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The most salient goals of neuroscience research on personality disorders (PDs) are to help determine the mechanisms of specific disorders and reduce the incidence and severity of personality disorders. However, authors often do not discuss neuroscience research in a context that highlights its clinical relevance. Frequently, converging evidence from clinical neuroscience could help us better characterize the mechanisms specific to personality disorders, which could be used to inform diagnosis and interventions. More pervasive efforts to describe clinical neuroscience research in terms of its clinical relevance could help better define progress made in understanding disorders, identify gaps in the research needed to be filled before the knowledge is clinically useful, and could potentially be useful to inform current clinical practice. This commentary outlines examples from Chan, Vaccaro, Rose, Kessler, and Hazlett’s review (this volume) in which the neuroscience research could be read in ways that emphasize its clinical relevance. In addition, it briefly highlights advances in neuroscience methods, as well as efforts to improve nosological systems that may help researchers in describing the clinical implications of neuroscience research.
This commentary presents some reflections on the peculiar position obsessive-compulsive personality disorder (OCPD) has among Cluster C PDs. Based on epidemiological, factor-analytic, and cognitive considerations, it is argued that OCPD deviates from avoidant and dependent PD. First, epidemiological research shows that in the general population OCPD is not associated with markers of poor functioning and unfortunate living circumstances. On the contrary, positive associations between OCPD and such markers are found. Moreover, disproportionally few people with OCPD seek mental health care. Second, based on a second-order factor analysis on a large data set that confirms the cluster structure in PDs, it is argued that OCPD has a deviant position, relatively weakly loading on the cluster-C factor. Third, research on cognitive processes and structures in PDs indicates that OCPD deviates from avoidant and dependent PD in several ways, including sharing an interpretation style with nonpatients, and in not reporting vulnerable cognitive-emotional states. Dysfunctional cognitive characteristics might be pushed out of awareness by powerful overcompensatory strategies that are more characteristic for Cluster B than for Cluster C. Alternatively, OCPD is characterized more by deviant cognitive processes than by specific content of schemas. OCPD’s dysfunctional core should be clarified.
This rejoinder notes that several key points were discussed in response to the authors' review of brief psychosocial interventions for personality disorders. In particular, the commentary suggested that understanding key mechanisms of change and moderators of treatment outcome were especially important to make forward progress in streamlining treatments for personality disorders. Here the authors highlight several shared candidate mechanisms of change across brief treatments for personality disorders, including a focus on education regarding emotion regulation, interpersonal processes, and instilling hope and expectancies for change. They also discuss the possibility that moderators of treatment outcome should be examined across types of outcomes. Moreover, some outcomes may be more amenable to brief treatments than others. Recommendations for future research in this area are discussed.
De Fruyt and De Clercq (this volume) and Sellbom (this volume) raise important issues surrounding the use of a five-factor model (FFM) of personality to conceptualize, assess, and diagnose personality disorder including how one includes a measure of impairment, the level of abstraction that is optimal (domains vs. facets), and the need for the development of formal test manuals, normative data, and means for identifying non-credible responding. In this response, the authors note their agreement with De Fruyt and De Clercq regarding the importance of assessing impairment but note that (a) it is already included to a large degree in the assessment of pathological FFM traits and (b) that they would prefer an approach that focuses explicitly on difficulties in occupational and social functioning. As to Sellbom’s comments suggesting that further work is necessary with regard to the development of test manuals, normative databases, and measures of valid responding – the authors agree and note some of the obstacles including the need for funding for the collection of normative data (and what consensus as to the kind – clinical only; community only; both) and development of test manuals. As to measures of credible responding, they note that many of these exist already for the family of FFM PD scales that they helped create and are aware of similar efforts for other popular measures of pathological traits.
