Borderline personality disorder (BPD) is one of the more vexing forms of psychopathology for researchers and clinicians alike to understand. Currently, the etiology and pathogenesis of the disorder remain unclear; however, steady progress has been made in several important areas that bear upon informing a more complete understanding of this condition. Long known to clinicians in office practice and mental health staff at clinics and hospitals, BPD is a heterogenous phenotype characterized by a complex array of features such as emotional dysregulation, interpersonal dysfunction, impulsivity, self-damaging behaviors, excessive anger and fear, and identity disturbance (American Psychiatric Association, 1994). The individual afflicted with BPD frequently experiences substantial social and occupational impairment, as well as frequent emotional turmoil. Those individuals who spend considerable time with a BPD-affected person, such as parents, partners, spouses, children, coworkers, and others, also encounter appreciable stresses and strains associated with the impact of BPD on the family, social, and occupational milieu.

We review the role of emotion regulation in borderline personality disorder (BPD). We briefly discuss the historical development of BPD as a disorder where emotional regulation plays a key role. We review the concept of emotion regulation in general and explore both one-factor and two-factor models of emotion regulation. We discuss cognitive and attentional aspects of emotion regulation, and explore these regulatory controls as operating as both voluntary as well as automatic processes. We then turn to other neurophysiological models of emotion regulation in general and examine how those models, both neurophysiologically and neuroanatomically, are expressed in individuals with BPD. We examine how neuroimaging, both anatomical and functional, reveals the roles that various neuroanatomical structures play in the regulation of emotion in BPD. We conclude by creating a neurodevelopmental model that describes how a complex matrix involving the interplay of constitutional/biological predispositions with environmental stressors as well as with parental effectiveness in response to the child's emotion expression can impact key aspects of adult cognitive, affective, interpersonal, and behavioral functioning that culminate in a diagnosis of BPD.

This article provides a contemporary view of the psychodynamics of borderline personality disorder (BPD) from a developmental psychopathology perspective. We first briefly describe the evolution of the borderline construct in psychoanalysis and psychiatry. Then we provide clinically and empirically informed model of domains of personality function and dysfunction that provides a roadmap for thinking about personality pathology from a developmental psychopathology standpoint and examine the nature and phenomenology of BPD in terms of these domains of functioning. Next, we describe prominent dynamic theories of etiology of BPD and examine these in relation to the available research. Finally, we describe psychodynamic conceptions of treatment and the way BPD phenomena manifest in treatment, followed again by consideration of relevant research, particularly on transference–countertransference constellations empirically identified in the treatment of patients with BPD.Preparation of this article was supported in part by NIMH Grants R01-MH62377 and R01-MH62378.

Borderline personality disorder (BPD) is a highly prevalent, chronic, and debilitating psychiatric problem characterized by a pattern of chaotic and self-defeating interpersonal relationships, emotional lability, poor impulse control, angry outbursts, frequent suicidality, and self-mutilation. Recently, psychopathology researchers and theorists have begun to understand fundamental aspects of BPD such as unstable, intense interpersonal relationships, feelings of emptiness, bursts of rage, chronic fears of abandonment and intolerance for aloneness, and lack of a stable sense of self as stemming from impairments in the underlying attachment organization. These investigators have noted that the impulsivity, affective lability, and self-damaging actions that are the hallmark of borderline personality occur in an interpersonal context and are often precipitated by real or imagined events in relationships. This article reviews attachment theory and research as a means of providing a developmental psychopathology perspective on BPD. Following a brief review of Bowlby's theory of attachment, and an overview of the evidence with respect to the major claims of attachment theory, I discuss individual differences, the evidence that these differences are rooted in patterns of interaction with caregivers, and how these patterns have important implications for evolving adaptations and development. Following this discussion, I present recent work linking attachment theory and BPD, focusing on the implications for understanding the etiology and treatment of BPD. In conclusion, I address some of the salient issues that point to the direction for future research efforts.

