Abstract

Borderline personality disorder (BPD) is a common and severe mental disorder that is associated with severe functional impairment and a high suicide rate. BPD is usually associated with other psychiatric and personality disorders, high burden on families and carers, continuing resource utilization, and high treatment costs. BPD has been a controversial diagnosis in adolescents, but this is no longer justified. Recent evidence demonstrates that BPD is as reliable and valid among adolescents as it is in adults and that adolescents with BPD can benefit from early intervention. Consequently, adolescent BPD is now recognized in psychiatric classification systems and in national treatment guidelines. This review aims to inform practitioners in the field of adolescent health about the nature of BPD in adolescence and the benefits of early detection and intervention. BPD diagnosis and treatment should be considered part of routine practice in adolescent mental health to improve these individuals’ well-being and long-term prognosis.

• borderline personality disorder
• adolescence
• self-injury
• suicidal behavior
• mental illness
• early intervention
• Abbreviations:

  AtR!Sk —

  outreach clinic for Adolescent Risk-taking and Self-harm behaviors

  BPD —

  borderline personality disorder

  CAT —

  cognitive analytic therapy

  DBT —

  dialectical behavior therapy

  DSM —

  Diagnostic and Statistical Manual for Mental Disorders

  ERT —

  emotion regulation training

  HPAA —

  hypothalamic-pituitary-adrenal axis

  HYPE —

  Helping Young People Early

  NSSI —

  nonsuicidal self-injury

  RCT —

  randomized controlled trial

This is the 4th in our series on Adolescent Health.

BPD in Adolescence

The Diagnosis of BPD

BPD is a severe mental disorder that is characterized by a pervasive pattern of instability in affect regulation, impulse control, interpersonal relationships, and self-image. BPD is defined by any 5 of the 9 criteria (see Table 1) in the Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition (DSM-5).The term “pervasive” indicates that these criteria should not be met exclusively in certain contexts or during periods of mental state disorder, such as depression. BPD has gained increased attention from the scientific and clinical communities and the public mainly because it is associated with a high risk of suicide, extensive use of mental health services, severe impairment in psychosocial functioning, and high social and economic costs.

• TABLE 1

  DSM-5 Diagnostic Criteria for BPD¹

  • Frantic efforts to avoid real or imagined abandonment

  • A pattern of unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation

  • Identity disturbance: markedly and persistently unstable self-image or sense of self

  • Impulsivity in at least 2 areas that are potentially self-damaging (eg, spending, sex, substance abuse, reckless driving, binge eating)

  • Recurrent suicidal behavior, gestures, or threats, or self-mutilating behavior

  • Affective instability due to a marked reactivity of mood (eg, intense episodic dysphoria, irritability, or anxiety usually lasting a few hours and only rarely more than a few days)

  • Chronic feelings of emptiness

  • Inappropriate, intense anger or difficulty controlling anger (eg, frequent displays of temper, constant anger, recurrent physical fights)

  • Transient, stress-related paranoid ideation or severe dissociative symptoms

   

TABLE 1

DSM-5 Diagnostic Criteria for BPD

Diagnosing BPD in Adolescence

Despite long-standing general agreement that personality disorders have their roots in childhood and adolescence, diagnosing BPD before age 18 years has been controversial. In many settings around the world, clinicians are still hesitant to diagnose BPD in youth, mainly because of 4 concerns: First, the diagnosis of BPD is not valid in adolescence. Second, typical features of BPD, such as affective instability or disturbed self-image, are normative among adolescents. Third, personality development is still in flux, and this precludes diagnosis. Fourth, and possibly most important, BPD is a pejorative term, and clinicians wish to protect their patients from stigmatizing and pessimistic attitudes. However, research over the past decade has disproven the first 3 assumptions, and greater knowledge of this has potential to influence the fourth.

There is increasing evidence in support of both diagnosing and treating BPD in adolescence. BPD has been found to be just as reliable and valid in adolescence as it is in adulthood, it shows similar stability in adolescence compared with adulthood, and it has incremental validity over and above common mental disorder diagnoses. Most important, disorder-specific treatment is beneficial, including early intervention. Thus, national treatment guidelines, Section 3 of the new DSM-5, and the proposed International Classification of Diseases, 11th Revision, personality disorder classification have all recently confirmed the legitimacy of the BPD diagnosis in adolescents. This highlights the need to communicate this new knowledge about BPD in adolescence to health care professionals.

Significance of Adolescent BPD

Prevalence and course

Epidemiologic data in adolescents are limited, with conservative point prevalence estimates ∼0.9%. Cumulative prevalence rates suggest that 1.4% of young people will meet diagnostic criteria for BPD by age 16 years, rising to 3.2% by age 22 years^. These data are comparable to adult prevalence data of 0.7% to 2.7%. BPD is a common and important disorder in adolescent mental health settings, with an estimated prevalence of 11% in psychiatric outpatients and up to 50% in inpatient settings.

Although the female-to-male ratio in clinical settings is usually reported to be at least 3:1, population-based studies do not show substantial gender differences in the prevalence of BPD in adults or children. The reasons for the unequal gender distribution in clinical settings might be an artifact of sampling or diagnostic biases or might reflect true biological, psychological, or social differences between males and females.

Longitudinal data show a normative increase in BPD traits after puberty (demarcating the onset of adolescence), reaching peak prevalence in early adulthood and subsequently declining in a linear fashion over subsequent decades. The diagnostic stability of BPD has been found to be similar in adolescents and adults. Ten years after initial diagnosis, 85% of adults with BPD will “remit” in terms of no longer meeting ≥5 BPD criteria; this number rises up to 99% after 16 years. These data confirm that BPD usually becomes clinically apparent during adolescence, peaks in young adulthood, and attenuates across the remainder of the life course.

Risk Taking and Self-Harm

Young people’s affinity to highly impulsive and self-damaging behavior places them at risk for adverse health outcomes. Both repetitive nonsuicidal self-injury (NSSI) and suicidal behavior are core features of BPD^, and most adults with BPD report a long-standing history of repetitive self-harm behaviors, dating back to childhood or adolescence. Among adolescents with BPD, “self-harm and suicidal behavior” (see Table 1) is the most frequently met BPD criterion. This differs from adulthood, when rates of self-harm and suicidal behavior decline. In young people, BPD features best predict continued engagement in NSSI over 1 year, and repetition of suicide attempts 6 months after hospitalization. Patients with BPD represent 9% to 33% of all suicides, and the lifetime suicide rate for BPD is estimated to be 8%. Specific data for suicide among adolescents with BPD are lacking, and 1 unresolved issue is the timing of suicide in the course of BPD. Higher suicide rates are found in studies with shorter duration of follow-up, suggesting that the early years after acute clinical care might be the period of highest risk. However, the study with the longest duration of follow-up (27 years) suggests that suicide occurs later in the course of BPD.

Adolescents with BPD are more likely to engage in risk-taking behaviors because of their tendency to act impulsively in response to aversive emotional states, not taking into account the possible consequences. Substance use is a serious problem in adolescent BPD, and like NSSI, it is often used for the purpose of affect-regulation in unbearable, aversive emotional states. Inpatients with BPD show a significantly higher prevalence of substance use disorder compared with their clinical controls. Additionally, adolescents with BPD are among the high-risk groups for sexual risk taking (eg, unprotected sexual intercourse, promiscuity) and consequent sexually transmitted diseases. Findings from adults show that sexual risk taking is exacerbated when BPD is comorbid with substance use.

Psychosocial Functioning and Mental Health Problems

When compared with their healthy peers, adolescents with BPD have substantial impairments in functioning, including social relationship problems and poor academic performance. In clinical studies, adolescents with a diagnosis of BPD also present with significantly reduced psychosocial functioning and quality of life comparable to child and adolescent psychiatric patients with other mental disorders.

Although BPD criteria tend to decline over time, functional impairment in adult BPD has been shown to be remarkably stable and more severe than for major depression. This is supported by one study in young people, which found that adolescent BPD uniquely predicts poor outcomes up to 2 decades into the future, such as a future BPD diagnosis, increased risk for other mental disorders (especially substance use and mood disorders), interpersonal problems, distress, and reduced quality of life.

Adult BPD is usually associated with a variety of comorbid mental health problems, and recent studies have found that the frequency of comorbid mental disorders might be even higher among adolescents with BPD. In 2 studies, almost all outpatients and 100% of adolescent inpatients with BPD presented with comorbid mental disorders, most of them with 2 or 3 additional psychiatric diagnoses. The most common comorbid mental disorders were mood disorders, followed by eating disorders, dissociative and posttraumatic stress disorders, other personality disorders and substance use disorders. When compared with patients with other mental disorders, the frequency of comorbid mental disorders was significantly higher among young people with BPD.

