10

Borderline Personality Disorder

Alexander L. Chapman, Nora H. Hope, and Brianna J. Turner

Introduction

Characterized by a combination of interpersonal, emotional, behavioral, and cognitive instability, BPD is a serious, fascinating, and often misunderstood condition. I (ALC) first encountered patients with BPD when I was an undergraduate working part-time at a transitional, residential crisis center. Patients lived at this center for a few days to a couple of weeks to have their risk monitored and ease the transition home following suicide-related hospitalizations. I knew next to nothing about BPD, aside from what I had gleaned from my abnormal psychology course. I admittedly had the stereotyped image of a distraught, unstable, out of control young woman in a hospital gown with long and unkempt hair, suffering after a breakup and resorting to self-cutting and pills to cope with her pain. I also had the sense that people with BPD were unpredictable, extremely sensitive, and could blow up or do something drastic at the drop of a hat.

In my work at this and other mental health centers, I learned that those with BPD are among the most misunderstood and stigmatized individuals in the mental health community. When patients presented interpersonal challenges, clinicians often labeled them “Axis II,” or said they had “characterological” issues; these terms often were euphemisms for BPD. Indeed, people with BPD often suffer intense relationship turmoil and rejection even from the treatment providers charged with their care (clinicians often are reluctant to diagnose or treat BPD). Further compounding these problems is the abundance of misinformation about the disorder, such as the myths that people with BPD cannot recover, are untreatable, or are manipulative and at high risk of violence (Chapman & Gratz, 2007). Some, but fortunately not all, of the clinicians I encountered spoke as if people with BPD were an entirely different kind of human being: oversensitive, unable to have normal relationships, unlikely to benefit from treatment, and uniformly difficult to work with.

The BPD patients I met, although often distraught, did not seem like members of a different species. They seemed sensitive, overwhelmed with their emotions, and sometimes confused and frustrated that their lives were fraught with such conflict and crisis. I probably would have felt and acted the same way if I were in their shoes. Moreover, they wanted their lives to change, often felt guilty and ashamed of their behavior, and had many strengths, chief among these being passion, sensitivity, and empathy. It was not until I was a young graduate student (and still knew next to nothing) that I had the opportunity to work in therapy with someone with BPD. I realized then that if I could help this person, there was hope for people with BPD. I refocused my interests and have continued to study (and treat) people suffering from BPD throughout my career, bringing several others along for the ride (including the co-authors of this chapter).

Within this chapter, we provide an overview of theory and research on and treatment of BPD. Research on BPD has consistently outpaced that of many other personality disorders over the past several years, with a quick PsychInfo search (conducted on February 15, 2018) for articles with “borderline personality disorder” in their titles revealing 327 publications (276 journal articles, 30 books, 21 dissertations) in 2015, 268 (248 journal articles, 5 books, 15 dissertations) in 2016, and 269 (246 journal articles, 9 books, 12 dissertations, 2 electronic collections) in 2017. Given the abundance of research on BPD since it first appeared in the Diagnostic and Statistical Manual for Mental Disorders, 3rd Edition (DSM-III; American Psychiatric Association, 1980), it would be impossible to cover BPD adequately in a single chapter. As such, we have selected some areas to focus on and others to largely neglect. Of note, our theoretical perspective is that BPD arises from a complex transaction of biological, social, and environmental forces resulting in core dysfunctions in the emotion regulation system (Chapman, 2009; Crowell, Beauchaine, & Linehan, 2009; Linehan, 1993a). Our aim is to provide an overview of BPD that is broad enough to provide a reasonable snapshot of the field and focused enough to provide cohesiveness, depth, and logical future directions for research and treatment on this fascinating disorder.

The Prevalence and Impact of Borderline Personality Disorder

A serious, severe, and complex disorder, BPD is associated with inordinate suffering and impact on health and mental health systems. Representative epidemiological surveys show that BPD affects about 1.4–5.9 percent of people in the general population (Grant et al., 2008; Lenzenweger, Lane, Loranger, & Kessler, 2007). In clinical settings, however, BPD is estimated to affect 15–25 percent of psychiatric outpatients and up to 30–50 percent of inpatients (Gunderson, 2001; Lieb, Zanarini, Schmahl, Linehan, & Bohus, 2004; Sar, Akyuz, Kugu, Ozturk, & Ertem-Vehid, 2006; Skodol et al., 2002). This discrepancy between community and clinical prevalence underscores the high rates of healthcare utilization in this population. Reflecting the complexity and profound suffering accompanying BPD, 70–80 percent of people with this disorder have a history of nonsuicidal self-injury and/or suicide attempts, and approximately 10 percent die by suicide (Black, Blum, Pfohl, & Hale, 2004; Gunderson, 2001; Paris & Zweig-Frank, 2001; Skodol et al., 2002). BPD is associated with frequent utilization of emergency, inpatient, outpatient psychiatric, and primary care services (Ansell, Sanislow, McGlashan, & Grilo, 2007; Bateman & Fonagy, 2003; Bender et al., 2006; Jackson & Burgess, 2004; Sansone, Farukhi, & Wiederman, 2011; Zanarini, Frankenburg, Hennen, & Silk, 2004). Accordingly, average yearly costs for inpatient and outpatient treatment range from $12,000 to $30,000 (USD) per patient (Comtois, Elwood, Holdcraft, Smith, & Simpson, 2007; Linehan & Heard, 1999). Further, estimates from research in Canada suggest that BPD is as burdensome as diabetes and rheumatic disease combined, costing approximately $20,000 to $50,000 (CDN) per quality of life year to treat (Van Busschbach, 2012).

BPD also is associated with considerable and persistent functional impairment. Although disorders such as schizophrenia and severe mood disorders often appear more strongly associated with disability and functional impairments, evidence suggests that similar impairments in social and occupational functioning occur among those with BPD, often reaching a level requiring public assistance, such as psychiatric disability support (Bateman & Fonagy, 2003, 2008; Grant et al., 2008; Jørgensen et al., 2009; Koons et al., 2006; Soloff & Chiappetta, 2017). In one study comparing patients with BPD to those with other personality disorders, those with BPD were approximately three times more likely to receive social security disability income benefits (Zanarini, Jacoby, Frankenburg, Reich, & Fitzmaurice, 2009). Although improvements are apparent over time, particularly among BPD patients who experience a remission in their diagnostic status (Zanarini, Frankenburg, Hennen, Reich, & Silk, 2005), psychosocial functioning can remain lower than optimal for several years, with one study finding that 51.2 percent of BPD patients remained at the level of poor psychosocial functioning over an eight-year follow-up period (Soloff & Chiappetta, 2017). Further, five years following mentalization-based treatment (MBT; Bateman & Fonagy, 2006), 54 percent of patients remained below a score of 60 on the General Assessment of Functioning (GAF) scale (Bateman & Fonagy, 2008). In our clinical experience, emotion dysregulation, intense interpersonal sensitivity, anxiety, negative beliefs about themselves, and co-occurring mood disorders often hamper functioning in school and occupational settings. Patients often describe intense frustration and sadness, knowing they have considerable potential but constantly hitting emotional and interpersonal roadblocks in their pursuit of important goals. Although good to outstanding functioning sometimes occurs in one or more areas of life (sometimes referred to as “apparent competence”; Linehan, 1993a), the impact of BPD on social and occupational functioning deserves considerable attention. Indeed, the development of educational initiatives and family-oriented programs (e.g., www.tara4bpd.org; www.borderlinepersonalitydisorder.org), and the publication of books to help loved ones navigate relationships with those with BPD (e.g., Manning, 2011), further underscore the important impact of this disorder on social functioning with family and loved ones.