Borderline personality disorder (BPD) is considered as a disorder of autonomy, and is related to both predisposing vulnerabilities and social relationships that fail to support basic psychological needs. Autonomy, which is defined within the self-determination theory as the capacity for self-endorsed action based on integrative, reflective awareness, is discussed as a developmental line that is dependent on specific supports from caregivers. Unresponsiveness, invalidation, or abuse by caregivers is argued to impair the capacity for autonomy and to catalyze an array of processes, both biological and psychological, which impact subsequent development and, in vulnerable individuals, can lead to BPD. Aspects of treatment, including the emphases on validation and acceptance of the patient's experience, and the cultivation of more reflective or mindful regulation of behavior, can be deduced from this analysis of autonomy disturbance, and these in turn have appeared as the cornerstones of effective treatments for BPD.

Although no prospective epidemiological studies have evaluated the relationship between family interactions and the development of borderline personality disorder (BPD), there is considerable evidence for the central role of family interactions in the development of BPD. This paper describes the role of family interactions or processes, especially those that might be regarded as invalidating or conflictual, negative or critical, and the absence of more validating, positive, supportive, empathic interactions, in the development of BPD. Perhaps more importantly, the proposed model considers how these parental and family behaviors transact with the child's own behaviors and emotional vulnerabilities, resulting in a developmental model of BPD that is neither blaming of the family member with BPD nor of her or his parents and caregivers, and has important and specific implications for both prevention and intervention.

Traditional theories regarding the etiology of borderline personality disorder have focused on poor attachment figures and/or traumatic experience. The present review posits an additional pathogenic course for this disorder. Specifically, the proposed mechanism involves a basic disruption of the neural hardware that supports the formation and maintenance of unconscious emotional memory, hardware essential for the formation of early attachments. It is further theorized that this early disruption has ongoing effects on both behavioral and concomitant neural development. Within this model, adolescence is described as a period of intense change that serves as the tipping point for the onset of borderline personality disorder.

Borderline personality disorder is a particularly devastating, yet understudied form of psychopathology. One of the most significant gaps in existing knowledge is the lack of systematic, prospective empirical attention to the developmental precursors of borderline personality. The present investigation was an exploratory attempt to address this limitation through (a) development of a psychometrically sound self-report instrument that assesses borderline personality features in childhood, the Borderline Personality Features Scale for Children (BPFS-C); (b) examination of the stability of BPF in childhood; (c) evaluation of gender differences in BPF in childhood; and (d) evaluation of the specificity of the BPFS-C for assessing borderline personality features. These goals were achieved through the prospective study of a normative sample of 400 (54% female) fourth though sixth graders who were assessed during the Fall of Year 1, Spring of Year 1, and Fall of Year 2. The use of linear mixed modeling techniques provided evidence for the construct validity of the BPFS-C. Further, borderline personality features as assessed with the BPFS-C were found to be moderately stable over the course of the study, with girls reporting higher levels of BPF than boys. Results also demonstrated that children's scores on the BPFS-C were uniquely related to indicators of borderline personality pathology above and beyond their scores on the Children's Depression Inventory. The implications of these results for the study of the development and etiology of borderline pathology are discussed.This research was supported by a grant to the first author from the National Institute of Mental Health (MH063684). We acknowledge Leslie Morey and Carol Rockhill for their extensive assistance with the development of the BPFS-C. We also thank the staff of the School Buddies Project and the teachers and children who participated in this study for their significant contributions.

Potential precursors to borderline personality disorder (BPD) were investigated in a sample of 185 maltreated and 175 nonmaltreated school-aged children attending a summer camp research program. Self-report, peer-report, and counselor-report measures were utilized to assess developmental constructs conceptualized to constitute vulnerability for later emerging BPD. These areas, including personality features, representational models of self, parent, and peers, interpersonal relationship difficulties with peers and adults, and suicidal/self-harm behavior, were used to develop a BPD precursors composite. Additionally, the efficiency of three attention networks was assessed with a computerized task. Maltreated children had higher mean scores on the BPD precursors composite, and children classified as having high levels of these precursors were more prevalent in the maltreatment group. No maltreatment group differences were found for the efficiency of the three attention networks; however, children with high levels of BPD precursors evinced less efficient processing of the conflict attention network, comparable to findings observed among adult patients with BPD. Child maltreatment and efficiency of the conflict attention network independently predicted scores on the BPD precursors composite. Experiential and biological contributions to risk for BPD and recommendations for prevention and intervention are discussed.This research was supported by funding from the National Institute on Drug Abuse (DA11741) and the Spunk Fund, Inc.