This is a commentary on Miller and Widiger’s (this volume) excellent chapter on personality disorders from the perspective of five factor personality models. In this commentary, the author discusses several issues of importance as the field moves forward with respect to dimensional personality-based diagnosis of personality disorder, most of which center on clinical application. First, a question is posed as to what level of personality abstraction is necessary for optimal formulation of personality disorders; although most five-factor models are established at the domain level, proposed personality disorder trait profiles appear at a much narrower facet level for which less scholarly consensus exist. Moreover, the author calls for more research into determining at what threshold on various trait dimensions clinical dysfunction begins to emerge. He also notes that most assessment devices currently available for dimensional trait models do not meet the Standards for Educational and Psychological Testing, which needs to be rectified prior to clinical application. Such tests also need to include validity scales to assess for noncredible responding. Finally, the author recommends that proposed personality inventories for these dimensional personality models show incremental utility above and beyond already well-established clinical assessment instruments.
This commentary begins by briefly reviewing and expanding upon some relevant factors of personality disorders that present challenges for clinicians. These factors include: lack of routine screening and assessment of personality disorders in routine clinical care; the vast heterogeneity both between and within personality disorder diagnoses; the high rates of comorbid psychological disorders; and the ego-syntonic nature of many personality disorders, which leads many clients to seek treatment for problems other than their personality disorders. The remainder of the commentary then outlines recommendations for clinicians to follow in their treatment of clients with personality disorders. It provides recommendations for the assessment, case conceptualization, treatment goal and target formation, target hierarchy creation, intervention selection, implementation and evaluation, and the creation and maintenance of rapport and therapeutic alliance when working with personality-disordered clients.
In this rejoinder the author responds to the commentaries to the chapter. While the commentaries favor taxomonetric/categorical vs. dimensional approaches, the author explores various possibilities to integrate these two perspectives. Such an approach would better fit research finding and allows for preservation of the merits of each approach. Such integration has to resolve such challenges as definition of conceptually and clinically meaningful dimensions, identification of the disorder-specific concepts that are not dimensional, conceptualization of orthogonal dimensions, and integration of the dimensional and categorical approaches through identification of moderators.
This chapter reviews Narcissistic and Histrionic Personality Disorders (NPD, HPD) from three current perspectives. The categorical approach is exemplified in the DSM-5 Section II chapter on personality disorders. The categorical/dimensional hybrid approach is characterized by the DSM-5 Section III Alternative Model for Personality Disorders. Finally, both personality disorders are also conceptualized by purely dimensional and multidimensional models (e.g., pathological narcissism, histrionism). Integrative, interdisciplinary research and theory on NPD and pathological narcissism is expanding rapidly, providing novel clinical insights into classification, etiology, maintenance, patient presentation, and treatment. The clinical science of narcissism is robust, and its future appears quite promising. In contrast, contemporary research and theory on HPD and histrionism is scant and declining. Some have called for its elimination as a diagnostic entity. If the current trend of waning empirical and clinical interest persists, it is unlikely that HPD will be retained in future revisions of the DSM and other personality disorder classification systems.
This commentary extends on Dixon-Gordon, Conkey, and Woods’ (this volume) review of studies on brief personality disorder treatments by exploring two ways in which this evidence base advances the state of personality disorder treatment, and, relatedly, ways in which findings from short-term and long-term treatment studies might be productively integrated toward the development and testing of better treatments. First, these studies improve the accessibility of personality disorder treatment by testing specific interventions of limited intensity and duration that may be implemented with greater ease by generalist clinicians with less specialized training, time, and program resources. Good Psychiatric Management for borderline personality disorder is offered as an example of a “stepped-care model” in which the delivery of specific short-term interventions could be stratified according to an evidence-based algorithm yielding maximal benefit for the largest number of patients within the shortest amount of time. Second, brief personality disorder treatment studies suggest ways to conceptualize change processes at the level of structural features of treatments and at the level of what is happening in patients’ minds. Change models derived from studies on longer-term personality disorder treatments, such as the generation of “epistemic trust” as posited by the developers of Mentalization-Based Treatment, might be productively applied and empirically evaluated in the setting of short-term treatments.
