposed (and rejected) revisions to personality disorder diagnosis for the DSM-V. Lara’s Affective and Emotional Composite Temperament (AFECTS) model integrates a number of emotional traits (e.g., volition/energy, drive, anger, fear, caution, emotional sensitivity, anxiety, control, coping, and stability) which represent neurobehavioral subsystems with four general categories of affective temperaments, which is divided into twelve global configurations. This complex AFECTS system allows clinicians and researchers to assess underlying emotional and temperamental factors associated with specific disorders in a finer grained fashion. Using this system, Lara and his collaborators are able to identify both the similarities and differences between depression, bipolar disorder, and BPD. All three disorders interface with characteristics of low volition, low coping, and high anxiety. BPD subjects maintain a profile of very high anger and desire as well as low coping and stability. Depressed subjects show lower anger and desire and higher coping and stability than those with BPD, but higher anger and desire and lower coping and stability than controls. These findings suggest that depression involves mild or moderate variations of features related to anger and coping, while BPD involves more severe variations. Similarly, BPD and bipolar subjects shared the same profile, but with higher anger scores distinguishing those with BPD from those with bipolar. In comparison to both mood disorders, BPD involves greater severity of dysfunctional traits.
These simple profiles derived from a complex system analyzing a wide number of temperamental and personality features allow clinicians to focus on key qualities, like high externalizing emotions and low self-regulating traits, as the organizing principles in treatment. However, this approach is limited by its lack of conceptual differentiation of disorders beyond an assessment of superficial description of traits. As noted, the differentiation of bipolar disorder from BPD is only by severity of anger, which may only perpetuate misdiagnosis and confusion between the two diagnoses. Treatment approaches tailored towards dimensional assessments of diagnosis have not been adequately proven, so the effectiveness of this approach in treatment of comorbid disorders is unclear. The clinical utility of dimensional and complex models such as Lara’s requires further study.
Yalch, Hopwood, and Zanarini present a model of hyperbolic temperament in BPD, in which the tendency towards intense emotional responses is combined with heightened interpersonal sensitivity. They note that negative affectivity, or a heightened tendency to experience negative emotions, is a heritable, stable trait associated with both depression and BPD and might explain the high level of co-occurrence and familial co-aggregation of these disorders. They also assert that the impulsivity, emotional dysregulation, and interpersonal hypersensitivity characteristics of BPD distinguish it from depression. These three characteristics importantly interact, resulting in what Zanarini and Frankenburg have called “emotional hypochondriasis” defined as “the transformation of unbearable feelings of rage, sorrow, shame, and/or terror into unremitting attempts to get others to pay attention to the enormity of emotional pain that one feels” [22]. Impulsive behaviors function as a way to remedy intense emotional pain as well as communicate interpersonally a bid for help, engaging another person to help regulate emotions. This model, for which Yalch, Hopwood, and Zanarini offer some empirical support, identifies more than a set of characteristics in BPD. It provides a model for interactions and functions between elements of the BPD syndrome as well as a model of transactions between an individual’s innate vulnerabilities and environment.
The model of hyperbolic temperament in BPD specifies both the overlaps and distinctions between BPD and depression as well as between acute and chronic symptoms of BPD. As Yalch, Hopwood, and Zanarini explain, the negative affectivity in depression confers a general vulnerability to develop negative emotions in response to stress, while in hyperbolic temperament, the vulnerability to intense negative emotion is developmentally rooted in and activated by interpersonal stress. Acute symptoms of BPD – that is, impulsive, self-destructive, and interpersonally focused behaviors – emerge episodically and remit, while temperamental symptoms persist, leading to chronic dysphoria and psychosocial dysfunction [23]. Negative affectivity, according to Yalch, Hopwood, and Zanarini, is a common factor driving vulnerability for and chronic features of both MDD and BPD, while more specific behavioral and interpersonal factors may differentiate manifestation of acute symptoms in the two disorders.
Related posts:
Is Borderline Personality Disorder Underdiagnosed and Bipolar Disorder Overdiagnosed?
Mood Disorders and Personality Disorders: Simplicity and Complexity
Depressive Disorders in Borderline Personality Disorder: Phenomenology and Biological Markers
Cognitive Behavioral Therapy-Based Interventions for Borderline Personality Disorder and Mood Disorders
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Psychodynamic Treatment for Borderline Personality Disorder and Mood Disorders: A Mentalizing Perspective
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