The Clinical Picture of Adolescent BPD

In summary, adolescent BPD is a severe mental disorder that is associated with frequent risk-taking and self-harm behavior, a particularly high burden of psychiatric comorbidity, and severe psychosocial impairment. Chanen and colleagues previously argued that being diagnosed with BPD at young age might indicate a more severe form of borderline personality disorder and/or a poorer prognosis. This clinical severity might also contribute to the high prevalence of service use among this group and might predict a possible lifelong functional impairment, high rates of usage of mental health services (including various forms of therapy, day treatment, and inpatient care) and emergency services, and increased mortality by both physical illness and suicide.

The Development of Adolescent BPD

BPD is increasingly seen as a life-span developmental disorder that exists on a dimensional continuum of severity. Despite increasing knowledge of neurobiological and psychosocial risk factors for BPD over the past decade, a detailed understanding of the developmental pathways to BPD has not yet been achieved, and prospective developmental data on adolescent BPD are rare.

Neurobiological Findings

To demonstrate that abnormalities found in adult BPD are implicated in its etiology, they should already be present early in the course of BPD. Studying adolescent BPD is a means of decreasing the influence of “duration of illness” effects (eg, treatment, chronicity) on research findings.

BPD is moderately heritable. However, no specific genes have been identified yet, and genetic vulnerability is more likely to be linked to certain temperamental factors such as negative emotionality, impulsivity, and introversion. Indeed, a BPD-specific temperamental pattern comprising opposing temperamental traits such as high novelty seeking and high harm avoidance has recently been found among adolescents with BPD, even when compared with clinical controls. Recent evidence from adults with BPD supports both gene–environment interaction and correlation in the development of BPD. This means that individuals with a “sensitive” genotype are at greater risk of BPD in the presence of a predisposing environment. Furthermore, the genes that influence BPD features also increase the likelihood of being exposed to certain adverse life events. One study found that the stability of BPD traits from mid to late adolescence is largely influenced by a combination of genetic and nonshared environmental factors. Recent research also focused on candidate genes from the serotonergic and dopaminergic systems but without stable and well-replicated findings.The only genetic data on adolescent BPD suggests that polymorphisms in the serotonin transporter gene might be a developmental risk factor for BPD.

Findings from structural imaging studies in adults consistently reveal volume reductions in the frontolimbic networks. Studies in adolescent BPD have only replicated findings for orbitofrontal cortex volumes and anterior cingulate cortex volumes. However, the common findings of volume reductions in the amygdala and hippocampus in adults with BPD do not seem to be present in the early course of BPD. Recent diffusion tensor imaging (DTI) studies of adolescents with BPD have revealed decreased fractional anisotropy in the inferior longitudinal fasciculus compared with healthy individuals and decreased fractional anisotropy in the fornix compared with clinical control participants. In the latter study, significant disorder-specific white matter alterations were found, including white matter pathways involved in emotion regulation as well as emotion recognition, suggesting that a large-scale network of emotion processing is disrupted in adolescent BPD.

Acute dysfunctional behaviors characteristic of BPD often occur in reaction to stressful situations. A specific vulnerability to stress (higher emotional intensity in response to stressors and a delayed return to baseline affect) has been proposed for individuals with BPD, which might be associated with the hypothalamic-pituitary-adrenal axis (HPAA). Adults with BPD show an attenuated cortisol response to acute stress, and this has also been found in adolescents engaging in repetitive NSSI. More numerous self-harm behaviors in adolescents with BPD were associated with increased pituitary volumes, suggesting greater basal activation of the HPAA. Given these findings, it is possible that prolonged activation of the HPAA in BPD individuals might induce HPAA hyporesponsiveness.

Altogether, the extant neurobiological findings in adolescent BPD are preliminary and need replication. Future research is needed, for example, to better address developmental processes (eg, brain maturation), or the interplay between different neurobiological systems and the environment.

Neuropsychological Findings

Alterations in emotion information processing have commonly been found in adults with BPD and have been proposed to be a key mechanism in the etiology of BPD. However, findings in adolescents are inconsistent. One study revealed that adolescent patients with BPD show stronger orienting to negative emotional stimuli, but a comparable study found no evidence of heightened sensitivity to emotional facial expressions.Nonetheless, adolescent borderline pathology has been linked to an inability to disengage attention from negative facial expressions during attentional maintenance when in a negative mood.

Adolescents with BPD have also been found to have impaired social perspective coordination and deficits in so-called theory of mind tasks. This latter deficit appears to be due to overinterpretive mental state reasoning (hypermentalizing = social-cognitive process that involves making assumptions about other people’s mental states that go so far beyond observable data that the average observer will struggle to see how they are justified), rather than the reduction or loss of theory of mind per se. Finally, youth with BPD have a preference for immediate gratification and a tendency to discount longer term rewards, which appears to be related to trait impulsivity.

Environmental Findings

Low family of origin socioeconomic status appears to be an independent prospective risk factor for BPD. This is confirmed by clinical data, with adolescents with BPD having lower socioeconomic status compared with healthy and clinical control subjects despite similar level of intelligence.

Strong associations between BPD and adverse childhood experiences have been found in clinical and population-based adult samples.The few studies including prospective data indicate that not only childhood maltreatment but also parenting variables such as attachment disorganization, maternal inconsistency and parental hostility are specifically associated with increased risk for BPD. In a recent population-based study, early BPD symptoms, at the age of 11, could be predicted by adverse family backgrounds and suboptimal parenting. A recent clinical study revealed that adolescent self-harm showed highest specific associations with maternal antipathy and neglect and only moderate associations with sexual abuse. It is still commonly believed that BPD is mostly a consequence of severe sexual abuse. However, although childhood sexual abuse is common in the histories of individuals with BPD, it is a rather weak and nonspecific risk factor. Taken together, the precise role of childhood adversity in the etiology of BPD remains contentious because putative risk factors, such as childhood abuse, adverse familial environment, and a family history of psychopathology might all contribute to the development of BPD and are often highly intercorrelated.

Although childhood experiences are predominantly influenced by parental relationships, peer relationships gain increasing importance during adolescent development. Difficulties with peer relationship might contribute to or accelerate the development of adolescent BPD. A history of being bullied in childhood is associated with BPD in adulthood and prospective data also show that being bullied during childhood is associated with BPD symptoms during early adolescence and increases the risk of self-harm in late adolescence by exacerbating the effects of exposure to an adverse family environment.

Recent research has increased our understanding of the developmental pathways to BPD. It is likely that individuals with a “sensitive” genotype are at greater risk of BPD in the presence of a predisposing environment, supporting the stress-diathesis model first proposed >30 years ago. However, the complexity of this interaction is likely to be high because of multiple interactions among predisposing biology (eg, genes), early environment (eg, low socioeconomic status, childhood adversity), reactive neurobiological alterations (eg, alterations of the HPAA), and a reactive environment (eg, having a higher risk of being bullied or maltreated because of particular temperamental characteristics), and further details are beyond the scope of this review.

Diagnosing Adolescent BPD

Early Detection

Diagnosing BPD is now justified and practical in adolescence and is supported in national treatment guidelines for BPD. Like most other disorders, there is likely to be a correlation between long duration of illness and worse prognosis for BPD. Early identification and treatment of young people with mental health problems is expected to reduce chronicity and related adverse health outcomes; thus, early detection of adolescent BPD is a crucial goal for health care systems.

Despite strong evidence supporting early identification of individuals with BPD, stigma is a key lingering barrier to early diagnosis in day-to-day clinical practice. BPD is highly stigmatized among professionals, and it is also associated with patient “self-stigma.” Although concerns about stigma are genuine and the response is well intentioned, this practice runs the risk of perpetuating negative stereotypes, reducing the prospect of applying specific beneficial interventions for the problems associated with BPD, and increasing the likelihood of incorrect diagnoses, inappropriate interventions and iatrogenic harm (such as polypharmacy).