A Brief History of Borderline Personality Disorder

In this section, we will briefly review the evolution of the construct and diagnosis of BPD, including current areas of active research and controversy. Descriptions of a syndrome marked by extreme interpersonal sensitivity, difficulty managing intense emotions, and impulsive, self-defeating, or aggressive behaviors date back hundreds of years (see Friedel, 2004; Millon, Grossman, & Meagher, 2004). Something resembling the construct of BPD was first described in the psychiatric nomenclature in 1938 (Stern, 1938). This modern name has its roots in psychoanalytic formulations of BPD as a syndrome on the borderline between psychotic and neurotic illness (Stern, 1938; Knight, 1953), given prominent mood disturbances combined with the loose associations and quasi-psychotic symptoms that sometimes emerged in unstructured situations. Features described by Stern (1938) that overlap with contemporary conceptualizations of BPD include hypersensitivity and interpersonal hypervigilance, difficulty coping under stressful conditions, idealization of others (including the treatment provider), feelings of inferiority, and difficulty effectively navigating treatment (and other) relationships (marked by dependency, hypersensitivity, etc.).

Although recent taxonomies no longer classify psychiatric illnesses along psychotic-neurotic dimensions, we still owe much to early formulations and case descriptions of BPD. For instance, early formulations correctly observed that BPD typically involves instability across affective, cognitive, and behavioral systems (Kernberg, 1967). Additionally, many early case histories noted that early childhood adversity, difficulty accurately perceiving and integrating contradictory thoughts and feelings, and predispositions toward intense emotional experiences figure prominently in the pathogenesis of this disorder (Kernberg, 1967; Masterson, 1972). Early conceptualizations also posited that different aspects of BPD might respond differently to treatment given its position between the more easily and successfully treated neurotic illnesses and the more chronic and persistent psychotic illnesses (Kernberg, 1967). Consistent with this hypothesis, we now know that some components of BPD respond very well to treatment, whereas others are more persistent (Zanarini, Frankenburg, Reich, & Fitzmaurice, 2010, 2012). Finally, the notion that BPD is optimally addressed through longer-term psychotherapy, rather than other forms of psychiatric intervention, has persisted (Kernberg, 1968; Masterson, 1972).

Following Kernberg’s pioneering theories in the 1960s (Kernberg, 1967, 1968), advances in defining BPD proceeded rapidly, sparked by increasing empirical research. Core features of BPD were defined in the late 1960s (Grinker, Werble, & Drye, 1968; Kernberg, 1967), interview criteria to assess these features were developed in 1975 (Gunderson & Singer, 1975), and by 1978, these observations had coalesced into a set of seven symptoms that could distinguish people with BPD from those with other psychiatric illnesses (Gunderson & Kolb, 1978). Soon after, BPD was officially recognized as a distinct diagnosis in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM; APA, 1980). Since this time, our knowledge of the prevalence, impact, course, and effective treatment of this disorder has grown considerably (Gunderson, 2009). We have quickly learned that BPD could be reliably and validly diagnosed using structured criteria (Hurt, Hyler, Frances, Clarkin, & Brent, 1989), clearly differentiated from other psychiatric syndromes (Gunderson & Phillips, 1991; Loranger, Oldham, & Tulis, 1982; Pope, Jonas, Hudson, Cohen, & Gunderson, 1983), and successfully treated using structured psychotherapies (Bateman & Fonagy, 1999; Linehan, Armstrong, Suarez, Allmon, & Heard, 1991; Silk et al., 1994). Yet, as research and practice continue to advance the frontiers of our knowledge, new controversies and challenges emerge. Below, we review the current state of knowledge regarding the definition and diagnosis of BPD, and some emerging areas of debate.

Current Criteria and Conceptualizations of Borderline Personality Disorder

BPD is recognized as a discrete diagnosis in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5; APA, 2013). In the tenth edition of the International Classification of Diseases (ICD-10; World Health Organization [WHO], 2016), symptoms of BPD are described under the label emotionally unstable personality disorder. According to these classification systems, core symptoms of BPD include disturbances in emotion (i.e., inappropriate and intense anger; marked reactivity of mood resulting in mood instability), cognition (i.e., persistently unstable self-image; chronic feelings of emptiness; stress-related paranoid ideation or dissociation), interpersonal relationships (i.e., frantic or excessive efforts to avoid real or perceived abandonment; persistent patterns of intense and unstable relationships), and behavior (i.e., impulsive and potentially self-damaging behavior; recurrent suicidal or self-harm behavior). The DSM requires a minimum of five of nine criteria to be met for a diagnosis of BPD. The ICD requires three of five criteria describing persistent impulsivity and at least two of six criteria describing symptoms unique to BPD. The upcoming eleventh revision of the ICD proposes to include a mild, moderate, or severe personality disorder category with a borderline pattern specifier to recognize symptoms of BPD (WHO, 2018).

Table 10.1Correspondence between DSM-5 and ICD-10 diagnostic criteria for BPD

DSM-5	ICD-10
Frantic efforts to avoid real or imagined abandonment	… excessive efforts to avoid abandonment
A pattern of intense and unstable interpersonal relationships characterized by alternating between extremes of idealization and devaluation	A liability to become involved in intense and unstable relationships …
Identity disturbance: Markedly and persistently unstable self-image or sense of self	… the patient’s own self-image, aims, and internal preferences (including sexual) are often unclear or disturbed.
Impulsivity in at least two areas that are potentially self-damaging	… marked tendency to act impulsively without consideration of the consequences … (general criterion: emotionally unstable personality disorder).
Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior	… series of suicidal threats or act of self-harm …
Affective instability due to a marked reactivity of mood	… characteristics of emotional instability
Chronic feelings of emptiness	… chronic feelings of emptiness.
Inappropriate, intense anger or difficulty controlling anger	… outbursts of intense anger may often lead to violence or “behavioral explosions” … (general criterion: emotionally unstable personality disorder).
Transient, stress-related paranoid ideation or severe dissociative symptoms

Although clinicians often experience BPD patients as distinctly different from people with other mental health problems (depression, anxiety disorders, etc.), BPD has been difficult to delineate. A seemingly heterogeneous assortment of symptoms together with heterogeneity among individuals meeting diagnostic thresholds presents challenges. Following DSM-5 criteria, there are 256 potential combinations of five of nine features, and, theoretically, many different clinical presentations that fall within the BPD category. Some evidence from factor analytic studies of DSM criteria has similarly suggested that BPD may be a multidimensional construct (Sanislow, Grilo, & McGlashan, 2000; Sanislow et al., 2002). Providing a single diagnostic label to a multidimensional syndrome potentially consisting of many different “types” of people with BPD may lead clinicians to assume that people with the BPD label are more similar than they actually are. People with BPD often do not fit neatly into other diagnostic categories, in part because of their episodic and varied symptoms that seem to encompass several other psychiatric problems and make it difficult to discern characteristics that are unique to BPD or secondary to other disorders. Indeed, with BPD, comorbidity is the norm, with BPD patients often meeting criteria for a host of co-occurring disorders, such as depression, anxiety disorders, eating disorders, substance use disorders, other personality disorders, and so forth (Grant et al., 2008; Lieb et al., 2004; Sar et al., 2006; Zanarini et al., 2004). Whereas the conceptualization of BPD on the border of psychosis and neurosis has been debunked and the name “borderline” remains anachronistic, the construct and presentation of BPD continue to present challenges to researchers and clinicians alike.

