Neural Changes in Borderline Personality Disorder After Dialectical Behavior Therapy–A Review

Abstract

The biological component of the biosocial theory of emotion regulation stipulates that borderline personality disorder (BPD) arises from biological vulnerabilities to heightened emotional reactivity. Comprehensive reviews have consistently implicated abnormalities in the amygdala, anterior cingulate cortex, and hippocampus in the neurobiology of BPD. While Dialectical Behavior Therapy (DBT) is the leading evidence-based psychotherapy for the treatment of BPD, there remains a paucity of literature examining changes in the neurobiology of BPD following DBT treatment. Nine studies were identified that examined neurobiological changes in BPD after the completion of DBT. Results indicated that there was significant deactivation of amygdala activity as well as the anterior cingulate cortex in patients with BPD after DBT treatment. As well, several studies found after DBT treatment, BPD patients had a decreased activity in the inferior frontal gyrus in response to arousing stimuli and increased activity in response to inhibitory control. Future research on the neurobiological change after DBT treatment can help clarify biological mechanisms of change in BPD.

Theta burst stimulation add on to dialectical behavioral therapy in borderline-personality-disorder: methods and design of a randomized, single-blind, placebo-controlled pilot trial

“…In addition to this, Mancke et al [ 9 ] found an increased grey matter volume in cortical regions connected with emotion regulation in women with BPD after receiving DBT treatment. These findings are supported by the review conducted by Iskric and Barkley-Levenson [ 10 ]. However, current published findings on the neural correlates of DBT effects are still scarce and much further research is needed to draw definitive conclusions.…”

Altered amygdalar emotion space in borderline personality disorder normalizes following dialectical behavioral therapy

“…Emotion dysregulation is a core symptom of BPD [55], and DBT focuses on this dysregulation by training patients to differentiate their emotions [3]. Functional neuroimaging studies of such emotion dysregulation in patients with BPD have used univariate analyses to consistently reveal altered activation levels of the amygdala in patients with BPD [56, 57], also with respect to treatment programs incorporating DBT [58]. However, the use of multivariate pattern analysis opens up new avenues for interpreting the role of the amygdala in BPD, as representational similarity analysis (RSA) allows one to hypothesize not only about the involvement of a brain region but more specifically about the representational content underlying its activity patterns [59].…”

“…As this study is the first to apply RSA to fMRI data of patients with BPD, follow-up work incoporating similar methodology, larger samples, and additional questionnaires (e.g., the Difficulties in Emotion Regulation Scale [68, 69]) is warranted in order to better characterize the relationship between neural representational spaces, emotion dysregulation, and BPD. One idea would involve carrying out several neuroimaging scans throughout the course of a DBT program in conjunction with a dismantling design [58]. This approach could help to constrain our understanding of the relationship between specific aspects of therapy and changes in the neural representational geometry, potentially revealing how such altered representational spaces map onto pathological behavior in BPD, thereby increasing the prognostic value of functional MRI in the clinic.…”

Amygdala response predicts clinical symptom reduction in patients with borderline personality disorder: A pilot fMRI study

“…For example, a recent meta-analysis reported functional hyperactivity of the left amygdala during aversive vs. neutral stimuli, as well as smaller gray matter volume of the amygdala in BPD ( Schulze et al, 2016 , 2019 ). This amygdala hyperactivation has been proposed to reflect the deviant salience of negative emotional stimuli and to be remediated by psychotropic medication ( Schulze et al, 2016 ) and psychotherapy ( Iskric and Barkley-Levenson, 2021 ) in BPD. We note that it is unclear whether remediation of amygdala hyperactivity is related to specific treatments or whether it is a general prerequisite for recovery from borderline symptomatology.…”

“…We note that it is unclear whether remediation of amygdala hyperactivity is related to specific treatments or whether it is a general prerequisite for recovery from borderline symptomatology. Notwithstanding this ambiguity, evidence shows that effects of DBT are also associated with changes in blood oxygen level-dependent (BOLD) signal in the amygdala ( Schnell and Herpertz, 2007 ; Krause-Utz et al, 2014 ; Salvador et al, 2016 ; Iskric and Barkley-Levenson, 2021 ). Here, we build on these previous findings by assessing the hypothesis that BPD is accompanied by abnormalities in aversive PIT and associated BOLD signal in the amygdala.…”