Most individuals with early BPD symptoms will be seen by a general practitioner, a pediatrician, or other health care worker. Therefore, early detection relies on knowledge of clinical indicators of BPD (suggested in Table 2), and appropriate referral networks to mental health professionals. Although these clinical indicators can be used to identify adolescents who might be at risk for having BPD, it is important to understand that their sensitivity and specificity will varying (eg, repetitive self-harm is more indicative of BPD than anger outbursts)

• TABLE 2

  Warning Signs That May Indicate a Possible Diagnosis of Adolescent BPD

  • Repetitive NSSI or suicide attempts

  • Impulsive risk-taking behaviors (eg, binge drinking, substance abuse, risky sexual behavior)

  • A mixture of high levels of both internalizing (depressive symptoms, anxiety) and externalizing problems (conduct problems, attention-deficit/hyperactivity disorder symptoms)

  • Frequent anger outbursts and disruptive behavior

  • Frequent interpersonal problems and fights (including unstable relationships)

  • Very low self-esteem, insecure identity, lack of goals in life

TABLE 2

Warning Signs That May Indicate a Possible Diagnosis of Adolescent BPD

Increasing knowledge about adolescent BPD and reductions in stigma among professionals are likely to make early detection of adolescent BPD feasible and maybe even routine. This would likely result in more timely and specific interventions that aim to reduce impairment of psychosocial functioning and reduce borderline and other psychopathology and consequently improve the prognosis for adolescents with BPD.

Diagnostic Characteristics

To date, the major diagnostic classification systems have not adopted developmentally focused criteria for BPD. Thus, adult BPD criteria are used for adolescents. Although there are some differences between adolescents and adults in diagnostic-related phenomena associated with BPD, a review concluded that these differences can be explained by the principle of heterotypic continuity in development.

Reported differences between adults and adolescents affect the dominance of diagnostic criteria at certain stages of development. Compared with adults, adolescents are more likely to present with the more “acute” symptoms of BPD, such as recurrent self-harm and suicidal behavior, other impulsive and self-damaging behaviors, and inappropriate anger while long-standing characteristics, such as unstable relationships, idenbances, or fear of abandonment, seem to be more strongly represented among adults with BPD. Because of this overrepresentation of acute symptoms in adolescent BPD, it is crucial to carefully distinguish acute mental states (that might occur during a mental state disorder or a developmental crisis) from features that indicate a more general pattern of maladaptive and dysfunctional behaviors.

Dimensional Diagnostic Approach

There is strong evidence from population and clinical studies supporting the notion that BPD is a dimensional construct, and subthreshold presentations are clinically important. An example of this appears in section 3 of the DSM-5 (conditions that require further research), but at present there is no consensus among the field as to which dimensional model should be adopted. Potential advantages of a dimensional approach are that (1) adolescents with BPD can be described much more in detail than previously possible, (2) subthreshold conditions can be easily identified and classified, (3) changes in BPD symptomatology over the course of illness can be more sensitively detected, and (4) therapeutic interventions could be more individually targeted.

Diagnostic Tools

Reliable diagnosis of BPD is essential and the use of a well-established diagnostic tool is highly recommended. The official tools of the fourth edition of the DSM (DSM-IV; Structured Clinical Interview for DSM-IV Axis II Personality Disorders) and International Classification of Diseases, 10th Revision (International Personality Disorder Examination) are widely used in clinical and research settings and have also successfully been used in adolescents. Recent developments in the field of adolescent BPD have also included the validation of the Childhood Interview for DSM-IV Borderline Personality Disorder, which shows good reliability and validity and is the first interview-based measure for adolescent BPD.

Self-report scales have been widely used in population-based studies of BPD and as screening measures in clinical settings. Examples from the adult population, which have also been successfully used in adolescent samples, are the BPD items of the Structured Clinical Interview for DSM-IV Axis II Personality Disorders Personality Questionnaire, the Borderline Personality Questionnaire, and the McLean Screening Instrument for BPD. The Borderline Personality Features Scale for Children has been developed specifically for children and adolescents and includes a newly developed parent report version. Adolescent BPD features may also be assessed by using the Personality Assessment Inventory for Adolescents.The Schedule for Nonadaptive and Adaptive Personality for Youth, a new self-report measure for the assessment of adolescent personality traits, relevant to both normal-range personality and the alternative DSM-5 model for personality disorder has recently been developed. The Borderline Personality Disorder Severity Index, IV, adolescent and parent versions have recently been validated for the assessment of BPD severity in adolescents.

Differential Diagnoses

Adolescents with BPD are characterized by a blend of externalizing (eg, impulsive-aggressive behavior, substance abuse) and internalizing (eg, anxiety, depression) symptoms. This variety of psychopathology means that adolescent BPD can easily be confused with other psychiatric diagnoses, and a thorough understanding of differential diagnoses aids precision. One of the key tasks of differential diagnosis is to distinguish “state” from “trait” psychopathology. To make a diagnosis of personality pathology, the feature must remain present to some extent outside distinct periods of abnormal mental state. For example, “affective instability” is a prominent feature of adolescent BPD that can be difficult to distinguish from affective mental state disorders (eg, depression). Moreover, many adolescents with BPD present with a co-occurring major depressive episode. The diagnosis of borderline affective instability is made when this feature predates or persists beyond distinct periods when the person has depressed mood accompanied by other features of major depression.

Clinical differentiation of bipolar II disorder from BPD can be challenging because of co-occurrence of phenomenologic features such as affective lability, difficulty controlling anger, impulsivity, and suicidality.This has previously led to the suggestion that BPD might in fact belong to the bipolar spectrum; however, this hypothesis is based largely on the observation of unstable mood, but there is little research to support this idea. Clinical characteristics such as family history, phenomenology, longitudinal course, comorbidity, and treatment response do differ significantly between the 2 conditions. Patients with BPD experience a higher and broader load of negative emotions (eg, anger, sadness, anxiety), and the fluctuation of their affective states is more rapid and chaotic, often in reaction to interpersonal events. Bipolar II disorder usually shows a sharp onset period in late adolescence or young adulthood, tends not to remit with age, and shows more agitated and autonomous mood episodes without interpersonal context. These episodes are rather cyclical and include sustained euphoric periods. Distinguishing the disorders is clinically important, because of the marked differences in treatments for BPD or bipolar II.

Adolescents with BPD often report transient and stress-related dissociative symptoms (eg, feeling that the self is strange or unreal, detached from emotions, feeling like a robot) and paranoid symptoms as well as auditory hallucinations. Thus, psychotic disorders are important differential diagnoses of BPD and require thorough differentiation because of the risk of unnecessary polypharmacy. Other diagnoses to be considered during the assessment of BPD include substance use disorders, which are common among youth with BPD. Although BPD can be diagnosed in the majority of adolescents with nonsuicidal self-injury, it is important to note that not all self-harming adolescents have BPD. Given the strong association between trauma and BPD, posttraumatic stress disorder is common among individuals with BPD and requires attention during assessment.

Early Intervention for BPD

BPD is a reliable and valid diagnosis in adolescence that is associated with acute risks and impairment and serious long-term consequences including poor psychosocial functioning and high morbidity and mortality. Therefore, specifically tailored, evidence-based interventions are crucial for this group.

Prevention

BPD has been identified as a leading candidate for developing empirically based prevention and early intervention programs because it is common in clinical practice, it is among the most functionally disabling of all mental disorders, it is often associated with help-seeking, and it has been shown to respond to intervention, even in those with established disorder. Data also suggest considerable flexibility and malleability of BPD traits in youth, making this a key developmental period during which to intervene, and adolescent BPD features have been shown to respond to intervention.

It has been strongly argued that stand-alone universal (whole population) prevention of BPD is not currently justified or feasible because the condition is not sufficiently prevalent, and it is unclear what form or dose of intervention would be appropriate. Similarly, selective prevention (targeting those with risk factors for BPD) is currently impractical because of the lack of specificity of most risk factors (particularly environmental factors, such as childhood adversity) associated with BPD. Both approaches are scientifically impractical because they cannot be adequately powered to reliably detect treatment effects. Indicated prevention is currently the only evidence-based form of prevention for BPD. This approach targets those individual displaying signs and symptoms that resemble aspects of the BPD phenotype and which presage its later appearance in adolescence or emerging adulthood. Certain early temperamental and personality features, internalizing and externalizing psychopathology, and specific BPD criteria are all candidate precursor signs and symptoms. Examples include features of disruptive behavior disorders, self-injury, substance use and depressive disorders, along with BPD diagnostic features. This approach is discussed in more detail elsewhere.

