10a
Lori N. Scott and Paul A. Pilkonis
We appreciate the cogent chapter on borderline personality disorder (BPD) provided by Chapman, Hope, and Turner (this volume). Our goal in this commentary is to provide additional emphasis and recommendations relevant to three themes – assessment, etiology, and treatment – that we hope can guide further research and innovation in these areas.
Assessment of BPD
Debates have emerged in recent years about how best to define and diagnose BPD, as well as personality disorders (PDs) in general. The most controversial issue has been whether to abandon the traditional categorical system of the DSM in favor of dimensional trait models. A related issue is whether BPD should be conceptualized as a multidimensional or unidimensional construct. As reviewed by Chapman et al., some factor analytic studies (Clarkin, Hull, & Hurt, 1993; Sanislow, Grilo, & McGlashan, 2000) identified three factors underlying the BPD criteria (i.e., affective dysregulation, behavioral dysregulation, and disturbed relatedness). Though these findings have been interpreted as evidence of multidimensionality, the high correlations between these factors (above .90) are more suggestive of a higher-order unidimensional construct than multiple independent domains. Accordingly, findings from several other studies (e.g., Clifton & Pilkonis, 2007; Feske, Kirisci, Tarter, & Pilkonis, 2007) demonstrated that a single-factor solution is the most psychometrically sound when compared to multidimensional structures, supporting the unidimensionality of BPD for measurement purposes. These findings suggest that the DSM criteria for BPD (despite their apparent diversity) form a single coherent construct, for which BPD severity can be assessed along a dimensional continuum.
However, Feske and colleagues (2007) found that the DSM criteria functioned best for the assessment of BPD at moderate to severe levels of symptom severity. Given evidence for significant functional impairment among people with subthreshold BPD symptoms (e.g., Trull, Useda, Conforti, & Doan, 1997), there is a need to develop criteria and measures by which to identify individuals with lower levels of symptoms (including prodromal symptoms) who could benefit from BPD-relevant interventions to prevent full development of the acute disorder. Evidence indicates that the presence of three or more BPD criteria has clinical significance in terms of functional outcomes (Clifton & Pilkonis, 2007). Studies with college student samples have identified a score of 38 or higher (T > 70) on the Personality Assessment Inventory – Borderline Features Scale (Morey, 1991) as a clinically meaningful threshold for BPD (Trull et al., 1997). These thresholds, however, rely on a conceptualization of BPD consistent with the DSM criteria. Clinically validated thresholds for dimensional trait measures of BPD (and PDs in general) are missing, limiting the clinical utility of a dimensional framework for assessment and diagnosis. If alternative models of PDs are to gain traction in clinical settings, measures capturing the full range of PD severity need to be developed, along with clinically valid cutoffs and corresponding recommendations for clinical care at various levels of severity and stages of the development of a disorder.
Etiology of BPD
Though diagnosis of BPD in children and adolescents has been controversial, considerable evidence has now accumulated to challenge the view that BPD cannot be diagnosed until adulthood (Winsper et al., 2016). In addition, much has been learned from longitudinal studies about risk factors for the development of BPD in childhood and adolescence (Stepp, Lazarus, & Byrd, 2016). Some of the most consistently identified early risk factors for BPD include low socioeconomic status, stressful life events, early adversity, maternal psychopathology, maladaptive parenting, maltreatment, and child temperamental characteristics (for a review, see Stepp et al., 2016). Unfortunately, however, there is a lack of specificity of identified risk markers for BPD, as all the identified factors are known risk factors for multiple types of psychopathology. Further, few studies have been able to identify predictors of onset of the disorder, which is important for achieving our goal of preventing BPD.
As noted in the target chapter, much of what is known about risk for BPD in children and adolescents has come from community-based longitudinal studies, such as the Pittsburgh Girls Study (PGS; for details, see Keenan et al., 2010). Findings from several analyses from the PGS support the stability and validity of BPD features in childhood and adolescence (Stepp & Lazarus, 2017; Stepp, Pilkonis, Hipwell, Loeber, & Stouthamer-Loeber, 2010). Analyses from the PGS have also elucidated how childhood temperament, environmental, and parenting factors interact (Scott, Zalewski, Beeney, Jones, & Stepp, 2017; Stepp, Scott, Jones, Whalen, & Hipwell, 2015) and transact (e.g., Stepp et al., 2014) to shape the course of BPD symptoms in adolescence. These results highlight the importance of longitudinal research during critical developmental periods to further assess the transactional nature of both static and dynamic child and environmental factors, especially in the parent–child context, as these are likely to be important targets in both individual and family-based interventions for emergent BPD in youth.
