Research on the brains of patients with BPD has been instrumental in changing the way we think about the disorder. With the advent of neuroscience, BPD’s conceptualization has changed from character flaw to mental illness. While this research is imperfect, fraught with contradictions and confounds, it provides a tangible basis for complex emotional, social, and behavioural symptoms. In Dialectical Behaviour Therapy (DBT), basic neuroscience is taught to patients in simplified terms: the cortex regulates emotion and thinks logically, and the amygdala produces emotional intensity. If amygdala activation is intense enough to push us past our Skills Breakdown Point, the connection between the amygdala and the cortex is severed and we are unable to access or use our skills. In DBT terms, the cortex is Reasonable Mind, the amygdala is Emotion Mind, and the connection of these two structures results in Wise Mind. Emotion Regulation and Interpersonal Effectiveness skills help us to engage our cortex to modulate the intensity of amygdala activation depending on the actual level of threat posed by the environment, while Distress Tolerance skills calm the amygdala by engaging the Mammalian Dive Response, slowing the heart rate and regulating breath.
Anterior Cingulate Cortex and Prefrontal Cortex
Typically, the anterior cingulate cortex (ACC) and prefrontal cortex (PFC) activate during tasks that require disengagement from emotional stimuli, like the emotional Stroop task. Individuals diagnosed with BPD do not display the same activation in the ACC and PFC as healthy comparisons during the Stroop task (Wingenfeld et al., 2009), suggesting impairment in these critical emotion regulation centres of the brain. In accord with these results, the ACC is smaller in patients with BPD. (Tebartz van Elst et al. cited in Domes et al., 2009).
Orbitofrontal Cortex and Amygdala
Similarly to the ACC and PFC discussed above, the amygdala and orbitofrontal cortex (OFC) typically activate in synchronicity to regulate appraisal of and response to emotional stimuli. As shown in the diagrams above, the amygdala are located just below the OFC. The amygdala is the accelerator, propelling us to react to threatening stimuli in our environment. The OFC is the brake: ensuring we don’t react to stimuli that are not actually threatening, like a social situation. This connection is impaired in individuals with BPD (New et al, 2007). What this means is the emotional activation of the amygdala in patients with BPD functions like a car with its brakes cut. Finally, the amygdalae of individuals with BPD are often significantly smaller and more powerful, with increased response to negative emotional images: a sports car with its brakes cut. (Herpertz et al., Tebartz van Elst et al., both cited in Domes et al., 2009).
Opioids. Natural opioids (ex. endorphins) regulate response to events that cause social, emotional, or physical pain. Lowered levels of opioids are found in the cerebrospinal fluid of people who engage in non-suicidal self-injury and people with BPD. The result of these low levels are chronic emptiness, dissociation, and dysphoria. It has been hypothesized that self-injury provides the relief that it does by stimulating the receptors for these opioids, that is: self-injury provides a sensation similar to that of a normally functioning opioid system (Stanley and Siever (2010).
Oxytocin. Oxytocin plays a role in attachment and prosocial behaviour and regulates the stress response (Stanley & Siever, 2010). Social symptoms of BPD (rejection sensitivity, expectation of judgement or abandonment by others, and impaired cognitive empathy) are regulated by the release and binding of oxytocin in the brain. Administration of intranasal oxytocin to patients with BPD has been found to lessen avoidance of angry faces and hypersensitivity to threat (Herpertz & Bertsch, 2015). Because of its central role in the social symptoms of BPD, oxytocin is an object of interest for new clinical trials and intervention experiments.
For a 3D exploration of the brain regions discussed, visit http://www.brainfacts.org/3d-brain
Take care of your brains this weekend!
Domes, G., Schulze, L., & Herpertz, S. C. (2009). Emotion recognition in Borderline Personality Disorder—A review of the literature. Journal of Personality Disorders, 23, 6–19. doi:10.1521/pedi.2009.23.1.6
Herpertz, S. C., & Bertsch, K. (2015). A new perspective on the pathophysiology of borderline personality disorder: A model of the role of oxytocin. American Journal of Psychiatry, 172, 840–851. doi:10.1176/appi.ajp.2015.15020216
New, A. S., Hazlett, E. A., Buchsbaum, M. S., Goodman, M., Mitelman, S. A., Newmark, R., … & Siever, L. J. (2007). Amygdala–prefrontal disconnection in borderline personality disorder. Neuropsychopharmacology, 32, 1629.
Stanley, B., & Siever, L. J. (2010). The interpersonal dimension of borderline personality disorder: Toward a neuropeptide model. American Journal of Psychiatry, 167, 24–39. doi:10.1176/appi.ajp.2009.09050744
Wingenfeld, K., Rullkoetter, N., Mensebach, C., Beblo, T., Mertens, M., Kreisel, S., … Woermann, F. G. (2009). Neural correlates of the individual emotional Stroop in borderline personality disorder. Psychoneuroendocrinology, 34, 571–586. doi:10.1016/j.psyneuen.2008.10.024