A couple of key advancements have begun to address these challenges. One advance has been the use of empirical and theoretical means to delineate core features of the disorder. For instance, factor analytic techniques show that criteria can be reduced to three latent features: disturbed relatedness consisting of identity problems, chronic emptiness, and interpersonal difficulties; affective dysregulation consisting of mood instability, inappropriate anger, and efforts to avoid abandonment; and behavioral dysregulation consisting of self-harm and impulsivity (Clarkin, Hull, & Hurt, 1993; Sanislow et al., 2000). Alternatively, evidence from genetic and neurobiological research has suggested two core biological predispositions underlying BPD: affective dysregulation and behavioral dyscontrol (Siever, Torgersen, Gunderson, Livesley, & Kendler, 2002). Still others have attempted to identify features that most clearly differentiate BPD from other syndromes, highlighting pervasive difficulties in emotion regulation (Glenn & Klonsky, 2009), impulsivity (Links, Heslegrave, & van Reekum, 1999; McCloskey et al., 2009), and interpersonal hypersensitivity (Gunderson, 2007) as candidate phenotypes or essential features of BPD. Nonetheless, consensus on the core, unique features of BPD remains elusive (Trull, Distel, & Carpenter, 2011). Further complicating this issue is the possibility that what appear to be core features of BPD are secondary to other, co-occurring disorders. For example, some research exploring impulsivity as a core feature of BPD has suggested that the co-occurrence of ADHD among individuals with BPD may largely account for the elevated impulsivity seen in this disorder, particularly when measured with laboratory impulsivity paradigms (Sebastian et al., 2013).

A second potential advance has been a renewed interest in dimensional models of personality pathology (Trull et al., 2011). The DSM-5 (APA, 2013) provides a framework for an alternative, dimensional model of BPD in Section III, which requires at least four of seven maladaptive traits, a minimum of mild interpersonal or personal impairment resulting from these traits, stable expression of traits across time and situation, and cultural incongruence of the traits compared to a person’s dominant culture. Dimensional systems, incorporating decades of personality science, may be more stable and valid than syndrome-based systems (Morey et al., 2003; Samuel et al., 2013) but can become complex and cumbersome for clinicians in everyday practice (Rottman, Ahn, Sanislow, & Kim, 2009; Rottman, Kim, Ahn, & Sanislow, 2011; Trull et al., 2011). Clinicians practicing within this type of system must grapple with many different traits and characteristics, synthesize them in a meaningful and valid manner, and use them to guide assessment and treatment. Some authors have suggested that further improvements to make these dimensional frameworks more user friendly could include reducing the number of criteria, weighting criteria to reflect their centrality or importance, and developing more objective markers for diagnosis (Trull et al., 2011). As it stands now, both the DSM-5 and the proposed eleventh edition of the ICD include both categorical and dimensional frameworks for diagnosing BPD. The next several years will be important in gauging their adoption in research and clinical settings.

In addition to issues related to the relative utility and validity of dimensional versus categorical diagnostic frameworks, a number of other controversies surround the conceptualization of BPD. First, given the high prevalence of childhood abuse and interpersonal trauma among people with BPD, debate has reemerged regarding whether BPD would be better conceptualized as a form of posttraumatic stress disorder, with vigorous arguments on both sides (see, for example, Cloitre, Garvert, Weiss, Carlson, & Bryant, 2014; Ford & Courtois, 2014; Trippany, Helm, & Simpson, 2006; van der Kolk, Pelcovitz, Roth & Mandel, 1996). Past abuse or trauma, however, is neither a necessary nor sufficient precondition for a BPD diagnosis (Zanarini, Williams, Lewis, & Reich, 1997). Further, given evidence (discussed below) that BPD is likely multiply determined through a complex transaction of environmental and individual (e.g., biological, genetic, temperament, behavioral) factors, it is perhaps most accurate to conclude that there are multiple pathways to the development of BPD, with trauma and related symptoms being important factors for some people with this diagnosis (Chapman & Gratz, 2007).

Second, although the most recent edition of the DSM eliminates the multiaxial system, there has been some debate as to whether BPD is more similar to the emotional disorders that were formerly recognized on Axis I than the personality disorders that were recognized on Axis II. On the one hand, BPD’s severity, unstable course, and positive response to treatment support its conceptualization alongside major emotional disorders, and this repositioning could provide much needed support for the value of providing reimbursement of psychotherapeutic services (Gunderson, 2009). On the other hand, placing BPD alongside other emotional disorders could increase the likelihood that this disorder would be overlooked during clinical assessment (Gunderson, 2010).

Third, there is some controversy regarding whether BPD should be diagnosed in adolescence (Kaess, Brunner, & Chanen, 2014; Larrivée, 2013). Initial arguments against earlier diagnosis held that many symptoms of BPD are developmentally normative in adolescence (e.g., unstable mood, intense relationships, and unstable sense of self), that personality may not be sufficiently stable to merit such a diagnosis, and that, given the unfortunate but persistent stigma that often accompanies this diagnosis, labeling adolescents with BPD may result in unintended harm. Emerging evidence, however, suggests that BPD can be reliably and validly differentiated from normal personality in adolescence and that these symptoms are stable from adolescence through later developmental stages, supporting the utility of earlier diagnosis (Chanen et al., 2004; Chanen, Jovev, McCutcheon, Jackson, & McGorry, 2008; Kaess et al., 2014; Miller, Muehlenkamp, & Jacobson, 2008; Winograd, Cohen, & Chen, 2008). Moreover, several authors have noted that diagnosis in adolescence would facilitate earlier intervention, and that adolescents with borderline personality pathology show favorable outcomes with psychotherapy (Miller et al., 2008). As a result of this emerging evidence, diagnosis of BPD in adolescence is permitted according to guidelines in Section III of the DSM-5 (APA, 2013) and the eleventh edition of the ICD (Tyrer, Crawford, Mulder, & the ICD-11 Working Group for the Revision of Classification of Personality Disorders, 2011; WHO, 2018). Whether this diagnostic category will be regularly applied to younger patients remains to be seen.

Course and Recovery from BPD

Although the symptoms associated with BPD can be debilitating and life-threatening, longitudinal research paints a relatively optimistic picture of the trajectory of the disorder. Looking at the prevalence of BPD across the lifespan, diagnosis of BPD peaks in young adulthood, and the prevalence decreases in middle age and beyond (Grant et al., 2008).¹ Contrary to the historical notion that BPD was chronic and not responsive to treatment, longitudinal studies have found that most individuals remit from the disorder with age. In an ongoing longitudinal study spanning 16 years, 78 percent of patients with BPD at the start of the study had achieved eight years of remission, while 99 percent had achieved two years of remission at some point during follow-up (Zanarini et al., 2012). Another study reassessed patients diagnosed with BPD after 27 years and found that 92 percent of the living patients who were reassessed no longer met diagnostic criteria for BPD (Paris & Zweig-Frank, 2001).

Research has also revealed that certain BPD symptoms are more likely to remit over time than others, supporting the notion that extreme behaviors may “burn-out” over the lifespan (as suggested by Stone, 1993). In a cohort study of BPD patients, Stepp and Pilkonis (2008) found significant differences in impulsivity and suicidality as a function of age, with both the over 30 and over 40 cohorts reporting significantly less impulsivity and suicidality than the younger cohorts. In contrast, emotional distress did not differ across the cohorts.

