Borderline personality disorder (BPD) is a heterogeneous disorder, and previous analyses have parsed its phenotype in terms of subtypes or underlying traits. We refined the BPD construct by testing a range of latent variable models to ascertain whether BPD is composed of traits, latent classes, or both. We also tested whether subtypes of BPD could be distinguished by anger, aggressiveness, antisocial behavior, and mis-trustfulness, additional putative indicators drawn from Kernberg's (1967, 1975) theory of BPD. In a mixed clinical and nonclinical sample (N = 362), a factor mixture model consisting of two latent classes (symptomatic and asymptomatic) and a single severity dimension fit the BPD criteria, as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), data better than latent class or factor analytic approaches. In the second analytic phase, finite mixture modeling of the symptomatic latent class (n = 100) revealed four BPD subtypes: angry/aggressive, angry/mistrustful, poor identity/low anger, and prototypical. Our results support a hybrid categorical-dimensional model of the BPD DSM-IV criteria. The BPD subtypes emerging from this model have important implications for treatment and etiological research.
"The methods and technology required for identification of biomarkers is emerging rapidly, and these approaches have the capability of identifying whole biological systems or networks that are involved in conferring risk for BPD (e.g., Neylan, Schadt, & Yehuda, 2014). To the extent that BPD consists of subtypes, including an aggression subtype (Hallquist & Pilkonis, 2012) as described in Mancke et al. (2015), these approaches are likely to assist in identifying such subtypes. "
[Show abstract][Hide abstract] ABSTRACT: Comments on the article by F. Mancke et al. (see record 2015-31349-001). The article presents a multidimensional model of aggression in the context of borderline personality disorder (BPD), with a selective review of the research literature. BPD is arguably the most widely researched personality disorder, and the review suggests that there has been extensive progress in characterizing behavioral and biological correlates of aggression. What is not clear from the review, and indeed, the broader literature, is whether the research cited in this review is specific to BPD or can generally be applied to reactive aggression in the context of other disorders (or by extension into the normative range of the behavior). The review by Mancke et al. also highlights the fact that there is a general lack of research establishing predictive validity of aggression in BPD, with most research comparing two groups sampled at one time point. (PsycINFO Database Record
(c) 2015 APA, all rights reserved).
"Conway, Hammen, and Brennan (2012) examined the latent structure of the DSM's nine BPD criteria in a large community sample (n = 700) of young adults at risk for psychopathology. They compared dimensional, categorical, and hybrid models (non-parametric factor analyses) finding that a fully dimensional latent structure best fit the data (i.e., Figure 6.1 Panel A). Hallquist and Pilkonis (2012) also examined BPD symptoms, but in a mixed clinical and non-clinical sample (n = 362), finding that a hybrid model best fit the data. Their model suggested that there was a largely symptomatic class and an asymptomatic class that differed along a shared dimension of BPD severity (i.e., Figure 6.1 Panel C). "
[Show abstract][Hide abstract] ABSTRACT: Rigorous science and effective treatment both rest on a foundation of valid and reliable assessment and diagnosis. In the consulting room, assessment and diagnosis should provide useful information for clear communication among professionals and to patients, establishing prognosis and ultimately deciding whether, and if so how, to treat. In the laboratory, assessment and diagnosis are necessary to decide which participants to include and exclude from studies, while also providing data of interest to examine as predictors and outcomes. In turn, assessment and diagnosis are predicated on the understanding of the nature and structure of the target phenomenon, in this case personality disorder (PD). Thoroughly and accurately assessing and diagnosing PD can be a demanding enterprise. Patients with severe PDs often lead chaotic lives and have a fragmented or diffuse sense-of-self that can become embodied in a frenzied assessment process and a muddled clinical picture. In contrast, milder but nevertheless impairing personality pathology often becomes apparent only as a clinician learns the patient’s characteristic manner of perceiving and responding to others, and set ways of regulating self and affect. These difficulties in the assessment process are understandable and to be expected given the nature of the pathology. However, a further challenge to this enterprise is that the current diagnostic framework more often than not serves to obfuscate as opposed to clarify clinical description. For more than 30 years, the modern era of the Diagnostic and Statistical Manual of Mental Disorders (DSM; APA, 2013) has furthered a model of personality pathology in which patients can receive one of ten putatively discrete, categorical PD diagnoses, or a diagnosis of PD not otherwise specified (PD-NOS). Despite a growing body of scientific work that calls its fundamental structure in to question (Widiger & Trull, 2007), this remains the model for the foreseeable future as it has been ported virtually verbatim from DSM-IV to DSM-5. Here we highlight a number of key questions that emerge when the extant PD model is applied in clinical practice, and demonstrate how they are directly amenable to investigation using contemporary quantitative methodology.
Personality disorders: Toward theoretical and empirical integration in diagnosis and assessment, Edited by Steven K. Huprich, 01/2015: chapter 5: pages 109-144; American Psychological Association., ISBN: 978-1-4338-1845-5
[Show abstract][Hide abstract] ABSTRACT: This review summarizes recent neurocognitive research to better delineate the nosology, prognostication and cause underlying borderline personality disorder (BPD).
BPD had marked clinical heterogeneity with high comorbidity. Executive dysfunction in this disorder was linked to suicidality and treatment adherence, and may serve as an endophenotype. BPD was also characterized by cognitive distortions such as risky decision-making, deficient feedback processing, dichotomous thinking, jumping to conclusion, monocausal attribution and paranoid cognitive style. Social cognition deficits recently described in BPD include altered social inference and emotional empathy, hypermentalization, poorer facial emotional recognition and facial expressions. In electrophysiological studies, BPD was found to have predominantly right hemispheric deficit in high-order cortical inhibition. Reduced left orbitofrontal activity by visual evoked potential and magnetoencephalography correlated with depressive symptoms and functional deterioration. Brain structures implicated in BPD include the hippocampus, dorsolateral prefrontal cortex and anterior cingulate cortex. Abnormal anatomy and functioning of frontolimbic circuitry appear to correlate with cognitive deficits.
Frontolimbic structural and functional abnormalities underlie the broad array of cognitive abnormalities in BPD. Further research should espouse broader considerations of effects of comorbidity and clinical heterogeneity, and include community samples and, possibly, longitudinal designs.
Current opinion in psychiatry 01/2013; 26(1):90-6. DOI:10.1097/YCO.0b013e32835b57a9 · 3.94 Impact Factor
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