SeminarBorderline personality disorder
Introduction
Borderline personality disorder (BPD) is a severe mental disorder that is characterised by a pervasive pattern of emotion dysregulation, inconsistent identity, and disturbed interpersonal function. The term was coined in 1938 by Adolf Stern, who viewed the disorder as existing at the border between psychosis and neurosis, and BPD was first classified as a mental disorder in the Diagnostic and Statistical Manual of Mental Disorders, 3rd edition in 1980.1, 2 Since then, much progress has been made in understanding and managing the condition. This Seminar reviews what has been discovered to date, and specifically addresses developments in early diagnosis, epidemiology, aetiology, and treatment options that have arisen since the publication of earlier reviews in this journal.3, 4
Section snippets
Case 1
A 17-year-old female patient was admitted to the emergency room after attempting suicide by overdose. Although her act had been impulsive, prompted by a break-up with her boyfriend, she had been hoarding the medication beforehand “in case she could no longer stand it”. Her home life was difficult, filled with violence, but she did not want to talk about that experience during admission. She reported having struggled with suicidal thoughts, self-harm, and significant bouts of loneliness since
Diagnosis and differential diagnosis
In the past decade, there have been substantial changes in the psychiatric nosology of personality disorders. At present, four classification systems are provided for BPD: the traditional criteria for diagnoses in section II of the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), an alternative model in section III of the DSM-5, and the models presented in the International Classification of Diseases, 10th and 11th revisions (ICD-10 and ICD-11).6, 7
Table 1 compares
Epidemiology and aetiology
Prospective community cohort studies show that although individual differences in maladaptive personality traits such as impulsivity, emotional reactivity, and negative affectivity can be observed in children, they do not crystalise into a coherent syndrome of BPD until the transition to adolescence (after age 12 years), marking adolescence as a sensitive period for the onset of BPD.19, 20 The validity and reliability of BPD diagnosis in adolescents are indicated by evidence supporting a
Pathophysiology
There is evidence that emotion dysregulation is a central mechanism closely linked to other BPD symptoms. Patients report intense, long-lasting, and strongly fluctuating emotions, which are often experienced as overwhelming and unpredictable.59 Emotional distress and dissociation can hinder executive functioning and goal-directed behaviour,60, 61 and when struggling with strong emotions, many patients impulsively turn to maladaptive coping strategies such as self-harm or substance abuse.5 By
Acute management
Clinical management in acute crisis situations depends to a large extent on whether the patient is already undergoing adequate psychotherapeutic treatment. If no previous treatment has been received, the following steps are recommended (see also panel 2).
The first priority must be addressing crisis behaviours, such as suicide attempts, serious attacks on other people, life-threatening self-injury, frequent unplanned hospital admissions, or dangerous high-risk behaviours. Interventions should be
Psychosocial interventions
Evidence-based guidelines agree that psychotherapy is the main treatment for BPD.18, 21 The latest Cochrane review of psychotherapies for BPD identified as many as 75 relevant randomised controlled trials (RCTs).104 Compared with unspecific control conditions, moderate clinically relevant effects have been observed for several parameters: overall BPD severity (standardised mean difference –0·52, 95% CI –0·70 to –0·33), self-harm (–0·32, –0·49 to –0·14), suicidality (–0·34, –0·57 to –0·11), and
Pharmacotherapy
Given the weakness of supporting evidence for pharmacotherapy, drugs that used to be routinely prescribed according to individually prevalent BPD symptom domains, such as impulsivity, emotional instability, or cognitive-perceptual symptoms, are no longer recommended (see panel 3).18, 21, 135, 136, 137
In particular, the evidence for selective serotonin reuptake inhibitors (SSRIs) is insufficient to support their use in the treatment of BPD pathology, unless a comorbidity is present that requires
Controversies and outstanding research questions
Although much progress has been made in the understanding and management of BPD, several controversies and as-yet unanswered research questions exist.
At present, there is no integrated aetiological model for the development of BPD that is empirically supported. Little is known about the genetic and neurobiological causes of postulated emotional hypersensitivity and the related transactional mechanisms with adverse childhood experience. Likewise, there is a dearth of robust evidence of early
Declaration of interests
MB is a cognitive-behavioural therapist, trained in DBT and with a special international activity in DBT training and dissemination. JSW is a cognitive-behavioural therapist, trained in DBT. CaS is a clinical psychologist with training in cognitive-behaviour therapy and mentalisation-based therapy. KL is a cognitive-behavioural psychotherapist with a special interest in schema therapy. AKU is a cognitive-behavioural therapist trained in DBT. ChS is a cognitive-behavioural therapist and has a
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