An important aim of research in this area is the early identification of youth at risk for developing BPD, as less is known about the trajectory of those at risk for this disorder (who do not yet met criteria for BPD) and early intervention may mitigate core symptoms of impulsivity and affective instability. Investigating the relationship between childhood psychopathology and later development of BPD in a large longitudinal cohort study (The Pittsburgh Girls Study; n = 1233), Stepp and colleagues (Stepp, Burke, Hipwell, & Loeber, 2012) found a correspondence between childhood symptoms of attention deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD), both of which are associated with poor impulse control and self-regulation, and symptoms of BPD in adolescence. Additionally, the Children in the Community (CIC) study, which followed 800 children in diverse socioeconomic areas of New York over 20 years, offers a unique glimpse into the early life of individuals who experience symptoms of BPD in adolescence versus those who do not (e.g., greater instances of childhood sexual abuse predicted BPD symptoms but not other PDs), as well as the correspondence between BPD symptoms in adolescence and adulthood (Cohen, Crawford, Johnson, & Kasen, 2005). Regarding the trajectory of BPD symptoms from adolescence to adulthood, BPD symptoms in early adolescence in the CIC (mean age = 14) were associated with BPD symptoms in early adulthood (mean age = 33), as well as lower academic and occupational attainment and greater psychosocial impairment (e.g., lower global assessment of functioning; lower role function), although age-related declines in symptoms were found (Winograd et al., 2008). Nonetheless, the CIC did not include any genetic, physiological, or neurobiological markers related to emotion dysregulation (Chapman, 2019a) or impulsivity, and future research should incorporate such markers in order to identify key person × environment transactions associated with the development and course of BPD. Finally, emerging research on evidence-based practice for children and adolescents with BPD and related problems has underscored the potential effectiveness of early intervention (Chanen & McCutcheon, 2013; Mehlum et al., 2014; Perepletchikova et al., 2017).

Together, findings thus far suggest that reliable early markers for BPD exist and predict future functioning, and that treatment of adolescents with BPD features and related behavioral problems (suicidality, self-harm) is promising. Future directions in this area should include multi-method longitudinal research, replication of treatment studies, and examination of preventative interventions.

Etiological Factors

Since BPD was first conceptualized, theorists, researchers, and clinicians have speculated on the origins of the disorder (e.g., Kernberg, 1975). Nonetheless, rigorous empirical investigations of the etiology of BPD have been scarce. The past few decades have marked significant advancement in scientific understanding of BPD, and many methods have been employed for identifying developmental factors that increase later risk for BPD or distinguish individuals with BPD from individuals with other psychiatric disorders or healthy controls. Longitudinal studies have helped to identify socio-developmental factors that predict later development of BPD, whereas translational experimental studies have helped identify neurobiological, emotional, interpersonal, and behavioral processes distinguishing those with BPD from other groups. In the brief review below, we focus primarily on longitudinal and translational research to circumvent some of the key limitations of cross-sectional, self-report data. We approach this research from a biopsychosocial framework, similar to Linehan’s (1993a; see also Crowell et al., 2009) biosocial theory of BPD and the models proposed by Zanarini and colleagues (Zanarini & Frankenburg, 1997; Zanarini et al., 2005), whereby BPD results from a transaction of core vulnerabilities in biology and temperament and socio-developmental factors, such as invalidating or adverse environments.

Genetic Factors

Genetic studies can help guide research and intervention by identifying candidate genes that are associated with BPD diagnosis, whereas twin and adoption studies allow for estimation of the heritability of BPD (e.g., the proportion of variability in BPD accounted for by genetic factors). Findings indicating that first-degree relatives of individuals with BPD are several times more likely to have BPD than the general population (Baron, Gruen, Asnis, & Lord, 1985; Links, Steiner, & Huxley, 1988; Zanarini, Gunderson, Marino, Schwartz, & Frankenburg, 1988) suggest that BPD may be heritable to some degree. Stronger evidence has emerged from twin studies suggesting a moderately high heritability of BPD. Torgersen et al. (2000) assessed 221 twin pairs for personality disorders using a reliable diagnostic interview and found a heritability of .69 for BPD, although the small sample size limits interpretability of these results and may overestimate heritability. In a large-scale study on over 5000 twins across three countries (The Netherlands, Belgium, and Australia), similar heritability estimates of .42 for BPD features were found in all three countries using a self-report measure of BPD features (Distel et al., 2008). More twin studies with multiple assessment methods and larger samples are needed to clarify the precise heritability of BPD.

Although no specific genes have been found to reliably predict BPD (or to differentiate vulnerability to BPD from vulnerability to other psychopathology), candidate genes have been identified that may confer risk. A focus of genetic research to date has been on genes involved in serotonin transport (e.g., 5-HTT), uptake (e.g., serotonin 1B receptor gene), and synthesis (e.g., trypotophan hydroxolase-1 gene); however, a recent systematic review and meta-analysis concluded that there was no reliable association of these genes with BPD (Amad, Ramoz, Thoma, Jardri, & Gorwood, 2014). Amad et al. (2014) have suggested that inconsistent results for candidate genes may support a “plasticity” theory in which genes confer vulnerability to environmental risk factors rather than directly to BPD itself. This hypothesis of an indirect genetic effect is congruent with transactional biosocial models (Crowell et al., 2009; Linehan, 1993a), which propose that biological vulnerabilities may contribute to and exacerbate environmental vulnerabilities (e.g., a child with a genetic vulnerability may experience more negative life events during development, contributing to development of emotion dysregulation) and vice versa. Combined longitudinal and genetic studies following youth over time are called for to fully test this plasticity hypothesis.

Adverse Environments

Numerous studies have found an association between BPD and negative early experiences. Zanarini et al. (2002) found that 62 percent of individuals with BPD in an inpatient sample reported childhood sexual abuse, and that level of abuse was correlated with BPD symptom severity. Compared to patients with other personality disorders, individuals with BPD report more experience of trauma, including greater frequency of childhood sexual abuse (Paris, Zweig-Frank, & Guzder, 1994; Yen et al., 2002) and physical abuse (Paris et al., 1994), and younger age of exposure to trauma (Yen et al., 2002). Corroborating self-report studies, Westen and colleagues (Westen, Ludolph, Misle, Ruffins, & Block, 1990) found documented childhood sexual abuse in the medical charts of over 50 percent of adolescents living with BPD in an inpatient sample. Nonetheless, as mentioned earlier, childhood trauma (including childhood sexual abuse) is not sufficient to explain the development of BPD. Further, most individuals who experience childhood sexual abuse do not go on to develop diagnosable personality disorders (Paris, 1998; Zanarini et al., 1997).

Experts have pointed out that childhood abuse does not usually occur in isolation, and is typically part of a pattern of family dysfunction (Zanarini et al., 1997). As suggested by genetic studies reviewed above, negative life events may also be intertwined with genetic vulnerability to BPD. An investigation by Distel at al. (2011) on a large sample of twins and siblings found that the impact of negative life events (including breakup, violent assault, sexual assault) on BPD features was moderated by genetic vulnerability, except for the impact of sexual assault. Sexual assault conferred increased risk for BPD features regardless of genetic predisposition. This finding suggests a unique impact of sexual trauma that cannot be explained by genetic predisposition, although replication studies with diagnostic assessment of BPD are warranted. Moreover, exposure to negative events was found to moderate heritability estimates for BPD, which were lower among those exposed to negative life events than for those who had not been exposed to such events. These findings suggest different pathways to the development of BPD, with adverse environments and trauma playing a larger role for some individuals than others, as well as the importance of person × environment transactions in the development of BPD.

Further reflecting the complex interplay of environmental and individual factors is research suggesting that parental psychopathology may play a role in the development of BPD. Parents of children with BPD are more likely to have BPD, other personality disorders (e.g., antisocial personality disorder), and substance use disorders (see Helgeland and Torgersen, 2004 for review). Likewise, in a systematic review of studies examining psychopathology in relatives of individuals with BPD, White and colleagues (White, Gunderson, Zanarini, & Hudson, 2003) found the greatest evidence for a relationship between BPD and both familial BPD and familial impulse control disorders (e.g., substance use disorders and antisocial personality disorder), whereas the link between BPD and familial schizophrenia was not supported and the link between BPD and familial depression was tenuous. White et al. also noted that studies that relied on indirect assessment of familial history of psychopathology tended to over-inflate effects, whereas studies with more rigorous methodologies (e.g., direct assessment of family members using reliable diagnostic interviews) yielded more conservative estimates. Finally, in a study of the etiological factors associated with BPD in a large nonclinical sample, the contribution of parental psychopathology to BPD features was not better explained by abuse in childhood (Trull, 2001). Family history of psychopathology likely confers both environmental and biological risks to the development of BPD. Genetic, twin, or adoption studies, however, are necessary to disentangle the pathways underlying the intergenerational transmission of BPD.

