Borderline personality disorder

Chapter 5
Borderline personality disorder


John M. Oldham


Senior Vice President and Chief of Staff, The Menninger Clinic, Barbara and Corbin Robertson Jr. Endowed Chair for Personality Disorders, Professor and Executive Vice Chair, Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, Texas, U.S.


Phenomenology


Borderline personality disorder (BPD) is a prevalent and disabling condition characterized by emotion dysregulation and interpersonal instability. In the early days when the term began to appear in the clinical literature, BPD was thought to be “on the border” between the psychoses and what were formerly called the neuroses [1]. In the United States, however, the criteria defining BPD that were included in the third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) [2] of the American Psychiatric Association (APA), published in 1980, characterized BPD as a disorder of emotion dysregulation and impulse dyscontrol, and schizotypal PD was recognized as the PD aligning more closely with the psychoses. These distinctions have remained applicable in DSM-IV [3] and in DSM-5, [4] and BPD might more accurately be thought of as a condition close to the border of the mood disorders and the impulse control disorders.


To make a DSM-5 BPD diagnosis, at least five of nine criteria must be present; abbreviated versions of these nine criteria are shown on Table 5.1. Since DSM-5 utilizes a polythetic system and any five of the nine criteria suffice to establish a BPD diagnosis, considerable heterogeneity is inevitable; it has been estimated that there can be 256 different criteria combinations in the case of BPD [5]. In addition to extensive heterogeneity of the borderline diagnosis, co-morbid conditions are common in patients with BPD. In one representative study, about 84 percent of patients with BPD also met criteria for at least one “Axis I” disorder (a term reflecting the multi-axial diagnostic system of DSM-III and DSM-IV, which was abandoned in DSM-5), principally mood disorders, anxiety disorders, and substance use disorders [6].


Table 5.1 DSM-IV diagnosis of borderline personality disorder (at least 5 must be present).





















Fear of abandonment
Difficult interpersonal relationships
Uncertainty about self-image or identity
Impulsive behavior
Self-injurious behavior
Emotional changeability or hyperactivity
Feelings of emptiness
Difficulty controlling intense anger
Transient suspiciousness or “disconnectedness”

Patients with BPD typically have severe impairment in functioning. In addition to emotion dysregulation and impulsivity, self-injurious behavior is common, and suicide risk is significant. It has been estimated that in clinical populations, between 8 and 10 percent of BPD patients die by suicide; risk factors include co-morbid mood or substance use disorders, history of sexual abuse, and family history of suicide [7]. Among emerging findings about other characteristics of patients with BPD are the presence of significantly disturbed sleep profiles [8], and possible alterations in inflammatory mechanisms [9].


Neurobiology


Patterns of family transmission of BPD have been identified for some time [10], and there has been growing interest in the heritability of BPD [11–15]. The estimated heritability of personality disorders as a group is in the 20–40 percent range, comparable to anxiety disorders and depressive disorders, and the heritability of BPD itself is estimated to be between 30 and 40 percent [16].


New technologies have been increasingly utilized to explore patterns of neuropathology and pathophysiology in all patients with brain disorders, including those with BPD. Volumetric abnormalities in limbic structures have been reported in patients with BPD, particularly reduced volume in the hippocampus and the amygdala [17]; a question has been raised, however, about whether these changes are accounted for by BPD itself or by co-morbid conditions such as post-traumatic stress disorder [18], but recent work suggests that the volume reductions are “candidate endophenotypes” for BPD and not secondary to co-morbid pathology [19]. One important hypothesis arising from neuroimaging studies is that the normally robust connectivity between the amygdala and the prefrontal cortex, thought to facilitate inhibitory control over the amygdala, is compromised in patients with BPD, hence their frequent failure to down-regulate amygdala-generated emotionality in response to aversive stimuli [20]. This pattern of emotion dysregulation has been observed and described clinically, and it has been documented using “ecological momentary assessment” technology, involving “real-time” computer-based assessment of affective states [21]. Earlier work had revealed that borderline patients show greater activation than controls particularly in the left amygdala when viewing facial expressions [22].


There has been recent interest in the role of neuropeptides in borderline pathology. Oxytocin has been shown to enhance the accuracy of recognition of facial expressions [23], and oxytocin levels have been reported to be low in BPD patients [24]. In one study of women with BPD, low oxytocin levels were suggested to have resulted from traumatic childhood experiences, particularly emotional neglect and abuse [25], and indeed a striking difference has been shown between borderline patients and controls with respect to interpersonal trust after the administration of intranasal oxytocin (enhancing trust in control subjects but not in borderlines) [26]. Similarly, a profound incapacity for borderline patients to maintain cooperation with a partner in an experimental paradigm has been demonstrated, correlated with altered activity of the anterior insular cortex in BPD patients, suggesting that the norms used in perception of social gestures are pathologically perturbed or missing altogether in patients with BPD [27]. These findings are particularly compelling in light of the growing recognition of disruptions in the attachment process early in the lives of many children and adolescents who later develop borderline pathology [28]. Gunderson has emphasized the importance of interpersonal hypersensitivity in borderline patients [29], and Koenigsberg has summarized work describing disturbed attachment styles in borderline patients as either “preoccupied” or “unresolved” [30].


Theoretical models of borderline pathogenesis and symptom formation


Figure 5.1 portrays a sequential theoretical model of the pathogenesis of borderline personality disorder [7], reflecting the bidirectional nature of heritable risk and disruptions in attachment, leading to instability of interpersonal relationships as the “signature” disturbance characteristic of borderline patients.

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Figure 5.1 Sequential theoretical model of BPD pathogenesis.


Figure 5.2 portrays a theoretical model of symptom expression in borderline patients, reflecting the vulnerability conferred by heritable risk factors in these patients. This vulnerability is activated by stressful stimuli, generally in the social and interpersonal realm, leading to highly symptomatic states of extreme distress. Behavior during these periods of stress, though listed as symptomatic criteria for borderline personality disorder, can actually be thought of as compensatory efforts to achieve relief, such as dissociative states, self-injurious behavior, or suicidality.

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Figure 5.2 Theoretical model of BPD symptom expression.


Longitudinal studies

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May 29, 2017 | Posted by in PSYCHIATRY | Comments Off on Borderline personality disorder
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