Borderline personality disorder (BPD) is characterized by a broad pattern of impulsivity and suicidality. BPD usually begins in adolescence; the full clinical picture of the disorder is associated with developmental increases in impulsivity. However, BPD also has childhood precursors. The developmental pathways are similar to those found in other impulsive spectrum disorders, but children who later develop BPD probably have both externalizing and internalizing symptoms. Research in this area has made use of retrospective data from adults, prospective data from community studies, follow-up studies from children at risk, as well as research on “borderline pathology of childhood” (a condition with symptoms similar to adult BPD). Existing evidence suggests that both temperamental and environmental risk factors play a role in the development of the behavioral patterns associated with the disorder. These pathways also help account for the life course and outcome of BPD in adulthood.This paper benefited from suggestions made by Jenny Macfie.

Although parasuicidal behavior in adolescence is poorly understood, evidence suggests that it may be a developmental precursor of borderline personality disorder (BPD). Current theories of both parasuicide and BPD suggest that emotion dysregulation is the primary precipitant of self-injury, which serves to dampen overwhelmingly negative affect. To date, however, no studies have assessed endophenotypic markers of emotional responding among parasuicidal adolescents. In the present study, we compare parasuicidal adolescent girls (n = 23) with age-matched controls (n = 23) on both psychological and physiological measures of emotion regulation and psychopathology. Adolescents, parents, and teachers completed questionnaires assessing internalizing and externalizing psychopathology, substance use, trait affectivity, and histories of parasuicide. Psychophysiological measures including electrodermal responding (EDR), respiratory sinus arrhythmia, and cardiac pre-ejection period (PEP) were collected at baseline, during negative mood induction, and during recovery. Compared with controls, parasuicidal adolescents exhibited reduced respiratory sinus arrhythmia (RSA) at baseline, greater RSA reactivity during negative mood induction, and attenuated peripheral serotonin levels. No between-group differences on measures of PEP or EDR were found. These results lend further support to theories of emotion dysregulation and impulsivity in parasuicidal teenage girls.This work was supported by grants from the Seattle Children's Hospital and Regional Medical Center, the Pediatric Clinical Research Center at Seattle Children's Hospital (M01-RR 00037), and the National Foundation for Suicide Prevention to Cindy J. Smith, and by a grant from the National Institute of Mental Health to Theodore P. Beauchaine (R01 MH63699). We express thanks to Trevor Aerts, Anna Amen, Tyson Bailey, Jordan Campbell, Breyen Engelhardt, Ashleigh Freize, Jennifer Gross, Barbara Kleine, Dana Kovalchick, Jenna Lee, Eileen Magill, Elise Mallman, Emily Miller, Andrea Moore, Seamus Morrone, Shelby Soike, and Aubriana Teeley.

We review different conceptions of inhibitory control that may be relevant to the regulatory problems featured in borderline personality disorder (BPD). These conceptions have often been framed with regard to personality traits of inhibitory control, but can also be related to cognitive measures of response suppression as well as affect regulation. Reactive behavioral inhibition is relatively unstudied in relation to BPD. A substantial amount of literature links executive function problems with BPD, but that literature has not isolated executive response inhibition nor been controlled for other personality disorder symptoms of antisociality, attention-deficit/hyperactivity disorder (ADHD), or depression, anxiety, or posttraumatic symptoms. We therefore conducted a study of this question looking at BPD symptoms in an adult sample with a small number of BPD subjects and other disorders. Results indicated that symptoms of BPD were correlated with response inhibition (measured by stop signal reaction time) even after controlling for the overlap of stop inhibition with ADHD, antisociality, and other Axis II disorder symptoms. We conclude by hypothesizing discrete developmental routes to BPD, based on different mechanism breakdowns, which would be amenable to empirical investigation at the cognitive or trait level of analysis.Portions of this work were supported by National Institute of Mental Health Grant R01-MH63146 (J.N., PI).