Neurobiological Factors

Advances in neuroimaging have allowed for the identification of neurobiological characteristics of individuals with BPD, compared with other groups (often, healthy controls, and less often, psychiatric controls). Some studies have found reduced hippocampal and amygdala volume (Schmahl, Vermetten, Elzinga & Bremner 2003; van Elst et al., 2003) among BPD patients compared with healthy controls. Functional MRI studies have found that individuals with BPD have greater amygdala activation when confronted with emotional stimuli compared to controls (Donegan et al., 2003; Goodman et al., 2014; Herpertz et al., 2001; Minzenberg, Fan, New, Tang, & Siever, 2007; Silvers et al., 2016), leading to speculation that overactivity of the amygdala underlies emotion dysregulation (Krause-Utz, Winter, Niedtfeld, & Schmahl, 2014). Multiple methodologies have found evidence of additional fronto-limbic dysfunction in BPD, with PET imaging showing decreased frontal metabolism of glucose (Schmahl, Vermetten, Elzinga, & Bremner, 2004) and fMRI showing aberrant activation of the anterior cingulate, superior temporal sulcus, and superior front gyrus compared to controls in response to a task requiring cognitive control in response to emotional pictures (Koenigsberg et al., 2009). Taken together, the findings broadly suggest poor frontal regulation of the limbic system in BPD (Baczkowski et al., 2017; Schulz, Schmahl, & Niedtfeld, 2016). These findings converge with behavioral and self-report research showing (a) heightened negative emotional reactivity among people with BPD (Rosenthal et al., 2008), particularly in certain contexts (e.g., social rejection; Chapman, Dixon-Gordon, Walters, & Butler, 2015; Chapman, Walters, & Gordon, 2014) and (b) difficulty inhibiting impulsive behavior in negative emotional contexts among individuals with BPD pathology (Chapman, Dixon-Gordon, Layden & Walters, 2010; Sebastian et al., 2013).

Nonetheless, there are some key limitations of the extant research on putative neurobiological factors contributing to BPD. First, much of the research has compared BPD patients to healthy, non-psychiatric controls, making it difficult to discern whether functional or anatomical characteristics are unique to BPD or attributable to co-occurring disorders or psychopathology in general. Reduced amygdala and hippocampal volumes, for example, are not specific to BPD and may be better accounted for by co-occurring PTSD (see Leichsenring, Leibing, Kruse, New, & Leweke, 2011). More research distinguishing BPD from other psychiatric groups is needed. Second, neuroanatomical differences demonstrated in cross-sectional studies do not necessarily represent etiological factors. Brain, behavior, and the environment all transact, and differences in brain function or anatomy could be associated with adverse environmental events or prolonged engagement in particular behaviors (e.g., self-injury, drug or alcohol use), among others. Additional longitudinal investigations involving neuroimaging and appropriate controls (e.g., both healthy controls and psychiatric controls) are necessary to determine the association between neurobiological factors and emergence of BPD over time.

Evidence-Based Treatment

Beyond the aforementioned challenges defining BPD and pinpointing the precise etiology of this disorder, clinicians often experience challenges in the treatment of people with BPD, and for good reasons. The combination of suicide risk, severe and out of control behaviors, rapidly shifting emotional states, impulsivity, and interpersonal relations characterized by idealization and devaluation of others (sometimes including the therapist) can make treatment a complex and challenging endeavor. Persons with BPD often show slow, inconsistent, and episodic progress in treatment (Linehan, 1993a). In our experience, people with BPD often want help but have hit many roadblocks in previous treatment. The notion that BPD patients have a difficult time finding the right therapeutic fit is underscored by data suggesting that the vast majority of such patients (97 percent) will receive outpatient treatment from an average of 6.1 therapists (Perry, Herman, Van Der Kolk, & Hoke, 1990; Skodol, Buckley, & Charles, 1983). Perhaps not surprisingly, when I (ALC) first began giving clinical workshops and asked how many people in the audience looked forward to treating their BPD patients, few courageous hands went up. Fortunately, over the past few decades, advances in our understanding of BPD, research on recovery from BPD, and studies showing that BPD can be effectively treated have increased clinicians’ enthusiasm to help this often disenfranchised group. I see more and more hands go up when I ask clinicians that fateful question. That said, research and public awareness campaigns targeting stigma around BPD lag well behind other disorders, such as bipolar disorder (Ellison, Mason, & Scior, 2013).

Dialectical behavior therapy (DBT), mentalization-based treatment (MBT), and transference-focused psychotherapy (TFP) have been described as “the big three” of evidence-based, specialized psychotherapeutic treatments for BPD (Gunderson, 2016). Chambless and Hollon (1998) established guidelines for deeming a specific therapy to be empirically supported, defining efficacious therapies as those that demonstrated superiority to no treatment in at least two randomized controlled trials and by at least two independent research teams (minimizing allegiance effects). In this section, we only consider psychotherapeutic interventions with at least two RCTs supporting the therapy in question above treatment-as-usual or against another evidence-based treatment.

Comprehensive Treatments

Dialectical Behavior Therapy

Stemming from Dr. Marsha Linehan’s attempts to develop and enhance treatment for highly suicidal individuals, DBT (Linehan, 1993a) has evolved into a comprehensive cognitive-behavioral approach addressing BPD and several other clinical problems. DBT is based on the biosocial theory (Crowell et al., 2009; Linehan, 1993a) that BPD results from the transaction of an invalidating rearing environment and a biological emotional vulnerability. Emotional vulnerability consists of proneness to a low threshold for emotional arousal, intense emotional reactions, and slow return to emotional baseline (often referred to as delayed recovery). The invalidating environment consists of the following characteristics: (a) indiscriminate rejection of the child’s communication of thoughts and emotions, (b) intermittent reinforcement of emotional escalation, and (c) oversimplification of the ease of coping and problem solving. The biosocial theory holds that, in a developmental context, emotional vulnerability transacts with the invalidating environment, such that both factors exacerbate each other. Intense emotion vulnerability, especially when expressed through emotional outbursts or tantrums, can occasion invalidating parenting, particularly among parents bereft of the skills to cope with and parent an emotional child. Invalidation can amplify emotionality and does not teach the child to understand, trust, or regulate her or his emotional responses. Within this framework, persons with BPD have core skill deficits in emotion regulation, and many of the behavioral problems seen in this disorder are thought to occur in response to emotion dysregulation or function to regulate emotions (e.g., nonsuicidal self-injury; Brown, Comtois, & Linehan, 2002) (Linehan, 1993a).

DBT addresses five key functions of treatment within four primary modes of treatment. The key functions include: (a) increasing client motivation to change, (b) structuring the environment (the treatment and natural environment), (c) improving client capabilities, (d) generalizing skills and capabilities to relevant environments, and (e) maintaining and improving therapist motivation and skills. The four components of DBT include weekly individual therapy, telephone consultation (availability of the therapist between sessions for skills coaching; see Chapman, 2019b, for a book on this mode of DBT), weekly group skills training, and a therapist consultation team meeting. See Table 10.2 for a description of how these modes and functions fit together.

