Dialectical Behavior Therapy was developed in the 1980s by Dr. Marsha Linehan, a psychologist who used her own insights from living successfully with borderline personality disorder to develop this therapy. DBT is a modified form of cognitive behavioral therapy and has been used to treat individuals with chronic suicidality and self-injurious behavior. In the first randomized control trial of DBT for borderline personality disorder, individuals who received DBT treatment versus treatment as usual had fewer suicidal episodes, fewer psychiatric hospitalizations, less treatment drop-out, and improved scores on global as well as social adjustment (Linehan et al., 1991). DBT was groundbreaking in its ability to target otherwise treatment resistant behaviors that could lead to adverse outcomes as fatal as suicide.
Since its inception, DBT has been more broadly applied to treat individuals struggling with substance use (Beckstead et al., 2015), treatment-resistant depression (Harley et al., 2008), eating disorders (Safer et al., 2010), and emotion regulation in general (Neacsiu et al., 2014). DBT is a multi-modal approach, and it involves individual psychotherapy, group skills training, and even phone consultations, with consistent coaching as part of treatment (Freedman & Duckworth, 2013). The Dialectics module of treatment refers to an approach of validation, where individuals are trained to accept their identified thoughts, emotions, and behavior rather than struggle with them. This validation facilitates a process of change (Dimeff & Linehan, 2001). The behavioral module focuses on specific behavioral coping skills that allow individuals to live with the symptoms of mental illness. Mindfulness practice is utilized in DBT to become conscious of one’s thoughts and feelings by paying attention to associated bodily sensations with an attitude of non-judgment and acceptance. Mindfulness practice is part of the process of validation, where one becomes tolerant of distressing thoughts and emotions without self-criticism. Mindfulness techniques such as progressive muscle relaxation and deep breathing are also utilized in the behavioral skills training module of DBT (Freedman & Duckworth, 2013).
DBT is a well-validated empirical approach to the treatment of borderline personality disorder as well as a range of other pathologies involving emotion dysregulation. To better appreciate the value of DBT, this blog will examine a less emphasized aspect of the treatment: its neurobiological effects on the brain and how the components of DBT may actually alter the brain’s capacity to respond to difficult emotions in a more adaptive way.
In their psychobiological framework of borderline personality disorder, Siever and Davis (1991) identify affective instability (AI) as a core dimension of the illness. Affective instability involves an inability to regulate intense and prolonged emotional intensity (Marwaha et al., 2014). This emotional intensity can manifest as rapid and dramatic oscillations of mood or affect in response to even small triggers in the environment, with these triggers usually being interpersonal in nature (Koenigsberg et al., 2010).
Neuroimaging data has linked the inefficient control of emotions in BPD to impaired regulatory control of the amygdala by the prefrontal cortex (Lis et al., 2007). The amygdala, part of the limbic system, is involved in emotional responses to stimuli (Davidson et al., 1999) and the frontal cortex is responsible for putting the breaks on these emotions. Dysfunctional coupling of fronto-limbic structures is thought to result in ineffective emotion regulation, the hallmark trait of BPD (New et al. 2007).
Growing evidence from fMRI studies shows increased amygdala activity in individuals with BPD in response to emotional faces (Donegan et al., 2003) and emotionally-triggering scripts (Beblo et al., 2006). In a recent meta-analysis, Schulze et al. (2016) found hyperactivity in the left amygdala, along with blunted activity in the bilateral dorso-lateral prefrontal cortex (DLPFC), during the processing of negative emotions in BPD. This pattern of an overactive amygdala and underactive PFC is consistent with the emotional instability that manifests in the presentation of the disorder. Structural abnormalities, including decreased gray matter in the left amygdala and hippocampus, as well as increased gray matter in subregions of the DLPFC may also be implicated in ineffective frontal inhibition of limbic hyperactivity (Shulze et al., 2016).
In a related line of research, Hazlett et al. (2012) showed that compared with healthy controls, individuals with BPD failed to show amygdala habituation to emotional stimuli (pleasant and unpleasant pictures). This means that no matter how many times individuals with BPD saw the same disturbing image, their amygdala reacted with the same intensity. This inability for the brain to adjust to a repeated emotional trigger in these individuals seems to reflect an overactive amygdala that is slow to return to baseline.
While limited research has explored the role of BPD treatment on activity in the prefrontal cortex, there is significant research suggesting a role of this treatment in tempering the emotional hypersensitivity associated with responsiveness in the amygdala. In a study looking at a 12-month course of DBT, treatment was found to normalize amygdala hyperactivity and lack of habituation to repeated stimuli in BPD (Goodman et al., 2014). These effects are similar to the absence of amygdala hyper-responsitivity found in individuals with BPD on psychotropic medications compared to individuals with a BPD diagnosis alone (Shulze et al., 2016). These findings suggest a neurobiological basis for the empirical support for DBT in managing affect instability in BPD and point toward the usefulness of further study in this field. To more fully understand the impact of DBT on the emotionally labile brain, future studies should target the neurobiological underpinnings of DBT in other clinical populations and should also explore the neurobiological correlates associated with specific sub-modules of DBT, such as mindfulness practice and acceptance or skills group training.
For example, mindfulness practice, a component of DBT training, has been shown to improve prefrontal regulation of emotionally sensitive brain regions. Even short-term mindfulness interventions have been associated with increased prefrontal activity and reduced amygdala activity when people were expecting to see negative or emotionally triggering images (Lutz et al., 2010). Expanding this type of research to explore each of the sub-modules of DBT may contribute to our understanding of how exactly this treatment affects the brain and the impact of these neural changes on treatment outcomes.
The emotional instability characteristic of borderline personality disorder has been associated with specific neurobiological patterns that lead to overactive emotions. Dialectical behavior therapy has been shown, not only to lead to clinical results, but also to produce changes in the brain that affect this neurobiological pattern and help put the brakes on emotional hypersensitivity. As we learn more about how treatments such as DBT target individual brain patterns, we can hope for more refined treatment recommendations that not only help individuals cope with emotional sensitivity, but actually improve resilience by boosting the brain’s capacity to hold responses to emotional triggers in check.
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