4c
Barbara De Clercq and Carla Sharp
The respective commentaries by Vernberg and Abel and Beauchaine provide unique perspectives on the developmental aspects of personality pathology. Vernberg and Abel took issue with some of the basic views espoused in our review, and appear to challenge the value of the assessment and diagnosis of personality pathology in adolescents. Beauchaine, on the other hand, did not challenge the basic premise of our review, but complemented it by providing important information on the biological aspects of personality pathology in youth. Given the complementary nature of the Beauchaine commentary, we spend our allotted word limit addressing the Vernberg and Abel commentary. However, we urge readers to seriously consider Beauchaine’s outstanding model of the etiopathophysiology of personality pathology, as we fully agree that much more research should focus on increasing our understanding of the biological mechanisms underlying the development of personality pathology. We thank the writers of both commentaries for their thoughtful and insightful input.
Vernberg and Abel agree with us that borderline personality disorder (BPD) may be an indicator of severity of general personality pathology (Criterion A function), rather than BPD per se. In turn, we agree with Vernberg and Abel that this view fits well with research showing that the self-system becomes more differentiated, domain-specific, and stable over the course of adolescence into early adulthood (Rosen, 2016; Sharp, Vanwoerden & Wall, 2018; Sharp & Wall, 2018b). However, we disagree with Vernberg and Abel that “the underlying dimensions of personality (and personality pathology) found in adults may not yet have emerged in children and adolescents.” Vernberg and Abel suggest that behavioral (especially externalizing) symptoms appear early on in childhood and adolescence, and that these symptoms can be treated “without these youth receiving a diagnosis [of personality pathology].” The first part of their thesis (that personality dimensions observed in adults have not yet emerged in youth) seems to negate more than a decade of research, including meta-analytic evidence, demonstrating the existence of underlying trait dimensions in children and adolescents that are the same as in adults, both in terms of structure, content, and course over time (although some stability parameters differ slightly in younger age groups; for a review, see Tackett, Herzhoff, Balsis, & Cooper, 2016). Doubting the existence of these traits (and their structure) seems thus unjustifiable.
The second part of their thesis brings into focus an important conceptual issue regarding the difference between clinical and personality related symptoms, or – as defined in earlier editions of the DSM – between Axis I and II disorders. Vernberg and Abel clearly equate symptoms of internalizing and externalizing disorders with personality pathology symptoms, and suggest that an actual screening for BPD adds no additional value since practitioners can merely focus on treating internalizing and externalizing symptoms. At a taxonomic level, however, we believe there is no need to contrast personality disorder conceptualizations with the traditional clinical approach of conceptualizing symptomatology in terms of internalizing–externalizing spectra. Already more than 15 years ago, a seminal publication (Krueger, 2005), followed by many others (e.g., Kotov et al., 2017; Krueger & Eaton, 2015), clearly showed that Axis I and II show a very similar empirical structure and can thus be represented from a unified perspective (Krueger, 2005). Indeed, the internalizing–externalizing spectra are by far the most empirically validated structural features accounting for all manifestations of psychopathology, including BPD (which is underscored by both trait and clinical psychologists). The point we aimed to make in our call for early detection of BPD, however, is that it is the co-occurrence and interplay of specific symptoms in BPD in particular that guide the cascading process of maladaptation from early adolescence onwards and lead to destructive outcomes. As BPD is thus more than a sum of its symptoms, looking at each of 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. To strengthen their argument, the authors refer to the descriptive review of Chorpita and Weisz (2009) to point out how therapeutic elements have been shown to be effective across RCTs for a number of individual symptoms in youth. Yet, precisely by referring to this review, the authors accentuate that even studies on transdiagnostic interventions focus solely on individual symptoms, providing no guidelines to clinicians on how exactly to treat youth who suffer from multiple symptoms, as always seen in BPD. Only by recognizing the subgroup of youth that suffers from the co-occurrence of multiple symptoms across both the internalizing and the externalizing spectra will BPD symptomatology in youth receive the clinical attention that it deserves. It is also worth noting that effective treatment components for internalizing versus externalizing symptoms differ heavily in the Chorpita and Weisz paper, which actually makes it a big challenge to treat BPD youth using transdiagnostic interventions only. A focused screening of BPD provides the necessary holistic picture of a young individual, which is particularly important given increasing evidence that the BPD constellation of symptoms does not necessarily represent a direct antecedent of adult BPD, but rather speaks to an overall vulnerability for maladaptive outcomes.
From an assessment perspective, these borderline phenotypic manifestations may be described along the traditional clinical perspective, or by using a trait conceptualization. Either way, we believe it is important to consider the construct of “personality functioning” as conceptualized in Criterion A of the DSM-5 AMPD (American Psychiatric Association, 2013). Whereas the exact definition of Criterion A is still a question of debate (Sharp & Wright, 2018), with some arguing that Criterion A can be readily observed in the general trait structure (Widiger et al., 2019), Criterion A may also be interpreted as an avenue for “going beyond traits.” Whether Criterion A is seen mainly as a measure of severity or impairment (Clark, Nuzum, & Ro, 2017) or as a more psychodynamic construct delineating process-oriented aspects of personality pathology that lies at a different level of explanation than the behavioral phenotype (Bender & Skodol, 2007; Fonagy, Gergely, Jurist, & Target, 2002; Kernberg, 1967; Sharp & Wall, 2018a), it offers a view of how traits interact with each other and with environmental factors to result in a level of functioning that is – from a trait perspective – closely aligned to the self-concept (defined by McCrae & Costa [1996] as a distinct mental construct that develops from characteristic maladaptations, the objective biography, and underlying basic dispositional tendencies). From the perspective of both internalizing–externalizing symptoms and trait personality pathology, the self-concept is conceptually differentiable from the internalizing/externalizing/trait symptoms themselves. We therefore see the developmental mapping of maladaptive Criterion A function as an important next step in further elucidating the developmental process of personality pathology.
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