This commentary focuses on the current state and recent developments within the field of research on drug treatments for borderline personality disorder. From an evidence-based medicine perspective, the relevance of the currently available evidence for clinical practice is critically discussed. Some research/practice gaps are highlighted, like polypharmacy and the widespread use of quetiapine, which both lack supporting, sufficiently reliable evidence. Sources for the lack of practically relevant research are outlined, and the example of recent research on Olanzapine for patients with borderline personality disorder is amplified. Last, new initiatives are presented which aim at improving the value of research, like the REWARD alliance, the AllTrials campaign, and the James Lind alliance that guide, inform, and support the design, conduct, and publication of studies that are of relevancy to consumers and clinicians, and have the potential to transform healthcare. Some first encouraging results of these endeavors are presented.
The following commentary on Jang and Choi’s chapter Issues and New Directions in Personality Disorder (PD) Genetics (This Volume) echoes their call to harness advances in PD assessment rather than rely on politically derived "top down" nosologies. We first discuss how recent work in the joint hierarchical structure of PD traits and psychopathology, as well as, personality dynamics (i.e., how personality manifests in different situations) likely offer fruitful avenues for exploring the more nuanced role of genetics in the development and maintenance of PD. Second, we highlight the need to better understand the role of environment in PD genetics and discuss emerging models (e.g., common pathway model). Third, we stress the need for more research and larger samples in order to arrive at stronger conclusions. Fourth, we consider how advances in gene-environment research can help to determine targets for PD prevention and treatment.
The purpose of this rejoinder is to emphasize several important areas of future research that were mentioned by one or both commentaries. First, the authors discuss issues related to multi-source assessment, such as the importance of further research on informant bias, and argue that the information gleaned from multiple sources is worth the added assessment burden. Second, they underscore the importance of longitudinal assessment both in capturing the treatment-relevant within-person processes through which personality pathology unfolds, as well as tracking therapeutic progress. They assert that a given measure’s ability to reliably and validly measure change over time should be considered when evaluating its clinical utility. Finally, they emphasize the need for greater attention to clinical utility of dimensional PD assessment measures.
In acknowledgment of the continued tension between the need to dimensionalize personality pathology in youth, and the reality of a categorical nosology in clinical settings, the goal of the present chapter is to review research on child and adolescent personality pathology from both these perspectives. While the review highlights several differences in constructs, methodology, and clinical implications of the two approaches, it also highlights significant commonalities in conclusions drawn from the traditions underlying categorical versus dimensional approaches. In particular, both categorical and dimensional approaches seem to support the idea that adolescence presents a unique developmental period for the crystallization of personality pathology.
Crowell, Kaliush, and Vlisides-Henry (this volume) provide a thought provoking chapter on assessment of mechanisms in personality disorders and describe the notable advancements for estimating genetic, temperamental, and environmental factors that arguably contribute to their development. To expand the depth and breadth of the target chapter, this commentary argues for a focus on the reciprocal and dynamic transactional processes that occur between an individual (genetic risk factors) and their environment. In this comment, the authors integrate findings from the broader genetics, personality, and psychopathology literature to illustrate the role of transactional mechanisms in developmental pathways to borderline personality disorder (BPD). Additionally, the authors highlight current gaps in the extant literature and discuss ways in which future research can investigate the person-environment transactions associated with BPD and related psychopathology. In addition to building our understanding of vulnerability to developing BPD, there are considerable prevention implications that may result from detection of malleable individual-based contributing factors to environmental exposure that may in turn reduce the risk of environmental stressor exposure in vulnerable individuals.
Flory (this volume) provides a compelling review of evidence bearing on the reliability and validity of diagnostic interviews for personality disorders (PDs). This commentary discusses several issues central to this topic, among the most important of which are: (1) the importance of distinguishing PD categories and constructs from the measures used to quantify them; and (2) the need to separate critiques of overarching conceptual frameworks (e.g., the dimensional perspective on personality) from criticisms of narrower assessment rubrics (e.g., the Five-Factor Model). Given the introspective limitations inherent in human information processing—limitations which are magnified in many forms of personality pathology—rigorous validation of PD assessment tools requires that researchers complement self-report outcome measures with behavioral and performance-based indices of personality dysfunction. To illuminate causal relationships among different features of personality pathology researchers must use experimental methods to alter PD-related psychological processes and assess the impact of these manipulations on affect, cognition, and behavior.