High Quality Clinical Care

Chanen and McCutcheon, who have pioneered early intervention in BPD for the past 15 years, have recently published basic principles for early intervention (see Table 3). These principles are drawn from the work of the Helping Young People Early (HYPE) program in Melbourne, Australia but are common to more recently established early intervention services for BPD, such as the Dutch emotion regulation training (ERT) program, or the German outreach clinic for Adolescent Risk-taking and Self-harm behaviors (AtR!Sk). Beyond these principles, the main differences among the programs are related to the model of individual psychotherapy that is practiced at each center.

• TABLE 3

  Basic Principles of Early Intervention in Adolescent BPD

  • Rigorous diagnoses of BPD criteria

  • Broad inclusion criteria, with limited exclusions for co-occurring psychopathology

  • A dimensional view of BPD, which means treating both subsyndromal (indicated prevention) and syndromal (early intervention) BPD

  • Assertive case management integrated with the delivery of individual psychotherapy and general psychiatric care

  • Active engagement of families and carers

  • A clear model of brief and goal-directed crisis and inpatient care

  • Individual and group supervision of staff including a quality assurance program

  • Access to support structures for social recovery

TABLE 3

Basic Principles of Early Intervention in Adolescent BPD

Psychotherapy

Individual psychotherapy is a key component of early intervention for BPD in addition to the underpinning service delivery models. To date, there are several disorder-specific psychotherapy treatment manuals available for adolescent BPD, but only some of the commonly used disorder-specific psychotherapeutic approaches are described in more detail here.

Cognitive analytic therapy (CAT) was the first individual therapy to be tested in a randomized controlled trial (RCT) in adolescent BPD. CAT has been adapted for early intervention in BPD and is used within the HYPE program in Australia. CAT is a time-limited, integrative, and “transdiagnostic” psychotherapy that arose from a theoretical and practical integration of elements of psychoanalytic object relations theory and cognitive psychology, subsequently developing into an integrated model of development and psychopathology. CAT is practical and collaborative in style, with a particular focus on identifying, understanding, and revising the individual’s problematic self-management and interpersonal relationship patterns and the thoughts, feelings, and behavioral responses that result from these patterns. A central feature in CAT is the joint (patient–therapist) creation of a shared understanding of the patient’s difficulties and their developmental origins, using plain-language written and diagrammatic “reformulations.” CAT has demonstrated effectiveness compared with “treatment as usual,” and more rapid recovery but similar 2-year outcome, compared with structured high-quality care available in the HYPE service model.

ERT is an adaptation of Systems Training for Emotional Predictability and Problem Solving (STEPPS). ERT is a 17-week, manual-based, cognitive-behavioral group treatment program for adolescent outpatients with borderline personality disorder. It combines cognitive behavioral elements and skills training with a systems component. In a recent RCT, ERT led to substantial improvement of adolescent BPD symptomatology but failed to demonstrate superiority over high qualitative treatment as usual.

Mentalization-based therapy has been developed in accordance to attachment theory and empirical research on psychotherapy. It is a psychodynamic approach that aims to improve the ability to make and use mental representations of their own and other people’s emotional states (“mentalization”). Mentalization-based therapy has recently been successfully applied to self-harming adolescents in the United Kingdom within a RCT but not yet proven effectiveness in a specific trial for adolescent BPD.

Other treatment approaches that have been successful in treating adults with BPD have been adapted for use in adolescents but have not been tested in RCTs in this age group. One of the most commonly used approaches for the psychotherapeutic treatment of adolescent BPD is dialectical behavior therapy for adolescents (DBT-A), which has been developed from Linehan’s DBT for adults and combines elements of cognitive-behavioral therapy with awareness and relaxation techniques from the Zen Buddhism. DBT has become well known for its skills-training groups, which aim to convey practical skills for the improvement of stress tolerance, emotion regulation, interpersonal difficulties, and awareness to individuals with BPD. DBT-A consists of 20 weekly individual psychotherapy sessions, weekly participation in the skills group and rigorous supervision of the therapists. In addition to adult DBT, the integration of families is a central component of DBT-A. DBT-A is currently used within the German program AtR!Sk. So far, there are some promising follow-up data available, and an RCT is under way.

Transference-focused psychotherapy is an analytic psychotherapeutic treatment approach that has been developed by Kernberg and his group in accordance with object relations theory. It combines classic analytic techniques with a more structured and presence-focused approach that fits the needs of adolescents with BPD. The transference-focused psychotherapy has been manualized and adapted for the treatment of adolescent BPD (adolescent identity treatment) but has not been evaluated.

Research has only begun to evaluate effectiveness of these disorder-specific treatments and has revealed some promising results. It appears highly likely that structured interventions for BPD are superior to treatment as usual in mental health services. However, true evidence is still lacking for almost all treatment approaches, and several specialized treatments have been studied with mixed results.

Pharmacotherapy

Recent meta-analyses for adult BPD concluded that there is no current evidence for any BPD specific pharmacotherapy. So called symptom-focused pharmacotherapy is controversial in adults with BPD and, given its lack of efficacy or effectiveness, should not be extrapolated to adolescent BPD. One preliminary study exists for the use of omega-3 fatty acids in adolescents with BPD and ultra high risk for psychosis. Overall, there is no current evidence for any specific pharmacotherapy as a first-line treatment of adolescent BPD, and the risks of polypharmacy and iatrogenic harm are high in these young people. Comorbid disorders should be treated according to their respective clinical guidelines for adolescents, and this might sometimes involve pharmacotherapy.

Conclusions

BPD is a reliable and valid diagnosis among adolescents. Importantly, it is associated with severe psychopathology and high risks for affected individuals’ health, development, and future. Adolescents with BPD benefit from early detection and intervention to alter the life-course trajectory of the disorder, reducing long-term adverse consequences of BPD, such as poor psychosocial functioning and high morbidity and mortality. Therefore, an important first step is to increase knowledge about adolescent BPD among clinicians in the field of child and adolescent health to reduce stigma and improve awareness with regard to adolescent BPD.

Footnotes

• Accepted May 6, 2014.
• Address correspondence to Michael Kaess, Department of Child and Adolescent Psychiatry, Centre for Psychosocial Medicine, University of Heidelberg, Blumenstrasse 8, 69115 Heidelberg, Germany. E-mail: michael.kaess@med.uni-heidelberg.de

• Dr Kaess participated in thorough literature research and wrote the first draft of the manuscript; Drs Brunner and Chanen participated in thorough literature research and critically revised the manuscript; and all authors approved the final manuscript as submitted.

• FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.

• FUNDING: No external funding.

• POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

References

1. ↵
   American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Publishing; 2013
2. ↵
   1. Leichsenring F,
   2. Leibing E,
   3. Kruse J,
   4. New AS,
   5. Leweke F

   . Borderline personality disorder. Lancet. 2011;377(9759):74–84pmid:21195251

3. ↵
   1. Chanen AM,
   2. McCutcheon LK

   . Personality disorder in adolescence: The diagnosis that dare not speak its name. Pers Ment Health. 2008;2(1):35–41

4. ↵
   1. Chanen AM,
   2. Jovev M,
   3. McCutcheon LK,
   4. Jackson HJ,
   5. McGorry PD

   . Borderline personality disorder in young people and the prospects for prevention and early intervention. Curr Psychiatry Rev. 2008;4(1):48–57

5. ↵
   1. Miller AL,
   2. Muehlenkamp JJ,
   3. Jacobson CM

   . Fact or fiction: diagnosing borderline personality disorder in adolescents. Clin Psychol Rev. 2008;28(6):969–981pmid:18358579

6. ↵
   1. Chanen AM,
   2. Jackson HJ,
   3. McGorry PD,
   4. Allot KA,
   5. Clarkson V,
   6. Yuen HP

   . Two-year stability of personality disorder in older adolescent outpatients. J Pers Disord. 2004;18(6):526–541pmid:15615665

7. ↵
   1. Kaess M,
   2. von Ceumern-Lindenstjerna I-A,
   3. Parzer P,
   4. et al

   . Axis I and II comorbidity and psychosocial functioning in female adolescents with borderline personality disorder. Psychopathology. 2013;46(1):55–62pmid:22890504

8. ↵
   1. Chanen AM,
   2. Jovev M,
   3. Jackson HJ

   . Adaptive functioning and psychiatric symptoms in adolescents with borderline personality disorder. J Clin Psychiatry. 2007;68(2):297–306pmid:17335330

9. ↵
   1. Chanen AM,
   2. McCutcheon L

   . Prevention and early intervention for borderline personality disorder: current status and recent evidence. Br J Psychiatry Suppl. 2013;54:s24–s29pmid:23288497