Future Directions in Treatment Development
Need for Psychosocial Rehabilitation
Despite increased optimism about the remission of BPD (defined as no longer meeting full diagnostic criteria for the disorder), many patients who remit in categorical terms remain functionally impaired. In one longitudinal study of BPD patients at 10-year follow-up (Soloff & Chiappetta, 2018), 44 percent still suffered from poor overall psychosocial, vocational, and economic functioning even though most participants showed significant decreases in BPD symptoms and substance abuse. Similarly, despite the high rate of remission in the McLean Study of Adult Development, 40 percent of patients demonstrated poor psychosocial functioning (defined as a Global Assessment of Functioning (GAF) score < 61) at 16- and 20-year follow-ups (Zanarini, Frankenburg, Reich, & Fitzmaurice, 2012; Zanarini, Temes, Frankenburg, Reich, & Fitzmaurice, 2018). We agree with others (e.g., Links, 1993; Zanarini et al., 2012, 2018) who have proposed a psychosocial rehabilitation model of treatment for BPD patients, regardless of any specific theoretical approach. Evidence from longitudinal studies supports the need to target improved social integration, engagement, and effectiveness in major social roles (i.e., work and love).
Improving Interpersonal Relatedness
Chapman and colleagues discuss emotion dysregulation as the central difficulty in BPD and the driving force behind other BPD symptoms (e.g., interpersonal conflict, self-harm, dissociation). We would argue that there is a more reciprocal relationship between emotion dysregulation and the challenging interpersonal behaviors seen in those with BPD, and that this relationship can be understood through the lens of attachment theory (Bowlby, 1969), which is fundamentally about emotion regulation within interpersonal contexts. One implication of this is that improving interpersonal relatedness, especially with important attachment figures, may be as valuable a target for treatments of BPD as enhancing intrapersonal capacities for emotion regulation.
A sense of felt attachment security serves a number of important self-regulatory functions, including the ability to regulate emotional experiences through constructive strategies (e.g., reappraisal, self-soothing, problem-solving) and to effectively seek and obtain support from others in times of distress (Shaver & Mikulincer, 2007). Both clinical and empirical observations (for a review, see Gunderson & Lyons-Ruth, 2008) suggest that persons with BPD lack a sense of felt security and are prone to a hyperactivation of the attachment system in the context of emotional distress or perceived threat of abandonment, resulting in hypervigilance to the availability of attachment figures, intensification and exaggeration of negative affect, and other maladaptive behaviors that exacerbate distress (e.g., impulsive self-destructive behaviors and frantic attempts to avoid abandonment). Hence, many of the interpersonal and mood-dependent behaviors of persons with BPD can be understood as ineffective attempts to seek support and soothing from important others and to modulate emotional distress through interpersonal relatedness.
Our previous work suggests that these behaviors are most pronounced in romantic relationships, which form the basis for most attachment bonds in adulthood (Hill et al., 2008, 2011). We have also demonstrated that, in BPD, a hyperactivated, anxious attachment to the romantic partner is displayed as both intense emotional reactivity (especially in terms of anger and hostility) in response to perceived rejection and attenuated positive emotions in response to acceptance from romantic partners (Lazarus et al., 2018). These findings, combined with evidence for the importance of positive relationships in predicting the longitudinal course of BPD symptoms (Links & Heslegrave, 2000; Pagano et al., 2004), suggest that enhancing patients’ ability for positive relatedness and modulation of emotions through transactions with attachment figures (including couples-based interventions) may lead to improved emotion regulation and a better chance for sustained recovery through the buffering effects of secure attachment.
Developing Personalized Interventions
Though evidence-based treatments for BPD now exist, their effects are modest, variable (including high rates of dropout; Levy, 2008), and unstable over follow-up (Cristea et al., 2017). One limitation to clinical trials is their focus on group differences in response to treatment, which have limited utility for conceptualizing and treating an individual patient. Such variable-centered approaches cannot address person-centered dynamic processes and heterogeneity in these processes. This limitation has impeded progress in understanding mechanisms of change and resulted in the use of one-size-fits-all treatment packages for patients who are heterogeneous. In this current era of evolving precision medicine, we must embrace methods that have greater sensitivity to the dynamic nature of both symptoms and therapeutic change processes and that examine change at both the group and person levels.
Of primary interest to most clinicians is how to predict when or under what conditions any specific individual may experience an increase in a specific symptom, or how a specific intervention or changes in a supposed mechanism may relate to change in a symptom within the same individual (Hoffart & Johnson, 2017). Such dynamic processes can now be captured more easily with available technologies. With mobile devices, patients can report on their moods, behaviors, and other experiences in real time. Continuous background data (e.g., ambient noise, sleep quality, social interactions, physical activity) can also be collected by mobile and wearable devices. Given such advances, clinicians should be encouraged to consider ambulatory assessment of patients and applications that promote the translation of real-time data into individually tailored adaptive interventions. Researchers should also be encouraged to embrace novel statistical methods for understanding heterogeneity in idiographic dynamic processes and developing person-specific models, e.g., group iterative multiple model estimation (Beltz, Wright, Sprague, & Molenaar, 2016) and machine learning (Patrick & Hajcak, 2016). Such work can lead to the development of personalized approaches to case conceptualization and intervention for BPD, ultimately providing hope for recovery to more patients and their loved ones.
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