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Personality Disorders

The Neural Networks in Borderline Personality Disorder

New research examines the neuroscience of borderline personality disorder.

People with borderline personality disorder (BPD) have what many consider a chronic and perhaps untreatable condition involving lifetime patterns of difficulty regulating moods, identity instability, problems in interpersonal relationships, and episodes of self-injury.

If you know someone with this disorder, you are perhaps aware of the seriousness of the symptoms, but also of the potential benefits of psychotherapy. However, you may also be aware that although therapy methods are being designed that have demonstrated efficacy, there still is not a “one-size-fits-all” approach that works for each individual with the disorder.

According to a new study by Melinda Westlund Schreiner and colleagues (2019), of the University of Minnesota, these generic approaches to BPD can only go so far. In reviewing the research on treatment with medication, Schreiner et al. note that such treatments as mood stabilizers may help some, but not all, BPD patients reduce episodes of anger and lack of impulse control. Antipsychotics work for other symptoms, such as anger and the so-called “cognitive-perceptual” symptoms of dissociation and reality testing. Antidepressants perhaps have the least therapeutic effect across all, but they may still be useful for some individuals.

Since no one approach works for everyone or all symptoms, Schreiner and colleagues believe that treatment must be tailored to the symptoms shown by the individual patient with BPD. Such individualized strategies are consistent with the priorities of the National Institutes of Mental Health (NIMH) “regarding greater precision in the treatment of mental illness” (p. 58). The University of Minnesota team believes that by understanding the neurobiology of BPD, therapies involving medication can better target and treat the individual’s symptoms.

The Schreiner et al. approach comes, then, from a biological perspective rather than one involving an understanding of the psychological contributions to BPD. The authors note that BPD can be treated successfully with psychotherapy, but many patients also require some form of psychopharmacological intervention. At present, though, the U.S. Food and Drug Administration has not approved any one BPD medication. Having medication as a treatment option, Schreiner and her colleagues believe, can “be valuable for those who may have limited access to qualified therapists and may provide added benefit to those engaged in an empirically supported psychotherapy” (p. 62).

Even if you are not a strong proponent of the biological approach, it is intriguing to think that BPD symptoms can be traced to reliable sources of variation in neural networks that uniquely characterize individuals with this disorder. Schreiner and her colleagues, reviewing the literature on functional magnetic resonance imaging (fMRI), note that people with BPD have been found to have increased activation (compared to controls) of the amygdala, the brain region involved in fear, when they are exposed to negative emotional stimuli.

Other neuroimaging methods combined with fMRI show, further, that people with BPD may have a hypersensitive response to information of a negative nature. However, the findings based on neuroimaging techniques also show variation among people with BPD depending on their behavioral symptoms. By matching functional connectivity patterns with specific symptoms, it may be possible, Schreiner et al. believed, to understand “how the neural circuits underpinning specific dimensions of BPD might change with treatment” (p. 59).

To explore this question, the University of Minnesota researchers recruited adults ranging from 18 to 45 years old with a diagnosis of BPD and no other current diagnosis. Participants were not on psychotherapeutic medications at the start of the study, and could not begin psychotherapy for the study’s duration. The final sample consisted of 19 individuals with baseline fMRI data, of whom 13 provided usable fMRI data at the end of an eight-week experimental intervention study.

Within this sample, the treatment group received an antipsychotic medication (with the brand name Seroquel), and the control received a placebo. Their psychological symptoms were assessed with a standard BPD measure that produces scores on scales of affective (emotional) disturbance, cognitive disturbance (distorted perceptions), impulsivity, and disturbances in relationships. Both participants and clinicians provided ratings on the presence of each symptom, but only the data from participants were used in the current study.

In the first test session, the research team administered fMRI for six minutes, during which they asked participants to relax with their eyes closed but to remain awake. The neuroimaging data also included maps of whole-brain connectivity. These data were used in a statistical model to predict the scores participants received on the BPD subscales.

Additionally, using the post-test scanning data, the researchers were able to calculate the changes in brain activity in relation to the psychological test scores, comparing treatment and placebo groups. Thus, although the sample was small, these analyses allowed the research team to explore both changes in brain scans before and after treatment as well as the relationship between these changes to types of BPD symptoms.

As the authors predicted, individuals with different BPD symptoms showed different patterns of activation in the brain, suggesting they differed in their susceptibility to negative stimuli. Those with higher impulsivity scores (self-injury, excessive drinking, and high spending) had increased functional connectivity at rest (RSFC) between the right amygdala and left hippocampus, another limbic system organ that is involved in processing short-term memory and may be involved in fear learning. Those high in cognitive disturbance (identity disturbance, paranoia, and dissociation) reduced their fear sensitivity as measured by the fMRI over the course of the study, but in the left amygdala, left temporal lobe, and left hippocampus. Thus, the authors conclude that dissociation may be related to different brain activation than impulsivity.

Finally, people high in disturbed relationships showed yet a third area of activation involving the right amygdala and right frontal lobe. As the authors conclude, “It is possible that the difficulties in interpersonal relationships may be a significant source of distress among those with BPD and lead to exacerbation of other symptoms” (p. 63), a conclusion consistent with psychological theories of BPD.

Because of the small sample size, and therefore the small numbers in control vs. treatment groups, the University of Minnesota study could not pinpoint the role of this specific type of medication in reducing BPD symptoms via changes in the brain or in psychological symptom scales. However, the apparent connection of BPD symptoms to differing patterns of brain activation suggests that the personalized treatment approach is worth pursuing further. At some point in the future, if this approach were to be further validated, it could potentially provide people with BPD yet another avenue for treatment, allowing their particular brain activation patterns to be matched with targeted therapies. Medication would be part of this picture, but psychotherapy could also become part of a broader biopsychosocial intervention.

To sum up, BPD is a complex disorder with multiple contributing factors and varying types of primary psychological dimensions. The Schreiner et al. study indicates that there is as yet untapped potential for neuroscience to advance our understanding and treatment of BPD.

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Schreiner, M. W., Klimes-Dougan, B., Mueller, B. A., Nelson, K. J., Lim, K. O., & Cullen, K. R. (2019). Neurocircuitry associated with symptom dimensions at baseline and with change in borderline personality disorder. Psychiatry Research: Neuroimaging, 290, 58–65. doi:// 10.1016/j.pscychresns.2019.07.001