10. ↵
    1. National Health and Medical Research Council

    . Clinical Practice Guideline for the Management of Borderline Personality Disorder. Melbourne, Australia: National Health and Medical Research Council; 2012

11. ↵
    1. National Collaborating Centre for Mental Health

    . Borderline Personality Disorder: Treatment and Management NICE Clinical Guideline. London, UK: National Institute for Health and Clinical Excellence; 2009

12. ↵
    1. Tyrer P,
    2. Crawford M,
    3. Mulder R,
    4. ICD-11 Working Group for the Revision of Classification of Personality Disorders

    . Reclassifying personality disorders. Lancet. 2011;377(9780):1814–1815pmid:21353696

13. ↵
    1. Johnson JG,
    2. Cohen P,
    3. Kasen S,
    4. Skodol AE,
    5. Oldham JM

    . Cumulative prevalence of personality disorders between adolescence and adulthood. Acta Psychiatr Scand. 2008;118(5):410–413pmid:18644003

14. ↵
    1. Lewinsohn PM,
    2. Rohde P,
    3. Seeley JR,
    4. Klein DN

    . Axis II psychopathology as a function of Axis I disorders in childhood and adolescence. J Am Acad Child Adolesc Psychiatry. 1997;36(12):1752–1759pmid:9401337

15. ↵
    1. Coid J,
    2. Yang M,
    3. Tyrer P,
    4. Roberts A,
    5. Ullrich S

    . Prevalence and correlates of personality disorder in Great Britain. Br J Psychiatry. 2006;188:423–431pmid:16648528

16. ↵
    1. Trull TJ,
    2. Jahng S,
    3. Tomko RL,
    4. Wood PK,
    5. Sher KJ

    . Revised NESARC personality disorder diagnoses: gender, prevalence, and comorbidity with substance dependence disorders. J Pers Disord. 2010;24(4):412–426pmid:20695803

17. ↵
    1. Chanen AM,
    2. Jovev M,
    3. Djaja D,
    4. et al

    . Screening for borderline personality disorder in outpatient youth. J Pers Disord. 2008;22(4):353–364pmid:18684049

18. ↵
    1. Grilo CM,
    2. Becker DF,
    3. Fehon DC,
    4. Walker ML,
    5. Edell WS,
    6. McGlashan TH

    . Gender differences in personality disorders in psychiatrically hospitalized adolescents. Am J Psychiatry. 1996;153(8):1089–1091pmid:8678180

19. ↵
    1. Lenzenweger MF,
    2. Lane MC,
    3. Loranger AW,
    4. Kessler RC

    . DSM-IV personality disorders in the National Comorbidity Survey Replication. Biol Psychiatry. 2007;62(6):553–564pmid:17217923

20. ↵
    1. Torgersen S,
    2. Kringlen E,
    3. Cramer V

    . The prevalence of personality disorders in a community sample. Arch Gen Psychiatry. 2001;58(6):590–596pmid:11386989

21. ↵
    1. Zanarini MC,
    2. Horwood J,
    3. Wolke D,
    4. Waylen A,
    5. Fitzmaurice G,
    6. Grant BF

    . Prevalence of DSM-IV borderline personality disorder in two community samples: 6,330 English 11-year-olds and 34,653 American adults. J Pers Disord. 2011;25(5):607–619pmid:22023298

22. ↵
    1. Skodol AE,
    2. Bender DS

    . Why are women diagnosed borderline more than men? Psychiatr Q. 2003;74(4):349–360pmid:14686459

23. ↵
    Tackett JL, Balsis S, Oltmanns TF, Krueger RF. A unifying perspective on personality pathology across the life span: developmental considerations for the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders. Dev Psychopathol. 2009;21(3):687–713
24. ↵
    1. Cohen P,
    2. Crawford TN,
    3. Johnson JG,
    4. Kasen S

    . The children in the community study of developmental course of personality disorder. J Pers Disord. 2005;19(5):466–486pmid:16274277

25. ↵
    1. Gunderson JG,
    2. Stout RL,
    3. McGlashan TH,
    4. et al

    . Ten-year course of borderline personality disorder: psychopathology and function from the Collaborative Longitudinal Personality Disorders study. Arch Gen Psychiatry. 2011;68(8):827–837pmid:21464343

26. ↵
    1. Zanarini MC,
    2. Frankenburg FR,
    3. Reich DB,
    4. Fitzmaurice G

    . Attainment and stability of sustained symptomatic remission and recovery among patients with borderline personality disorder and axis II comparison subjects: a 16-year prospective follow-up study. Am J Psychiatry. 2012;169(5):476–483pmid:22737693

27. ↵
    1. Chanen AM,
    2. Kaess M

    . Developmental pathways to borderline personality disorder. Curr Psychiatry Rep. 2012;14(1):45–53pmid:22009682

28. ↵
    1. Zanarini MC,
    2. Frankenburg FR,
    3. Reich DB,
    4. Fitzmaurice G,
    5. Weinberg I,
    6. Gunderson JG

    . The 10-year course of physically self-destructive acts reported by borderline patients and axis II comparison subjects. Acta Psychiatr Scand. 2008;117(3):177–184pmid:18241308

29. ↵
    1. Glenn CR,
    2. Klonsky ED

    . Prospective prediction of nonsuicidal self-injury: a 1-year longitudinal study in young adults. Behav Ther. 2011;42(4):751–762pmid:22036002

30. ↵
    1. Wilcox HC,
    2. Arria AM,
    3. Caldeira KM,
    4. Vincent KB,
    5. Pinchevsky GM,
    6. O’Grady KE

    . Longitudinal predictors of past-year non-suicidal self-injury and motives among college students. Psychol Med. 2012;42(4):717–726pmid:21906421

31. ↵
    1. Yen S,
    2. Weinstock LM,
    3. Andover MS,
    4. Sheets ES,
    5. Selby EA,
    6. Spirito A

    . Prospective predictors of adolescent suicidality: 6-month post-hospitalization follow-up. Psychol Med. 2013;43(5):983–993pmid:22932393

32. ↵
    1. Kullgren G,
    2. Renberg E,
    3. Jacobsson L

    . An empirical study of borderline personality disorder and psychiatric suicides. J Nerv Ment Dis. 1986;174(6):328–331pmid:3711874

33. ↵
    1. Runeson B,
    2. Beskow J

    . Borderline personality disorder in young Swedish suicides. J Nerv Ment Dis. 1991;179(3):153–156pmid:1997663

34. ↵
    1. Pompili M,
    2. Girardi P,
    3. Ruberto A,
    4. Tatarelli R

    . Suicide in borderline personality disorder: a meta-analysis. Nord J Psychiatry. 2005;59(5):319–324pmid:16757458

35. ↵
    1. Paris J,
    2. Zweig-Frank H

    . A 27-year follow-up of patients with borderline personality disorder. Compr Psychiatry. 2001;42(6):482–487pmid:11704940

36. ↵
    1. Chen EY,
    2. Brown MZ,
    3. Lo TTY,
    4. Linehan MM

    . Sexually transmitted disease rates and high-risk sexual behaviors in borderline personality disorder versus borderline personality disorder with substance use disorder. J Nerv Ment Dis. 2007;195(2):125–129pmid:17299299

37. ↵
    1. Feenstra DJ,
    2. Hutsebaut J,
    3. Laurenssen EMP,
    4. Verheul R,
    5. Busschbach JJV,
    6. Soeteman DI

    . The burden of disease among adolescents with personality pathology: quality of life and costs. J Pers Disord. 2012;26(4):593–604pmid:22867509

38. ↵
    1. Crawford TN,
    2. Cohen P,
    3. First MB,
    4. Skodol AE,
    5. Johnson JG,
    6. Kasen S

    . Comorbid Axis I and Axis II disorders in early adolescence: outcomes 20 years later. Arch Gen Psychiatry. 2008;65(6):641–648pmid:18519822

39. ↵
    1. Winograd G,
    2. Cohen P,
    3. Chen H

    . Adolescent borderline symptoms in the community: prognosis for functioning over 20 years. J Child Psychol Psychiatry. 2008;49(9):933–941pmid:18665882

40. ↵
    1. Zanarini MC,
    2. Frankenburg FR,
    3. Hennen J,
    4. Reich DB,
    5. Silk KR

    . Axis I comorbidity in patients with borderline personality disorder: 6-year follow-up and prediction of time to remission. Am J Psychiatry. 2004;161(11):2108–2114pmid:15514413