Table 10.2DBT modes and functions

Mode	Function
Individual Therapy	Improve motivation, generalize treatment gains, solve life problems, build a life worth living
Group Skills Training	Increase capabilities (mindfulness, distress tolerance, interpersonal effectiveness, emotion regulation, self-management/regulation)
Telephone Consultation	Generalize new behaviors to relevant situations
Consultation Team	Maintain and improve therapist motivation and capability

Source: Chapman & Hope (in press).

DBT is dialectical in that the treatment involves the balancing and synthesis of acceptance and change-oriented therapeutic styles, interventions, and skills. In developing DBT, Linehan discovered that the predominantly change-oriented approach to CBT was upsetting to clients who received the message that they simply needed to change their thinking and behavior to conquer longstanding, complex suffering. As a result, Linehan began to incorporate acceptance-oriented strategies stemming from both client-centered approaches and Zen practice. DBT, therefore, balances a problem solving and skills-training oriented treatment with validation and acceptance of clients, and teaches clients how to accept themselves. The DBT skills, similarly, involve a balance of change-oriented (interpersonal effectiveness, emotion regulation) and acceptance-oriented (reality acceptance skills, mindfulness) skills (Linehan, 1993b, 2014).

In the decades since the first RCT comparing DBT to treatment as usual (TAU) for the reduction of parasuicidal behavior (i.e., suicide attempts and self-injury; Linehan et al., 1991) among BPD patients, evidence has supported DBT as a well-established treatment. More than 20 published RCTs have examined standard DBT (all modes and functions as described above), and others have examined components of DBT, such as DBT skills training (nearly 20 studies). In addition, numerous open and uncontrolled trials and effectiveness and other studies have examined standard DBT, DBT-informed adaptations, or components of DBT (such as DBT skills training) for a variety of other clinical problem areas and in many settings (e.g., correctional, inpatient, outpatient, community, university). Overall, the findings have supported the efficacy of standard DBT for BPD and related problems, and suggest promise for DBT skills training for BPD, emotion regulation problems, depression, anxiety, and disordered eating (bingeing and purging), among other difficulties (see Neacsiu, Eberle, Kramer, Wiesmann, & Linehan, 2014, for a recent review, and McMain, Guimond, Barnhart, Habinski, & Streiner, 2017, for a recent study examining DBT skills group alone for suicidal patients with BPD). In a systematic Cochrane review, Stoffers et al. (2012) found moderate to large effects supporting DBT over TAU for reducing inappropriate anger and parasuicidal behavior (including suicide attempts and nonsuicidal self-injury) and improving psychiatric symptoms (Stoffers et al., 2012). DBT has been widely disseminated and recognized as an efficacious treatment for BPD, with both the Australian National Health and Medical Resource Council and the United Kingdom’s National Collaborating Centre for Mental Health concluding that DBT has the most evidence among current treatments for BPD (NHMRC, 2012; NICE, 2009). Until relatively recently, it was difficult to find a psychosocial treatment other than DBT that had been subject to carefully designed randomized trials. The field of promising treatments for BPD, however, has expanded to include other treatments described below.

Mentalization-Based Treatment

Developed by two experts with a psychoanalytic orientation, Anthony Bateman and Peter Fonagy, MBT is based on the theory that BPD results from impairments in early attachment relationships leading to poor mentalization, the ability to understand the internal states (e.g., thoughts, emotions) of oneself and others (Bateman & Fonagy, 1999). As such, a major focus of MBT is on monitoring mentalization and attachment in the therapeutic relationship and improving mentalization through patient–therapist interactions. For example, in individual therapy, the therapist expresses her or his own states of mind and their relation to the patient’s behaviors, invites patients to verbalize their own states of mind, and collaboratively addresses misunderstandings with patients (“understand misunderstanding”; Fonagy et al., 2014, p. 319). The MBT therapist retains a stance of curious inquiry into the patient’s thoughts, emotions, and interpretations and their relations to the therapist’s internal states.

MBT has been developed for delivery in both partial-hospitalization and outpatient settings. In the initial development of MBT, treatment was delivered in the context of routine psychiatric care for patients with BPD in a partial hospital program with one MBT group and individual therapy session per week. In outpatient MBT, patients typically meet with their individual therapist for one session of individual therapy and one session of group therapy per week.

To date, findings of the four existing RCTs on MBT have shown positive outcomes. One RCT examined the efficacy of MBT in the partial hospitalization program compared to TAU, finding that 18 months of MBT led to significantly greater improvement in BPD symptoms, fewer suicide attempts, greater psychosocial functioning, and more stable employment compared to TAU (Bateman & Fonagy, 1999, 2001). Upon follow-up five years later, the MBT group continued to maintain gains, evidencing fewer suicide attempts, lower use of psychiatric services, and higher rates of remission from BPD, compared to the TAU participants (Bateman & Fonagy, 2008). In the first RCT of outpatient MBT, results revealed that this treatment outperformed structured clinical management in several domains (Bateman & Fonagy, 2009). Patients assigned to outpatient MBT experienced greater reductions in suicide attempts and hospitalization after 12 months compared to patients in structured clinical management. Jørgensen et al. (2013) conducted the first independent investigation of the efficacy of MBT, comparing two years of more intensive outpatient MBT to two years of less intensive biweekly supportive group therapy. They found that MBT resulted in superior outcomes in therapist-rated global functioning, whereas both treatments resulted in comparable improvements in depression, social functioning, and BPD symptom severity (number of diagnostic criteria met in SCID-II assessment). Lastly, one RCT has examined MBT for adolescents with comorbid depression and self-harm (Rossouw & Fonagy, 2012). Whereas this study was not conducted on a sample selected for BPD diagnosis or features, emergent BPD symptoms were assessed in the study. Rossouw and Fonagy found that 12 months of MBT, adapted for adolescents, outperformed TAU in reducing the primary outcomes of self-harm and depression, and that improved mentalization, changes in attachment style (less avoidance), and reduced emergent BPD symptoms accounted for these group differences in outcomes.

Transference-Focused Psychotherapy

Rooted in Kernberg’s theory of the borderline personality organization (Kernberg, 1967), TFP is a psychoanalytically oriented therapy for BPD. TFP posits that the primitive defense mechanisms engaged in by the individual with BPD, such as splitting (e.g., rigidly categorizing others into “good” and “bad”), cause substantial impairment in relationships, identity, and self-regulation. TFP aims to correct both interpersonal dysfunction and the emotional reactivity that follows by exploring dynamics in the therapeutic relationship (Choi-Kain, Finch, Masland, Jenkins, & Unruh, 2017). For example, in individual therapy, the therapist addresses defense mechanisms by analyzing transference in the therapeutic relationship. TFP typically involves two weekly individual therapy sessions for three years. As such, this is the longest and most time-intensive of the “big three” treatments for BPD.

Three RCTs have been conducted on TFP to date, and two have supported the efficacy of TFP. Clarkin and colleagues (Clarkin, Levy, Lenzenweger, & Kernberg, 2007) evaluated one year of TFP, DBT, or supportive psychotherapy for patients with BPD in an RCT with three active treatment conditions. They found that both TFP and DBT outperformed supportive psychotherapy in reducing suicidality, and that TFP resulted in greater improvements in anger than DBT or supportive psychotherapy. A second RCT was conducted by an independent research team on schema-focused therapy (SFT) versus TFP in the treatment of BPD and found both to reduce symptoms of BPD and general psychopathology, with SFT outperforming TFP on all outcome measures (Giesen-Bloo et al., 2006). Most recently, Doering et al. (2010) evaluated one year of TFP versus an enhanced TAU condition of treatment by community experts. TFP resulted in greater reductions in symptoms of BPD, fewer suicide attempts, less hospitalization, and greater psychosocial functioning than TAU, whereas improvements in depression and anxiety occurred in both conditions but did not significantly differ between conditions. There was no significant change in self-harm in either condition. Reviewing this accumulated empirical evidence from these three RCTs, TFP seems to be a possibly efficacious treatment for certain clinical problem areas among BPD patients, although more well-controlled efficacy studies with consistent findings are needed before concluding that TFP has robust empirical support. As of the writing of this chapter, additional RCTs have been published on TFP since the latest Cochrane review of treatments for BPD (Stoffers et al., 2012).