The aim of this paper is to clarify how neural mechanisms at the molecular level, specifically the serotonergic (5-HT) system and the hypothalamic–pituitary–adrenal axis system (HPA) in conjunction with early life stress may contribute to the emergence of aggression, self-directed and otherwise, in borderline personality disorder (BPD). Chronic dysregulation of these biological systems, which function to regulate stress and emotion, may potentiate the development of impulsive aggression in borderline personality conditions. Our central premise in this paper is that brain development, stress regulation, and early pathonomic experience are interactive and cumulative in their mutual influence on the development of impulsive aggression in BPD. We review the parameters of impulsive aggression in BPD, followed by a discussion of the neurobiological and neuroendocrine correlates of impulsive aggression with and without BPD. We then focus on the developmental continuities in BPD with attention to brain maturation of 5-HT and HPA axis function during the life span and the influence of early adverse experiences on these systems. Finally, we comment on the data of the relative stability of aggression in BPD, adolescence as a developmental stage of potential vulnerability, and the course of aggressive behavior during the life span.The authors thank Caroline Cozza, Michael McCloskey, and Kurt Knoblett for their comments during the preparation of this manuscript. This research was supported by research funding from the American Foundation of Suicide Prevention (J.K.G.), Grant MH066888-01 (R.L.), and the Borderline Personality Disorder Research Foundation (E.F.C.).

Borderline personality disorder (BPD) is characterized by a pervasive instability of interpersonal relationships, affects, self-image, marked impulsivity, dissociation, and paranoia. The cognitive dimension of the disorder has received relatively little attention and is poorly understood. This paper proposes that neurocognitive impairment is a key moderator in the development of BPD and elaborates a possible pathway for the expression of the cognitive domain. Neurocognitive impairment is hypothesized to moderate the relationship between caretaking and insecure disorganized attachment and pathological dissociation in the formation of the disorder contributing to impaired metacognition and a range of cognitive difficulties. The empirical evidence from studies of cognitive processes, brain function, attachment, and dissociation that support this theory are reviewed and discussed. Areas for future research that might verify or refute this theory are suggested.The author thanks Geralyn Windt for assistance in manuscript preparation, Dr. Jack Maser for early review of the manuscript, and Dr. Elizabeth Twamley for her invaluable consultation and expert review of the manuscript.

Functional neuroimaging recently has been used to localize brain dysfunction in borderline personality disorder (BPD). Initial studies have examined baseline activity or emotional reactivity, and our group has investigated what we consider to be a crucial interaction between negative emotion and behavioral (dys)control. This research is beginning to identify abnormal frontolimbic circuitry likely underlying core clinical features of this condition. We review the evidence for dysfunction in specific frontolimbic regions, leading to a mechanistic model of symptom formation in BPD. In addition, we offer an integration of these neuroimaging findings with developmental perspectives on the emergence of borderline psychopathology, focusing on the ways in which early psychosocial experience may interact with developing brain systems. We also consider possible mechanisms of psychotherapeutic change at the neural systems level in BPD. Finally, we propose that future neuroimaging studies of BPD should integrate multiple levels of observation (structural, functional, neurochemical, genetic, and clinical) in a model-driven fashion to further understand the dynamic relationship between biological and psychological factors in the development and treatment of this difficult condition.

The natural history and course of borderline personality disorder (BPD) has long been the focus of speculation, typically guided by impressions from clinical work with BPD-affected individuals. Not unlike the other personality disorders (PDs), it has long been assumed that BPD is relatively stable, traitlike, and enduring in nature. The extent to which BPD is or is not a plastic construct has implications not only for understanding its longitudinal course, but also for understanding its development and, ultimately, its treatment and/or prevention. This paper consists of two parts. The first part reviews the longitudinal research corpus that bears directly upon the issue of stability of BPD in both adolescents and adults. The consistent trend in very nearly all studies, whether using a categorical or dimensional approach to assessment, is one of considerable change over time. This literature presents complexities, however, because most of the extant studies examine BPD-affected individuals who have been exposed to treatment. However, at least two large-scale longitudinal studies, which include both treated and untreated persons, also provide support for viewing BPD as a malleable disorder that declines in severity over time. The second part presents original data from the Longitudinal Study of Personality Disorders that specifically examine the predictors of change in BPD using a neurobehavioral model of personality within an individual growth curve (IGC) analytical framework. This IGC analysis revealed important predictors of both overall level of BPD features as well as rate of change in BPD features, with particularly important roles played by the agentic positive emotion (i.e., incentive motivation) and anxiety (negative emotion) systems. The benefits of the IGC approach for understanding the developmental psychopathology of BPD is also stressed.This research was supported in part by NIMH Grant MH 45448 to Mark F. Lenzenweger for the Longitudinal Study of Personality Disorders.