J Psychiatry Neurosci 2013; 38(3): 164-172
Gitta A. Jacob, PhD; Kerstin Zvonik, PhD; Susanne Kamphausen, MD; Alexandra Sebastian, MSc; Simon Maier, MSc; Alexandra Philipsen, MD; Ludger Tebartz van Elst, MD; Klaus Lieb, MD; Oliver Tüscher, MD
Jacob, Zvonik, Kamphausen, Sebastian, Maier, Philipsen, Tebartz van Elst, Lieb, Tüscher — Department of Psychiatry and Psychotherapy, University Medical Center Freiburg; Jacob — Clinical Psychology and Psychotherapy, University of Freiburg; Zvonik — Center for Translational Research in Systems Neuroscience and Psychiatry, Department of Psychiatry, Georg August University Göttingen; Kamphausen — Department of Psychiatry and Psychotherapy, University Medical Center Tübingen; Sebastian, Lieb, Tüscher — Department of Psychiatry and Psychotherapy, University Medical Center Mainz; Tüscher— Department of Neurology, University Medical Center Freiburg, Germany
Background: Both emotion regulation and impulsivity are core aspects of borderline personality disorder (BPD) pathology. Although both problems may be combined specifically in BPD, few studies to date have investigated the emotional modulation of impulsivity in BPD.
Methods: Women with BPD and matched healthy controls performed go/no-go tasks after induction of anger, joy or a neutral mood by vocally presented short stories. Dependent variables were the behavioural results and functional magnetic resonance imaging data.
Results: We included 17 women with BPD and 18 controls in our study. No behavioural group differences were found. However, patients with BPD showed stronger activation of the left amygdala and weaker activation of the subgenual anterior cingulate during anger induction than controls. Inhibition in the go/no-go task after anger induction increased activity in the left inferior frontal cortex in controls, but not in women with BPD, who, in turn, showed increased activation in the subthalamic nucleus.
Limitations: Findings cannot be generalized to men, and 4 patients were taking antidepressant medication (selective serotonin reuptake inhibitors). In addition, no patient control group was investigated, thus we do not know whether findings are specific to BPD compared with other disorders.
Conclusion: Our findings are consistent with the view that a disturbed amygdala–prefrontal network in patients with BPD is compensated by a subcortical loop involving the subthalamic nucleus, leading to normal behavioural inhibition in these patients.
Submitted Feb. 7, 2012; Revised June 10, July 23, 2012; Accepted July 25, 2012.
Acknowledgements: This work was funded by the German Research Foundation (grant JA1785/1-1), a fellowship grant from the Freiburg University Medical School to O. Tüscher, and a grant from the German Federal Ministry of Research and Education (grant 01GV0606) to L. Tebartz van Elst.
Competing interests: G.A. Jacob receives royaltees from Beltz, Elsevier and Junfermann. A. Philipsen sits on the advisory boards of and has received lecture fees from Lilly, Medice and Shire. L. Tebartz van Elst declares having received lecture and travels fees from Elli Lilly, Medtronic, Pfizer and UCB. O. Tüscher received support through his institution from the German Federal Ministry of Research and Education (grant 01GW0730). None declared for K. Zvonik, S. Kamphausen, A. Sebastian, S. Maier and K. Lieb.
Contributors: G.A. Jacob, K. Zvonik, L. Tebartz van Elst, K. Lieb and O. Tüscher designed the study. K. Zvonik, S. Kamphausen, S. Maier, A. Philipsen and O. Tüscher acquired the data. G.A. Jacob, K. Zvonik, A. Sebastian, S. Maier, A. Philipsen, K. Lieb and O. Tüscher analyzed the data. G.A. Jacob and O. Tüscher wrote the article. K. Zvonik, S. Kamphausen, A. Sebastian, S. Maier, A. Philipsen, L. Tebartz van Elst, K. Lieb and O.
Correspondence to: G.A. Jacob, Clinical Psychology and Psychotherapy, Institute of Psychology, Engelbergerstraße 41, 79106 Freiburg, Germany; email@example.com