Non-Comprehensive or Ancillary Approaches

Systems Training for Emotional Predictability and Problem Solving (STEPPS)

STEPPS is a short-term group treatment for BPD designed to serve as an adjunct to a patient’s TAU (Blum et al., 2008). Patients attend a weekly, seminar-style, group session where they are provided psychoeducation about BPD, emotion management skills training, and behavioral skills training (e.g., goal setting; building healthy habits around eating, sleep and exercise; stopping self-harm) based on cognitive behavioral principles. Additionally, the treatment is considered “systems-based” in that participants are encouraged to share their new skills with other people in their lives to help build support, and a one-time group psychoeducation session is offered to participants’ family members and friends.

Evidence for STEPPS. The first RCT, conducted by the treatment developers, found that STEPPS plus TAU resulted in greater reductions in BPD symptoms, impulsivity, and negative affectivity than TAU alone, although patients in the STEPPS condition had a higher drop-out rate (31 percent versus 14 percent; Blum et al., 2008). There were no differences in self-harm or suicide attempts between the two conditions. In a second RCT, STEPPS plus a complementary individual therapy (based on STEPPS principles, and offered every two weeks) was compared to TAU (Bos, van Wel, Appelo, & Verbraak, 2010). STEPPS recipients demonstrated greater reductions in general psychiatric symptoms and BPD symptoms, and gains were maintained at six-month follow-up. As with the first RCT, no differences were observed in terms of engagement in impulsive or self-damaging behaviors. Although initial evidence for STEPPS is promising, it is still unknown whether STEPPS is efficacious as a stand-alone treatment. As a brief intervention, STEPPS seems to be a beneficial adjunct to TAU and may serve patients and healthcare providers well when specialized comprehensive treatments for BPD are unavailable. Nonetheless, it will be important for future RCTs to compare STEPPS to enhanced TAU (e.g., treatment by community experts) or to treatments that have been established to be superior to TAU, such as DBT or MBT.

Emotion Regulation Group Therapy

Emotion regulation group therapy (ERGT) (Gratz & Gunderson, 2006; Gratz, Tull, & Levy, 2014) is another short-term group therapy designed as an adjunct to TAU for BPD. The focus of ERGT is on the treatment of self-harm within BPD by targeting the proposed underlying mechanism of emotion dysregulation. In ERGT, patients with repeated self-harm and BPD attend a weekly group for 14 weeks focused on teaching skills related to emotion regulation and acceptance, emphasizing acceptance of emotions and control of behaviors (Gratz & Gunderson, 2006; Gratz et al., 2014).

Two RCTs (Gratz & Gunderson, 2006; Gratz et al., 2014) and two open trials (Gratz & Tull, 2011; Sahlin et al., 2017) have evaluated the efficacy/utility of ERGT as an adjunct to TAU for BPD. Initial results have supported the possible efficacy of this brief intervention, with ERGT plus TAU reducing self-harm, emotion dysregulation, and BPD symptoms more than TAU alone in all four trials (Gratz & Gunderson; 2006; Gratz & Tull, 2011; Gratz et al., 2014; Sahlin et al., 2017). Further, upon follow-up nine months after treatment in the largest RCT, participants in the ERGT condition experienced significant post-treatment improvements in self-harm, emotion dysregulation, BPD symptoms, and quality of life compared to TAU, indicating that benefits of attending ERGT may continue to materialize even after patients end group (Gratz et al., 2014). Aside from DBT, ERGT has been identified as the only other psychotherapy with two or more controlled trials examining efficacy for reducing deliberate self-harm (see Turner, Austin & Chapman, 2014 for systematic review of psychotherapy for self-harm). Nonetheless, all controlled trials to date have been conducted by the treatment developer, and independent evaluation of the efficacy of ERGT is needed in order to define ERGT as efficacious.

Generalist Approaches

Following the emergence of evidence-based, specialized psychotherapeutic treatments for BPD, generalist approaches are gaining momentum. Accumulating evidence suggests that these approaches may offer sufficient treatment for core symptoms of BPD with the benefit of requiring less intensive training of clinicians for treatment delivery. Choi-Kain and colleagues (2017) classified the latest “wave” of efficacy studies on psychotherapeutic treatments for BPD as that of specialist therapies (e.g., DBT; MBT; TFP) vs. generalist approaches, such as general psychiatric management (Gunderson, 2014), and identified three RCTs (Bateman & Fonagy, 2009; Jørgensen et al., 2013; McMain et al., 2009) that fit into this wave. Based on these three RCTs, the authors concluded that “these enhanced, structured, and well-informed generalist treatment approaches performed as well in most ways to their already established specialized counterparts” (Choi-Kain et al., 2017, p. 22). Both Gunderson (2016) and Choi-Kain et al. (2017) posit that well-structured generalist approaches may fill the pressing need for less-intensive, more cost-effective treatment when specialized manualized treatments, such as DBT, are unavailable.

Medications

Although there are no “anti-BPD” medications approved for use by the US Food and Drug Administration or any other national authority, there is some evidence for a role of pharmacology in the treatment of specific symptoms. The most comprehensive review of high quality evidence for pharmacological intervention is presented in a Cochrane review (Lieb, Völlm, Rücker, Timmer, & Stoffers, 2010) including 27 RCTs from 1979–2008. On one hand, certain medications were found to be somewhat effective at treating specific symptoms of BPD, including the first-generation antipsychotic medications of haloperidol (for anger) and flupentixol (for suicidal behavior), second-generation antipsychotic medications of aripiprazole (for anger, psychotic symptoms, impulsivity, depression, and anxiety) and olanzapine (for anger, psychotic symptoms, anxiety), the mood stabilizers valproate, divalproex sodium, and topiramate (for interpersonal problems, anger, and impulsivity), and supplementary omega-3 fatty acids (for suicidality and depression²). On the other hand, there is little support for the use of antidepressants in treating symptoms of depression or affective instability among patients with BPD. No significant effects were found for the use of SSRI antidepressants compared to placebo, and only one significant effect was found for other antidepressants (the tricyclic amitriptyline; see Lieb et al., 2010). The authors noted that the overall quality of evidence for pharmacological treatment of BPD is low, due to few RCTs and small sample sizes. Additionally, actively suicidal clients were excluded from most RCTs, eliminating a sizable subset of the BPD patient population and resulting in uncertainty as to the helpfulness of medications for suicidal patients with BPD.

Descriptive research on the common medication prescription practices of physicians for patients with BPD paints a different picture that deviates from the empirical evidence on their efficacy. Despite the lack of evidence for SSRIs on symptoms of BPD in clinical trials, SSRIs are widely prescribed to patients with BPD (Baken-Glenn, Steels, & Evans, 2010; Knappich, Hörz-Sagstetter, Schwerthöffer, Leucht, & Rentrop, 2014; Zanarini, Frankenburg, Khera, & Bleichmar, 2001). Additionally, patients with BPD may be at particular risk of poly-pharmacy (Tyrer & Bateman, 2004), given the presence of multiple symptom domains and common co-occurrence of BPD with other disorders. An update to the Cochrane review by two of the original authors, Stoffers and Lieb, concluded that the current evidence is “unsatisfying” and suggested that the way patients with BPD tend to be treated with medication in community and hospital settings does not reflect the limited evidence base (Stoffers & Lieb, 2015). In addition, Paris (2002) has warned of physicians responding to limited effectiveness of any one medication for BPD by over-prescribing with multiple medications. This warning is particularly important given evidence that BPD patients were found to have substantially higher rates of prescribed opioid medications than a clinical comparison group of patients with other personality disorders (Frankenburg, Fitzmaurice, & Zanarini, 2014).