41. ↵
    1. Cailhol L,
    2. Jeannot M,
    3. Rodgers R,
    4. et al

    . Borderline personality disorder and mental healthcare service use among adolescents. J Pers Disord. 2013;27(2):252–259pmid:23514188

42. ↵
    1. Bender DS,
    2. Dolan RT,
    3. Skodol AE,
    4. et al

    . Treatment utilization by patients with personality disorders. Am J Psychiatry. 2001;158(2):295–302pmid:11156814

43. ↵
    1. Oldham JM

    . Borderline personality disorder and suicidality. Am J Psychiatry. 2006;163(1):20–26pmid:16390884

44. ↵
    1. Chen H,
    2. Cohen P,
    3. Crawford TN,
    4. Kasen S,
    5. Guan B,
    6. Gorden K

    . Impact of early adolescent psychiatric and personality disorder on long-term physical health: a 20-year longitudinal follow-up study. Psychol Med. 2009;39(5):865–874pmid:18775086

45. ↵
    1. Miller JD,
    2. Morse JQ,
    3. Nolf K,
    4. Stepp SD,
    5. Pilkonis PA

    . Can DSM-IV borderline personality disorder be diagnosed via dimensional personality traits? Implications for the DSM-5 personality disorder proposal. J Abnorm Psychol. 2012;121(4):944–950pmid:22428791

46. ↵
    1. Chanen AM,
    2. Velakoulis D,
    3. Carison K,
    4. et al

    . Orbitofrontal, amygdala and hippocampal volumes in teenagers with first-presentation borderline personality disorder. Psychiatry Res. 2008;163(2):116–125pmid:18395424

47. ↵
    1. Kendler KS,
    2. Aggen SH,
    3. Czajkowski N,
    4. et al

    . The structure of genetic and environmental risk factors for DSM-IV personality disorders: a multivariate twin study. Arch Gen Psychiatry. 2008;65(12):1438–1446pmid:19047531

48. ↵
    1. Kaess M,
    2. Resch F,
    3. Parzer P,
    4. von Ceumern-Lindenstjerna I-A,
    5. Henze R,
    6. Brunner R

    . Temperamental patterns in female adolescents with borderline personality disorder. J Nerv Ment Dis. 2013;201(2):109–115pmid:23364119

49. ↵
    1. Distel MA,
    2. Middeldorp CM,
    3. Trull TJ,
    4. Derom CA,
    5. Willemsen G,
    6. Boomsma DI

    . Life events and borderline personality features: the influence of gene-environment interaction and gene-environment correlation. Psychol Med. 2011;41(4):849–860pmid:20594379

50. ↵
    1. Bornovalova MA,
    2. Hicks BM,
    3. Iacono WG,
    4. McGue M

    . Stability, change, and heritability of borderline personality disorder traits from adolescence to adulthood: a longitudinal twin study. Dev Psychopathol. 2009;21(4):1335–1353pmid:19825271

51. ↵
    1. Hankin BL,
    2. Barrocas AL,
    3. Jenness J,
    4. et al

    . Association between 5-HTTLPR and borderline personality disorder traits among youth. Front Psychiatry. 2011;2:6pmid:21556276

52. ↵
    1. Brunner R,
    2. Henze R,
    3. Parzer P,
    4. et al

    . Reduced prefrontal and orbitofrontal gray matter in female adolescents with borderline personality disorder: is it disorder specific? Neuroimage. 2010;49(1):114–120pmid:19660555

53. ↵
    1. Goodman M,
    2. Hazlett EA,
    3. Avedon JB,
    4. Siever DR,
    5. Chu K-W,
    6. New AS

    . Anterior cingulate volume reduction in adolescents with borderline personality disorder and co-morbid major depression. J Psychiatr Res. 2011;45(6):803–807pmid:21145068

54. ↵
    1. Whittle S,
    2. Chanen AM,
    3. Fornito A,
    4. McGorry PD,
    5. Pantelis C,
    6. Yücel M

    . Anterior cingulate volume in adolescents with first-presentation borderline personality disorder. Psychiatry Res. 2009;172(2):155–160pmid:19299113

55. ↵
    1. New AS,
    2. Carpenter DM,
    3. Perez-Rodriguez MM,
    4. et al

    . Developmental differences in diffusion tensor imaging parameters in borderline personality disorder. J Psychiatr Res. 2013;47(8):1101–1109pmid:23628384

56. ↵
    1. Maier-Hein KH,
    2. Brunner R,
    3. Lutz K,
    4. et al

    . Disorder-specific white matter alterations in adolescent borderline personality disorder. Biol Psychiatry. 2014;75(1):81–88pmid:23768862

57. ↵
    1. Stiglmayr CE,
    2. Ebner-Priemer UW,
    3. Bretz J,
    4. et al

    . Dissociative symptoms are positively related to stress in borderline personality disorder. Acta Psychiatr Scand. 2008;117(2):139–147pmid:18028248

58. ↵
    1. Stiglmayr CE,
    2. Grathwol T,
    3. Linehan MM,
    4. Ihorst G,
    5. Fahrenberg J,
    6. Bohus M

    . Aversive tension in patients with borderline personality disorder: a computer-based controlled field study. Acta Psychiatr Scand. 2005;111(5):372–379pmid:15819731

59. ↵
    1. Zimmerman DJ,
    2. Choi-Kain LW

    . The hypothalamic-pituitary-adrenal axis in borderline personality disorder: a review. Harv Rev Psychiatry. 2009;17(3):167–183pmid:19499417

60. ↵
    1. Nater UM,
    2. Bohus M,
    3. Abbruzzese E,
    4. et al

    . Increased psychological and attenuated cortisol and alpha-amylase responses to acute psychosocial stress in female patients with borderline personality disorder. Psychoneuroendocrinology. 2010;35(10):1565–1572pmid:20630661

61. ↵
    1. Kaess M,
    2. Hille M,
    3. Parzer P,
    4. Maser-Gluth C,
    5. Resch F,
    6. Brunner R

    . Alterations in the neuroendocrinological stress response to acute psychosocial stress in adolescents engaging in nonsuicidal self-injury. Psychoneuroendocrinology. 2012;37(1):157–161pmid:21676550

62. ↵
    1. Jovev M,
    2. Garner B,
    3. Phillips L,
    4. et al

    . An MRI study of pituitary volume and parasuicidal behavior in teenagers with first-presentation borderline personality disorder. Psychiatry Res. 2008;162(3):273–277pmid:18304783

63. ↵
    1. Crone EA,
    2. Ridderinkhof KR

    . The developing brain: from theory to neuroimaging and back. Dev Cogn Neurosci. 2011;1(2):101–109pmid:22436435

64. ↵
    1. Cicchetti D,
    2. Rogosch FA

    . Gene × environment interaction and resilience: effects of child maltreatment and serotonin, corticotropin releasing hormone, dopamine, and oxytocin genes. Dev Psychopathol. 2012;24(2):411–427pmid:22559122

65. ↵
    1. von Ceumern-Lindenstjerna I-A,
    2. Brunner R,
    3. Parzer P,
    4. Mundt C,
    5. Fiedler P,
    6. Resch F

    . Initial orienting to emotional faces in female adolescents with borderline personality disorder. Psychopathology. 2010;43(2):79–87pmid:20068378

66. ↵
    1. Jovev M,
    2. Chanen A,
    3. Green M,
    4. et al

    . Emotional sensitivity in youth with borderline personality pathology. Psychiatry Res. 2011;187(1-2):234–240pmid:21269710

67. ↵
    1. von Ceumern-Lindenstjerna I-A,
    2. Brunner R,
    3. Parzer P,
    4. Mundt C,
    5. Fiedler P,
    6. Resch F

    . Attentional bias in later stages of emotional information processing in female adolescents with borderline personality disorder. Psychopathology. 2010;43(1):25–32pmid:19893341

68. ↵
    1. Jennings TC,
    2. Hulbert CA,
    3. Jackson HJ,
    4. Chanen AM

    . Social perspective coordination in youth with borderline personality pathology. J Pers Disord. 2012;26(1):126–140pmid:22369170

69. ↵
    Sharp C, Pane H, Ha C, Venta A, Patel AB, Sturek J, et al. Theory of mind and emotion regulation difficulties in adolescents with borderline traits. J Am Acad Child Adolesc Psychiatry. 2011;50(6):563–573.e1
70. ↵
    1. Sharp C,
    2. Ha C,
    3. Carbone C,
    4. et al

