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.
Highlights
Borderline Personality Disorder (BPD) is a debilitating mental illness characterized by emotion dysregulation, poor impulse control, identity disturbances, recurrent suicidal or self-harming behaviors, and unstable interpersonal relationships (1, 2)
Several studies focused on neural changes observed using functional magnetic resonance imaging (fMRI) resulting from 12-week Dialectical Behavior Therapy (DBT) treatment programs for individuals with borderline personality disorder (BPD)
Five longitudinal fMRI scans were completed, wherein participants viewed a set of images designed to induce emotional arousal
Summary
Borderline Personality Disorder (BPD) is a debilitating mental illness characterized by emotion dysregulation, poor impulse control, identity disturbances, recurrent suicidal or self-harming behaviors, and unstable interpersonal relationships (1, 2). This review article will primarily focus on the biological components of BPD. Comprehensive reviews have consistently demonstrated the multifaceted neurobiology of BPD in adults (2, 4, 5) as well as adolescents (6), along with the neurobiology of non-suicidal self-injury, a prominent and pervasive symptom among individuals with BPD (7). Abnormalities in the amygdala and anterior cingulate cortex (ACC) have been consistently implicated in the neurobiology of both BPD as well as individuals who engage in non-suicidal self-injury (2, 5– 7). A meta-analysis of neuroimaging studies on emotion processing showed left amygdala hyperactivity and reduced dorsolateral prefrontal cortex (dlPFC) among individuals with BPD (8, 9). Abnormalities in the hippocampus have been linked with BPD in adults (2, 5)
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