Common Ground among Evidence-Based Psychosocial Approaches

Despite differing theoretical foundations (object relations, psychodynamic, psychoanalytic, behavioral, etc.), psychosocial treatments with empirical support for BPD have some common elements, including an emphasis on the therapeutic relationship, emotion regulation and self-control, and interpersonal processes. Treatments vary in their degree of emphasis on these variables, with DBT most strongly emphasizing emotion and self-regulation, and MBT and TFP emphasizing interpersonal processes and the therapy relationship as a vehicle for change. In DBT, the therapy relationship is considered necessary but not sufficient, although the therapist ideally takes the opportunity to use interpersonal transactions in the therapy room to help the client develop skills to navigate interpersonal contexts in daily life. In addition, each of the treatments discussed here emphasizes the effectiveness of a fairly structured approach, consistent with the notion that therapeutic structure has a regulating effect and provides a “contained” context in which BPD patients can engage in the therapeutic process (whether that process involves increasing or decreasing specific behaviors, as in DBT, or processing interactions between the therapist and client, as in MBT and TFP).

Commonalities across empirically supported treatments for BPD suggest the possibility of transtheoretical processes of change that could be used in routine clinical practice. In other areas, treatment developers have distilled commonalities in discrete treatment manuals into broader, flexible approaches, such as the emerging transdiagnostic protocol to emotional disorders (Barlow, Allen, & Choate, 2004) and the transdiagnostic approach for eating disorders (Fairburn, Cooper, & Shafran, 2003). It is fortunate that the growing treatment literature suggests that BPD can be treated successfully; however, practitioners who provide specific, manualized treatments often are hard to find, even in large, urban areas. Further, as described above, there is some evidence that more general approaches to BPD treatment, based on common principles rather than specific techniques, such as general psychiatric management (McMain & Pos, 2007), have promise and may ease dissemination and implementation.

Predictors of Outcome and Mechanisms of Change

For the refinement of treatments for BPD to proceed efficiently, more research is needed to identify predictors of treatment outcome and mechanisms of change. The key questions here are: (1) How do treatments for BPD result in positive outcomes (mechanisms of change)? (2) For whom do treatments for BPD result in positive outcomes, and relatedly, for which groups of BPD patients do we need to modify or refine treatment? If key mechanisms of change were identified, treatment elements targeting these mechanisms could be emphasized to provide a more efficient and easily disseminated intervention. If we knew the patients for whom specific treatments were more or less likely to work, it would be easier to determine key research and treatment priorities targeting subgroups of patients who do not respond to existing treatments.

In terms of predictors of outcome for BPD, a review by Barnicott and colleagues (Barnicot, Katskou, Bhatti, Fearns, & Priebe, 2012) found some evidence that greater pre-treatment BPD severity predicted greater change in BPD symptoms (but only inconsistently change in diagnostic status) over the course of treatment, and that patients with a history of self-injury pre-treatment showed greater improvements in self-injury. Further, some studies showed evidence that therapeutic alliance positively predicted outcome.

In terms of mechanisms of change, one review of 14 studies addressing mechanisms in DBT or CBT found the most consistent evidence for the use of skills (Rudge, Feigenbaum, & Fonagy, 2017). From a DBT framework (and to some extent, a CBT framework), one key aim is for patients with BPD to increase their behavioral capabilities (skills) in key areas. In one study examining DBT skills use as a potential mechanism of change, Neacsiu and colleagues (Neacsiu, Rizvi, & Linehan, 2010) found that DBT skills use mediated decreases in suicide attempts and depression and increases in control of anger, and partially mediated decreases in self-injury. Other studies have examined a variety of potential mechanisms falling broadly under the category of skills, such as mindfulness (O’Toole, Diddy, & Kent, 2012; Perroud, Uher, Dieben, Nicastro, & Huguelet, 2010), negative/compensatory thinking patterns (Gibbons et al., 2010), and DBT skills use (Barnicot et al., 2012; Stepp, Epler, Jahng, & Trull, 2008).

Other studies have examined whether treatments change putative neurocognitive and neurobiological mechanisms associated with BPD. Thomsen and colleagues (Thomsen, Ruocco, Uliaszek, Mathiesen, & Simonsen, 2017) examined changes in neurocognitive functioning following six months of MBT among 18 women with BPD, compared with changes observed among non-psychiatric controls during a similar period (with no treatment). The study examined a range of neurocognitive measures and found that both patients and controls showed improvement on some of these measures, such as processing speed and perceptual reasoning. Results, however, revealed a significant interaction for only sustained attention, such that whereas patients began with lower performance than controls, these differences were non-significant at post-treatment. Another line of research has examined whether DBT changes the neurobiological fronto-limbic dysfunction often observed in some of the studies reviewed previously. Goodman et al. (2014), for example, compared changes in amygdala activation to pleasant, unpleasant, or neutral images among patients receiving 12 months of standard DBT versus healthy controls not receiving treatment. Findings suggested that the patients with BPD displayed significant reductions in both amygdala activity and self-reported emotion regulation difficulties (assessed via the Difficulties in Emotion Regulation Scale [DERS]; Gratz & Roemer, 2004), and that reductions in amygdala activity were associated with reductions in DERS scores. The findings of this and other studies (Schmitt, Winter, Niedtfeld, Herpertz, & Schmahl, 2016) suggest that DBT may have promise in reducing amygdala hyperactivity, increasing prefrontal connectivity to the amygdala, and increasing activity in prefrontal areas associated broadly with executive functioning and behavioral control (e.g., dorsolateral prefrontal cortex).

Conclusions and Future Directions

A severe, complex, and often stigmatized disorder, BPD has mystified clinicians and researchers alike. Developments over the past three to four decades have helped to shape and define the conceptualization of BPD, clarify potential causes and contributing factors, and highlight effective treatments. We know that (a) BPD characterized by impulsivity, emotional dysregulation, and interpersonal dysfunction, (b) the course of BPD is much more variable and positive than previously thought, and (c) psychosocial treatments work for BPD. For the field to move forward, several important future directions include: (a) research examining the validity and acceptability of alternative (e.g., dimensional, trait-based) conceptualizations of BPD, (b) increased longitudinal and translational research highlighting the dynamic interplay of factors conferring risk for BPD, and (c) treatment research highlighting predictors of outcome, the characteristics of treatment responders and non-responders, and potential mechanisms of change that could inform the development of streamlined, targeted, and efficient treatments. In addition, although we believe that inroads have been made in reducing the stigma associated with BPD and countering common myths about this disorder, there is the need to devote more resources to public education on BPD and efforts to reduce stigma. Finally, although treatment works for many people with BPD, it is still very hard for patients to find evidence-based treatment. More work is needed to increase access to treatment for this group of patients, who, in many cases, wish to overcome suffering, improve their lives and relationships, and make meaningful contributions to others’ lives.

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A Michael Smith Foundation for Health Research Career Investigator to the first author supported the writing of this chapter. Author Email: alchapma@sfu.ca.

¹In a nationally representative sample of American adults (n = 34,653), the prevalence of BPD for ages 20–29 was 9.3%, while it was 5.5% for ages 45–64 (Grant et al., 2008).

²Two small studies (n = 49 and n = 27) included in the Cochrane review have suggested efficacy for dietary supplements of omega-3 fatty acids reducing suicidality (study 1 only) and depressive symptoms.