    . Hypermentalizing in adolescent inpatients: treatment effects and association with borderline traits. J Pers Disord. 2013;27(1):3–18pmid:23342954

71. ↵
    1. Lawrence KA,
    2. Allen JS,
    3. Chanen AM

    . Impulsivity in borderline personality disorder: reward-based decision-making and its relationship to emotional distress. J Pers Disord. 2010;24(6):786–799pmid:21158600

72. ↵
    1. Cohen P,
    2. Chen H,
    3. Gordon K,
    4. Johnson J,
    5. Brook J,
    6. Kasen S

    . Socioeconomic background and the developmental course of schizotypal and borderline personality disorder symptoms. Dev Psychopathol. 2008;20(2):633–650pmid:18423098

73. ↵
    1. Zanarini MC,
    2. Williams AA,
    3. Lewis RE,
    4. et al

    . Reported pathological childhood experiences associated with the development of borderline personality disorder. Am J Psychiatry. 1997;154(8):1101–1106pmid:9247396

74. ↵
    1. Afifi TO,
    2. Mather A,
    3. Boman J,
    4. et al

    . Childhood adversity and personality disorders: results from a nationally representative population-based study. J Psychiatr Res. 2011;45(6):814–822pmid:21146190

75. ↵
    1. Carlson EA,
    2. Egeland B,
    3. Sroufe LA

    . A prospective investigation of the development of borderline personality symptoms. Dev Psychopathol. 2009;21(4):1311–1334pmid:19825270

76. ↵
    1. Johnson JG,
    2. Cohen P,
    3. Brown J,
    4. Smailes EM,
    5. Bernstein DP

    . Childhood maltreatment increases risk for personality disorders during early adulthood. Arch Gen Psychiatry. 1999;56(7):600–606pmid:10401504

77. ↵
    1. Winsper C,
    2. Zanarini M,
    3. Wolke D

    . Prospective study of family adversity and maladaptive parenting in childhood and borderline personality disorder symptoms in a non-clinical population at 11 years. Psychol Med. 2012;42(11):2405–2420pmid:22475090

78. ↵
    1. Kaess M,
    2. Parzer P,
    3. Mattern M,
    4. et al

    . Adverse childhood experiences and their impact on frequency, severity, and the individual function of nonsuicidal self-injury in youth. Psychiatry Res. 2013;206(2–3):265–272pmid:23159195

79. ↵
    1. Fossati A,
    2. Madeddu F,
    3. Maffei C

    . Borderline personality disorder and childhood sexual abuse: a meta-analytic study. J Pers Disord. 1999;13(3):268–280pmid:10498039

80. ↵
    1. Bradley R,
    2. Jenei J,
    3. Westen D

    . Etiology of borderline personality disorder: disentangling the contributions of intercorrelated antecedents. J Nerv Ment Dis. 2005;193(1):24–31pmid:15674131

81. ↵
    1. Crowell SE,
    2. Beauchaine TP,
    3. Linehan MM

    . A biosocial developmental model of borderline personality: Elaborating and extending Linehan’s theory. Psychol Bull. 2009;135(3):495–510pmid:19379027

82. ↵
    1. Sansone RA,
    2. Lam C,
    3. Wiederman MW

    . Being bullied in childhood: correlations with borderline personality in adulthood. Compr Psychiatry. 2010;51(5):458–461pmid:20728001

83. ↵
    1. Wolke D,
    2. Schreier A,
    3. Zanarini MC,
    4. Winsper C

    . Bullied by peers in childhood and borderline personality symptoms at 11 years of age: a prospective study. J Child Psychol Psychiatry. 2012;53(8):846–855pmid:22380520

84. ↵
    Lereya ST, Winsper C, Heron J, Lewis G, Gunnell D, Fisher HL, et al. Being bullied during childhood and the prospective pathways to self-harm in late adolescence. J Am Acad Child Adolesc Psychiatry. 2013;52(6):608–618.e2
85. ↵
    1. Linehan M

    . Cognitive Behavior Therapy of Borderline Personality Disorder. New York, NY: Guilford; 1993

86. ↵
    1. Patel V,
    2. Flisher AJ,
    3. Hetrick S,
    4. McGorry P

    . Mental health of young people: a global public-health challenge. Lancet. 2007;369(9569):1302–1313pmid:17434406

87. ↵
    1. McGorry P

    . Early clinical phenotypes and risk for serious mental disorders in young people: need for care precedes traditional diagnoses in mood and psychotic disorders. Can J Psychiatry. 2013;58(1):19–21pmid:23327752

88. ↵
    1. Aviram RB,
    2. Brodsky BS,
    3. Stanley B

    . Borderline personality disorder, stigma, and treatment implications. Harv Rev Psychiatry. 2006;14(5):249–256pmid:16990170

89. ↵
    1. Rüsch N,
    2. Hölzer A,
    3. Hermann C,
    4. et al

    . Self-stigma in women with borderline personality disorder and women with social phobia. J Nerv Ment Dis. 2006;194(10):766–773pmid:17041289

90. ↵
    1. Sharp C,
    2. Romero C

    . Borderline personality disorder: a comparison between children and adults. Bull Menninger Clin. 2007;71(2):85–114pmid:17666001

91. ↵
    1. Lawrence KA,
    2. Allen JS,
    3. Chanen A

    . A study of maladaptive schemas and borderline personality disorder in young people. Cognit Ther Res. 2011;35(1):30–39

92. ↵
    1. Zimmerman M,
    2. Chelminski I,
    3. Young D,
    4. Dalrymple K,
    5. Martinez J

    . Does the presence of one feature of borderline personality disorder have clinical significance? Implications for dimensional ratings of personality disorders. J Clin Psychiatry. 2012;73(1):8–12pmid:22054015

93. ↵
    1. Widiger TA,
    2. Simonsen E

    . Alternative dimensional models of personality disorder: finding a common ground. J Pers Disord. 2005;19(2):110–130pmid:15899712

94. ↵
    1. Schmeck K,
    2. Schlüter-Müller S,
    3. Foelsch PA,
    4. Doering S

    . The role of identity in the DSM-5 classification of personality disorders. Child Adolesc Psychiatry Ment Health. 2013;7(1):27pmid:23902698

95. ↵
    1. Chanen AM,
    2. McCutcheon LK,
    3. Germano D,
    4. Nistico H,
    5. Jackson HJ,
    6. McGorry PD

    . The HYPE Clinic: an early intervention service for borderline personality disorder. J Psychiatr Pract. 2009;15(3):163–172pmid:19461389

96. ↵
    1. First MB,
    2. Spitzer RL,
    3. Gibbon M,
    4. Williams JBW

    . User’s Guide for the Structured Clinical Interview for DSM-IV Personality Disorders (SCID-IV). Washington, DC: American Psychiatric Press; 1996

97. ↵
    1. Loranger AW

    . International Personality Disorder Examination: DSM-IV and ICD-10 Interviews. Odessa, FL: Psychological Assessment Resources; 1999

98. ↵
    1. Henze R,
    2. Barth J,
    3. Parzer P,
    4. et al

    . Validation of a screening instrument for borderline personality disorder in adolescents and young adults—psychometric properties and association with the patient’s self-esteem [in German]. Fortschr Neurol Psychiatr. 2013;81(6):324–330pmid:23775165

99. ↵
    1. Zanarini MC

    . The Childhood Interview for DSM-IV Borderline Personality Disorder (CI-BPD). Belmont, MA: McLean Hospital and Harvard Medical School; 2003

100. ↵
     1. Sharp C,
     2. Ha C,
     3. Michonski J,
     4. Venta A,
     5. Carbone C

     . Borderline personality disorder in adolescents: evidence in support of the Childhood Interview for DSM-IV borderline personality disorder in a sample of adolescent inpatients. Compr Psychiatry. 2012;53(6):765–774pmid:22300904

101. ↵
     1. Poreh AM,
     2. Rawlings D,
     3. Claridge G,
     4. Freeman JL,
     5. Faulkner C,
     6. Shelton C

     . The BPQ: a scale for the assessment of borderline personality based on DSM-IV criteria. J Pers Disord. 2006;20(3):247–260pmid:16776554

102. ↵
     1. Noblin JL,
     2. Venta A,
     3. Sharp C

     . The validity of the MSI-BPD among inpatient adolescents. Assessment. 2013; 21(2):210–217 pmid:23344914

