Putting the Brakes on Emotional Reactions: Dialectical Behavior Therapy in the Treatment of Borderline Personality Disorder

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.



Beblo, T., Driessen, M., Mertens, M., Wingenfeld, K., Piefke, M., & Rullkoetter, N. (2006). Functional MRI correlates of the recall of unresolved life events in borderline personality disorder. Psychological Medicine, 36(6), 845-856. doi:S0033291706007227.

Beckstead, D. J., Lambert, M. J., DuBose, A. P., & Linehan, M. (2015). Dialectical behavior therapy with American Indian/Alaska native adolescents diagnosed with substance use disorders: Combining an evidence based treatment with cultural, traditional, and spiritual beliefs. Addictive Behaviors, 51, 84-87. doi: http://dx.doi.org/10.1016/j.addbeh.2015.07.018

Davidson, R. J., Abercrombie, H., Nitschke, J. B., & Putnam, K. (1999). Regional brain function, emotion and disorders of emotion. Current Opinion in Neurobiology, 9(2), 228-234. doi:http://dx.doi.org/10.1016/S0959-4388(99)80032-4

Dimeff, L., & Linehan, M. M. (2001). Dialetical behavior therapy in a nutshell. The California Psychologist, 34, 10-13.

Donegan, N. H., Sanislow, C. A., Blumberg, H. P., Fulbright, R. K., Lacadie, C., & Skudlarski, P. (2003). Amygdala hyperreactivity in borderline personality disorder: Implications for emotional dysregulation. Biological Psychiatry, 54(11), 1284-1293. doi:http://dx.doi.org/10.1016/S0006-3223(03)00636-X

Freedman, J. L., & Duckworth, K. (2013). Dialectical behavioral therapy fact sheet. Retrieved April 17, 2016, from https://www2.nami.org/factsheets/DBT_factsheet.pdf

Goodman, M., Carpenter, D., Tang, C. Y., Goldstein, K. E., Avedon, J., & Fernandez, N. (2014). Dialectical behavior therapy alters emotion regulation and amygdala activity in patients with borderline personality disorder. Journal of Psychiatric Research, 57, 108-116. doi:http://dx.doi.org/10.1016/j.jpsychires.2014.06.020

Harley, R., Sprich, S., Safren, S., Jacobo, M., & Fava, M. (2008). Adaptation of dialectical behavior therapy skills training group for treatment-resistant depression. The Journal of Nervous and Mental Disease, 196(2) Retrieved from http://journals.lww.com/jonmd/Fulltext/2008/02000/Adaptation_of_Dialectical_Behavior_Therapy_Skills.8.aspx

Hazlett, E. A. (2016). Neural substrates of emotion-processing abnormalities in borderline personality disorder. Biological Psychiatry, 79(2), 74-75. doi:10.1016/j.biopsych.2015.10.008 [doi]

Hazlett, E. A., Zhang, J., New, A. S., Zelmanova, Y., Goldstein, K. E., & Haznedar, M. M. (2012). Potentiated amygdala response to repeated emotional pictures in borderline personality disorder. Biological Psychiatry, 72(6), 448-456. doi:http://dx.doi.org/10.1016/j.biopsych.2012.03.027

Koenigsberg, H. W. (2010). Affective instability: Toward an integration of neuroscience and psychological perspectives. Journal of Personality Disorders, 24(1), 60-82. doi:10.1521/pedi.2010.24.1.60 [doi]

Linehan M.M., Armstrong H.E., Suarez A., Allmon D., & Heard H.L. (1991). Cognitive-behavioral treatment of chronically parasuicidal borderline patients. Archives of General Psychiatry, 48(12), 1060-1064. doi:10.1001/archpsyc.1991.01810360024003

Lis, E., Greenfield, B., Henry, M., Guilé, J. M., & Dougherty, G. (2007). Neuroimaging and genetics of borderline personality disorder: A review. Journal of Psychiatry & Neuroscience, 32(3), 162-173. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1863557/

Lutz, J., Herwig, U., Opialla, S., Hittmeyer, A., Jancke, L., & Rufer, M. (2014). Mindfulness and emotion regulation–an fMRI study. Social Cognitive and Affective Neuroscience, 9(6), 776-785. Retrieved from http://europepmc.org/abstract/MED/23563850

Marwaha, S., He, Z., Broome, M., Singh, S. P., Scott, J., & Eyden, J. (2014). How is affective instability defined and measured? A systematic review. Psychological Medicine, 44(09), 1793-1808. doi:10.1017/S0033291713002407