This commentary discusses the value of considering general interpersonal mechanisms across personality disorders, argues that specific strategies for addressing personality disorder problems may lie in the specifics of different relationship contexts, and notes the importance of developing a model of how psychotherapy targets relationship contexts so as to improve psychological health.
Antisocial personality disorder (ASPD) and psychopathy are related but distinguishable conditions with long histories in the mental health field. Recent years have seen a shift toward viewing these diagnostic conditions as dimensional and multifaceted, as opposed to discrete and unitary. This chapter covers historic and contemporary conceptualizations of these conditions and current approaches to assessing each. The authors describe the new dimensional system for personality disorders in the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders. In addition, they discuss the triarchic model, an integrative framework for clarifying similarities and differences between ASPD and psychopathy, and guiding etiological research on these conditions. In particular, they consider how the three constructs of the triarchic model – boldness, meanness, and disinhibition – relate to distinct biobehavioral systems and measures. The chapter concludes with suggestions for future research that can help to advance our understanding of ASPD and psychopathy, with a focus on multi-method assessments and targeted treatments.
This rejoinder is aimed at responding to the respective commentaries by Vernberg and Abel and Beauchaine; however, most of the rejoinder focuses on the commentary by Vernberg and Abel given the fact that Vernberg and Abel appear to challenge the basic premise that maladaptive traits denote personality disturbance beyond that of externalizing and internalizing disorder, which according to them, renders the concept of youth BPD obsolete. The authors of this rejoinder provide two points of rebuttal in this regard. First, while it is true that Axis I and II show a very similar empirical structure and can thus be represented from a unified perspective, the construct of youth BPD lies in the co-occurrence and interplay of specific symptoms. BPD is therefore more than a sum of its symptoms, and assessing these symptoms individually from established internalizing-externalizing measures (as Vernberg and Abel suggest) would not adequately capture the dynamics between symptoms that largely account for the downward spiral of BPD functioning. Second, they view the DSM-5 Criterion A function as the feature of personality pathology that distinguishes it from trait function; in particular the self-concept manifestations of Criterion A that are not readily captured by trait (Criterion B) personality function.
Traditionally, studies of personality disorder development have focused on (1) whether adult symptoms are expressed among children and adolescents, and if so (2) ages of onset at which full syndrome criteria are met. Although such studies are necessary and important, they provide limited understanding of etiopathophysiology—the complex and interactive biological and social determinants of PDs across the lifespan. This commentary presents a brief update to our conceptual model of antisocial (ASPD) and borderline (BPD) development among boys and girls. It focuses on (1) complexity of genetic, environmental, and neurohormonal influences on subcortical vulnerability to impulsivity; (2) increasing contributions of cortically mediated emotion dysregulation in adolescence and adulthood; and (3) moderation of common genetic and neural vulnerabilities to ASPD and BPD by sex. Importantly, neural correlates of ASPD and BPD are already observed among teens who are at risk for the disorders. Implications for prevention are discussed.
Diagnostic reliability receives cursory attention in the literature with wide ranges of kappa coefficients often interpreted as “adequate.” Moreover, the vast majority of personality disorder (PD) kappa estimates, including those reviewed by Flory (this chapter), are derived from the audio/video recording method. This method results in inflated estimates of diagnostic reliability, which provides limited insight into whether patients would receive the same diagnosis at different hospitals or clinics and whether researchers are studying similar patients. A more rigorous and ecologically valid method for assessing diagnostic reliability is the test-retest method. Although echoing some of Flory’s points, the authors here disagree with her assertion that categorical PDs demonstrate acceptable reliability. In fact, the reliability of categorical PDs assessed using the test-retest method is far lower than the DSM-5 conceptualization would indicate. Moreover, the test-retest diagnostic reliability of categorical PDs fails to achieve minimal benchmarks established in the “normal” personality literature, indicating critical problems for the DSM-5 categorical model. If the goal is to provide optimal patient care and advance clinical science, then adopting the trait-based dimensional model of personality pathology from section III of DSM-5 is necessary.