103. ↵
     1. Sharp C,
     2. Mosko O,
     3. Chang B,
     4. Ha C

     . The cross-informant concordance and concurrent validity of the Borderline Personality Features Scale for Children in a community sample of boys. Clin Child Psychol Psychiatry. 2011;16(3):335–349pmid:20921039

104. ↵
     1. Chang B,
     2. Sharp C,
     3. Ha C

     . The criterion validity of the Borderline Personality Features Scale for Children in an adolescent inpatient setting. J Pers Disord. 2011;25(4):492–503pmid:21838564

105. ↵
     1. Morey LC

     . Personality Assessment Inventory—Adolescents Professional Manual. Lutz, FL: Psychological Assessment Resources; 2007

106. ↵
     1. Linde JA,
     2. Stringer D,
     3. Simms LJ,
     4. Clark LA

     . The Schedule for Nonadaptive and Adaptive Personality for Youth (SNAP-Y): a new measure for assessing adolescent personality and personality pathology. Assessment. 2013;20(4):387–404pmid:23794180

107. ↵
     1. Schuppert HM,
     2. Bloo J,
     3. Minderaa RB,
     4. Emmelkamp PMG,
     5. Nauta MH

     . Psychometric evaluation of the Borderline Personality Disorder Severity Index-IV—adolescent version and parent version. J Pers Disord. 2012;26(4):628–640pmid:22867512

108. ↵
     1. Ruggero CJ,
     2. Zimmerman M,
     3. Chelminski I,
     4. Young D

     . Borderline personality disorder and the misdiagnosis of bipolar disorder. J Psychiatr Res. 2010;44(6):405–408pmid:19889426

109. ↵
     1. Paris J

     . Personality disorders and mood disorders: phenomenological resemblances vs. pathogenetic pathways. J Pers Disord. 2010;24(1):3–13pmid:20205495

110. ↵
     1. Bayes A,
     2. Parker G,
     3. Fletcher K

     . Clinical differentiation of bipolar II disorder from borderline personality disorder. Curr Opin Psychiatry. 2014;27(1):14–20pmid:24270482

111. ↵
     1. Parker G

     . Is borderline personality disorder a mood disorder? Br J Psychiatry. 2014;204:252–253pmid:24692750

112. ↵
     1. Renaud S,
     2. Corbalan F,
     3. Beaulieu S

     . Differential diagnosis of bipolar affective disorder type II and borderline personality disorder: analysis of the affective dimension. Compr Psychiatry. 2012;53(7):952–961pmid:22560773

113. ↵
     1. Nock MK,
     2. Joiner TE Jr,
     3. Gordon KH,
     4. Lloyd-Richardson E,
     5. Prinstein MJ

     . Non-suicidal self-injury among adolescents: diagnostic correlates and relation to suicide attempts. Psychiatry Res. 2006;144(1):65–72pmid:16887199

114. ↵
     1. Yen S,
     2. Shea MT,
     3. Battle CL,
     4. et al

     . Traumatic exposure and posttraumatic stress disorder in borderline, schizotypal, avoidant, and obsessive-compulsive personality disorders: findings from the collaborative longitudinal personality disorders study. J Nerv Ment Dis. 2002;190(8):510–518pmid:12193835

115. ↵
     1. Lenzenweger MF,
     2. Desantis Castro D

     . Predicting change in borderline personality: Using neurobehavioral systems indicators within an individual growth curve framework. Dev Psychopathol. 2005;17(4):1207–1237pmid:16613438

116. ↵
     1. Chanen AM,
     2. Jackson HJ,
     3. McCutcheon LK,
     4. et al

     . Early intervention for adolescents with borderline personality disorder using cognitive analytic therapy: randomised controlled trial. Br J Psychiatry. 2008;193(6):477–484pmid:19043151

117. ↵
     1. Schuppert HM,
     2. Giesen-Bloo J,
     3. van Gemert TG,
     4. et al

     . Effectiveness of an emotion regulation group training for adolescents—a randomized controlled pilot study. Clin Psychol Psychother. 2009;16(6):467–478pmid:19630069

118. ↵
     1. Cuijpers P

     . Examining the effects of prevention programs on the incidence of new cases of mental disorders: the lack of statistical power. Am J Psychiatry. 2003;160(8):1385–1391pmid:12900296

119. ↵
     Kaess M, Fischer G, Parzer P, Resch F, Brunner R. Is detection and treatment of adolescent self-harm a suitable strategy for the treatment of borderline personality disorder? Presented at the International Congress for Borderline Personality Disorder; 2014
120. ↵
     Ryle A, Kerr IB. Introducing Cognitive Analytic Therapy: Principles and Practice. Chichester, UK: Wiley; 2002
121. ↵
     1. Chanen AM,
     2. Jackson HJ,
     3. McCutcheon LK,
     4. et al

     . Early intervention for adolescents with borderline personality disorder: quasi-experimental comparison with treatment as usual. Aust N Z J Psychiatry. 2009;43(5):397–408pmid:19373700

122. ↵
     1. Blum N,
     2. St John D,
     3. Pfohl B,
     4. et al

     . Systems Training for Emotional Predictability and Problem Solving (STEPPS) for outpatients with borderline personality disorder: a randomized controlled trial and 1-year follow-up. Am J Psychiatry. 2008;165(4):468–478pmid:18281407

123. ↵
     Schuppert HM, Timmerman ME, Bloo J, et al. Emotion regulation training for adolescents with borderline personality disorder traits: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012;51(12):1314–1323.e2
124. ↵
     1. Bateman A,
     2. Fonagy P

     . Mentalization based treatment for borderline personality disorder. World Psychiatry. 2010;9(1):11–15pmid:20148147

125. ↵
     Rossouw TI, Fonagy P. Mentalization-based treatment for self-harm in adolescents: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012;51(12):1304–1313.e3
126. ↵
     1. Rathus JH,
     2. Miller AL

     . Dialectical behavior therapy adapted for suicidal adolescents. Suicide Life Threat Behav. 2002;32(2):146–157pmid:12079031

127. ↵
     1. Fleischhaker C,
     2. Böhme R,
     3. Sixt B,
     4. Brück C,
     5. Schneider C,
     6. Schulz E

     . Dialectical behavioral therapy for adolescents (DBT-A): a clinical trial for patients with suicidal and self-injurious behavior and borderline symptoms with a one-year follow-up. Child Adolesc Psychiatry Ment Health. 2011;5(1):3pmid:21276211

128. ↵
     1. Goldstein TR,
     2. Axelson DA,
     3. Birmaher B,
     4. Brent DA

     . Dialectical behavior therapy for adolescents with bipolar disorder: a 1-year open trial. J Am Acad Child Adolesc Psychiatry. 2007;46(7):820–830pmid:17581446

129. ↵
     Mehlum L. Study NCT00675129: Treatment for adolescents with deliberate self-harm. Available at: http://www.clinicaltrials.gov/ct2/show/NCT00675129?term=suicide&age=0&rank=22. Accessed April 10, 2014
130. ↵
     1. Clarkin JF,
     2. Foelsch PA,
     3. Levy KN,
     4. Hull JW,
     5. Delaney JC,
     6. Kernberg OF

     . The development of a psychodynamic treatment for patients with borderline personality disorder: a preliminary study of behavioral change. J Pers Disord. 2001;15(6):487–495pmid:11778390

131. ↵
     1. Foelsch PA,
     2. Odom AE,
     3. Kernberg OF

     . Treatment of adolescents with identity diffusion: a modification of transference focused psychotherapy [in French]. Sante Ment Que. 2008;33(1):37–60pmid:18795195

132. ↵
     1. Biskin RS

     . Treatment of borderline personality disorder in youth. J Can Acad Child Adolesc Psychiatry. 2013;22(3):230–234pmid:23970912

133. ↵
     1. Stoffers J,
     2. Völlm BA,
     3. Rücker G,
     4. Timmer A,
     5. Huband N,
     6. Lieb K

     . Pharmacological interventions for borderline personality disorder. Cochrane Database Syst Rev. 2010;(6):CD005653pmid:20556762

134. ↵
     1. Amminger GP,
     2. Chanen AM,
     3. Ohmann S,
     4. et al

     . Omega-3 fatty acid supplementation in adolescents with borderline personality disorder and ultra-high risk criteria for psychosis: a post hoc subgroup analysis of a double-blind, randomized controlled trial. Can J Psychiatry. 2013;58(7):402–408pmid:23870722

• Copyright © 2014 by the American Academy of Pediatrics

Source: Borderline Personality Disorder in Adolescence | State-of-the-Art Review Articles | Pediatrics