Neacsiu, A. D., Eberle, J. W., Kramer, R., Wiesmann, T., & Linehan, M. M. (2014). Dialectical behavior therapy skills for transdiagnostic emotion dysregulation: A pilot randomized controlled trial. Behaviour Research and Therapy, 59, 40-51. doi:http://dx.doi.org/10.1016/j.brat.2014.05.005

New, A. S., Hazlett, E. A., Buchsbaum, M. S., Goodman, M., Mitelman, S. A., & Newmark, R. (2007). Amygdala-prefrontal disconnection in borderline personality disorder. Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology, 32(7), 1629-1640. Retrieved from http://dx.doi.org/10.1038/sj.npp.1301283

Safer, D. L., & Jo, B. (2010). Outcome from a randomized controlled trial of group therapy for binge eating disorder: Comparing dialectical behavior therapy adapted for binge eating to an active comparison group therapy. Behavior Therapy, 41(1), 106-120. doi:http://dx.doi.org/10.1016/j.beth.2009.01.006

Schulze, L., Schmahl, C., & Niedtfeld, I. (2016). Neural correlates of disturbed emotion processing in borderline personality disorder: A multimodal meta-analysis. Biological Psychiatry, 79(2), 97-106. doi:http://dx.doi.org/10.1016/j.biopsych.2015.03.027

Siever, L. J., & Davis, K. L. (1991). A psychobiological perspective on the personality disorders. American Journal of Psychiatry, 148(12), 1647-1658.

van Zutphen, L., Siep, N., Jacob, G. A., Goebel, R., & Arntz, A. (2015). Emotional sensitivity, emotion regulation and impulsivity in borderline personality disorder: A critical review of fMRI studies. Neuroscience & Biobehavioral Reviews, 51, 64-76. doi:http://dx.doi.org/10.1016/j.neubiorev.2015.01.001

Deep Brain Stimulation: Tourette Syndrome

Much of Tourette Syndrome is unknown and there lies an aura of mystery around the predispositions and treatment approach to this disorder. Tourette syndrome is a chronic neurological disorder typically diagnosed through motor or vocal tics. Tics are repetitive movements, either in movement or speech, which are uncontrollable and involuntary (McNaught, 2011). It is typically seen with an onset around 5-8 years old although it currently impacts those of all ages (Jankovic, 2011). Those with milder cases of Tourette syndrome may be able to suppress the tics but it will still cause detrimental impairments in various aspects of their lives. Many of those who have a Tourette Syndrome often exhibit other symptoms other than tics such as hyperactivity, impulsivity, obsessions and compulsions, anxiety, and depression as well (Jankovic, 2011). These often lead to comorbid diagnoses, the two most common ones being Attention Deficit Hyperactivity Disorder (ADHD) and Obsessive Compulsive Disorder (OCD) (Jankovic, 2011)

The mystery around Tourette syndrome is that so much of the etiology of the disorder is unknown. There is current research to show that the abnormalities are targeting specific regions of the brain such as basal ganglia, frontal lobe, and prefrontal cortex (Cannon, 2012). The evidence points to an impact on the dopamine, serotonin, and norepinephrine neurotransmitters with the main abnormal metabolism of dopamine. A significant twin study shows that a large component of Tourette syndrome is genetic and that there are implications that Tourette syndrome can be inherited as though it were an autosomal dominant condition (Müller-Vahl, 2011). Other non-genetic factors such as gestational stress, severe trauma, drug/alcohol abuse, or gestational infections may play a big factor in causing Tourette syndrome (McNaught, 2011). Similar to the cause of Tourette syndrome being unknown, there is currently no evidence to show that there is a cure for this psychiatric condition. Treatment modalities are focused on behavioral therapy with occupational therapy, psychological counseling therapy, and pharmacological therapy to aid in managing the symptoms (McNaught, 2011).

Diverging away from the more conventional approaches to treatment, research shows that there has been one mode of treatment that has shown promising efficacy in improving symptoms of Tourette syndrome. Deep brain stimulation is a neurosurgical procedure involving a plantation of electrodes to parts of the brain that will be stimulated by electrical pulses (Ackermans, 2006). Essentially, the procedure induces neuromodulation so that the abnormal nerve activity for those with Tourette syndrome will be altered to mimic normal impulses (Bajwa, 2007). Deep brain stimulation still has yet to be FDA-approved for Tourette syndrome but is currently FDA-approved for Parkinson’s disease, tremors and dystonia (Cannon, 2012). Because of its efficacy and safety in Parkinson’s disease, deep brain stimulation has been applied to other movement disorders, such as Tourette syndrome (Black, 2009). This method of treatment is reserved for patients who have undergone significant behavioral and pharmacologic treatments without seeing significant improvements for their involuntary tics (Cannon, 2012). Those considered for this mode of treatment would also show that their impairments are detrimental and cannot be alleviated.

As Tourette syndrome is believed to have loop dysfunction in the basal ganglia-thalamocortical circuits, deep brain stimulation attempts to regulate the abnormal communication that causes the involuntary tics (Priori, 2013). The surgical procedure for deep brain stimulation would involve implanting two different components: electrodes, implanted into specific regions in the brain, to deliver electrical pulses and an impulse generator, implanted under the collarbone, to stimulate the pulses (Houeto, 2005). The delivery of the electricity would generate impulses to the affected parts of the brain to alter the abnormal circuitry seen in those with Tourette syndrome (Hariz, 2010). These affected parts have been many and include the frontal lobe, the limbic system, the thalamus, and the cerebellum (Shahed, 2007). The two sites that seem to prove best are “the internal globus pallidus (GPi) and the centromedian-parafascicular nuclei of the thalamus, near the middle of the brain (CM-Pf)” (Black, 2009). Side effects are concurrent with any other neurosurgical procedures (Hariz, 2010). However, with regulation of abnormal impulses that cause these severe tics, clients may show noteworthy improvements for their symptoms.

The research behind deep brain stimulation for the use of Tourette syndrome and tic disorders is still emerging (Krack, 2010). However, there is enough evidence to show that this treatment modality has proven efficacy in clients with a debilitating tic disorder and severe impairments in the major aspects of their lives (Piedad, 2012). In cases where medication and behavioral therapy has proven ineffective, deep brain stimulation can serve as an option to improve severely disruptive motor and vocal tics (Lyons, 2011). This will be an interesting mode of treatment to follow and continued research on the neurobiological process of Tourette syndrome and the neuromodulation of deep brain stimulation will only further psychiatric understanding of this disorder (Servello, 2010).





Ackermans, L., Y. Temel, et al. (2006). “Deep brain stimulation in Tourette’s syndrome: two targets?” Mov Disord 21(5): 709-13.

Bajwa, R. J., A. J. de Lotbiniere, et al. (2007). “Deep brain stimulation in Tourette’s syndrome.”Mov Disord22(9): 1346-50.

Cannon, E., Silburn, P., Coyne, T., O’Maley, K., Crawford, J. D., & Sachdev, P. S. (2012). Deep brain stimulation of anteromedial globus pallidus interna for severe Tourette’s syndrome. American Journal of Psychiatry.

Hariz, M. I., & Robertson, M. M. (2010). Gilles de la Tourette syndrome and deep brain stimulation. European Journal of Neuroscience, 32(7), 1128-1134.

Houeto, J. L., C. Karachi, et al. (2005). “Tourette’s syndrome and deep brain stimulation.” J Neurol Neurosurg Psychiatry 76(7): 992-5.

Jankovic, J., & Kurlan, R. (2011). Tourette syndrome: evolving concepts. Movement disorders, 26(6), 1149-1156.

Krack, P., Hariz, M. I., Baunez, C., Guridi, J., & Obeso, J. A. (2010). Deep brain stimulation: from neurology to psychiatry?. Trends in neurosciences, 33(10), 474-484.

Lyons, M. K. (2011, July). Deep brain stimulation: current and future clinical applications. In Mayo Clinic Proceedings (Vol. 86, No. 7, pp. 662-672). Elsevier.

McNaught, K. S. P., & Mink, J. W. (2011). Advances in understanding and treatment of Tourette syndrome. Nature Reviews Neurology, 7(12), 667-676.

Müller-Vahl, K. R., Cath, D. C., Cavanna, A. E., Dehning, S., Porta, M., Robertson, M. M., … & ESSTS Guidelines Group. (2011). European clinical guidelines for Tourette syndrome and other tic disorders. Part IV: deep brain stimulation. European child & adolescent psychiatry, 20(4), 209-217.

Piedad, J. C. P., Rickards, H. E., & Cavanna, A. E. (2012). What patients with gilles de la tourette syndrome should be treated with deep brain stimulation and what is the best target?. Neurosurgery, 71(1), 173-192.

Servello, D., Sassi, M., Brambilla, A., Defendi, S., & Porta, M. (2010). Long‐Term, Post‐Deep Brain Stimulation Management of a Series of 36 Patients Affected With Refractory Gilles de la Tourette Syndrome. Neuromodulation: Technology at the Neural Interface, 13(3), 187-194.

Shahed, J., J. Poysky, et al. (2007). “GPi deep brain stimulation for Tourette syndrome improves tics and psychiatric comorbidities.” Neurology 68(2): 159-60.