J Psychiatry Neurosci 2018;43(3):161-170
Katja Bertsch, PhD; Karin Roelofs, PhD; Paul Jonathan Roch, MD; Bo Ma, MSc; Saskia Hensel, MSc; Sabine C. Herpertz, MD; Inge Volman, PhD
Background: Difficulty in controlling emotional impulses is a crucial component of borderline personality disorder (BPD) that often leads to destructive, impulsive behaviours against others. In line with recent findings in aggressive individuals, deficits in prefrontal amygdala coupling during emotional action control may account for these symptoms.
Methods: To study the neurobiological correlates of altered emotional action control in individuals with BPD, we asked medication-free, anger-prone, female patients with BPD and age- and intelligence-matched healthy women to take part in an approach-avoidance task while lying in an MRI scanner. The task required controlling fast behavioural tendencies to approach happy and avoid angry faces. Additionally, before the task we collected saliva testosterone and self-reported information on tendencies to act out anger and correlated this with behavioural and functional MRI (fMRI) data.
Results: We included 30 patients and 28 controls in our analysis. Patients with BPD reported increased tendencies to act out anger and were faster in approaching than avoiding angry faces than with healthy women, suggesting deficits in emotional action control in women with BPD. On a neural level, controlling fast emotional action tendencies was associated with enhanced activation in the antero- and dorsolateral prefrontal cortex across groups. Healthy women showed a negative coupling between the left dorsolateral prefrontal cortex and right amygdala, whereas this was absent in patients with BPD.
Limitations: Specificity of results to BPD and sex differences remain unknown owing to the lack of clinical control groups and male participants.
Conclusion: The results indicate reduced lateral prefrontal–amygdala communication during emotional action control in anger-prone women with BPD. The findings provide a possible neural mechanism underlying difficulties with controlling emotional impulses in patients with BPD.
Submitted May 19, 2017; Revised Aug. 24, 2017; Accepted Sept. 6, 2017; Published online first Jan. 16, 2018
Acknowledgements: The study was supported by the German Research Foundation (HE 2660/12-1 and BE5292/1-1). I. Volman was supported by a Marie Curie Individual Fellowship (MSCA-IF-2014_EF_660397) within the European Union’s Horizon 2020 Framework Program. The authors thank P. Gaalman, Dr. S. Heiland and Dr. T. Kaestel for technical support and Dr. J. Cook for language editing. Furthermore, the authors thank the members of the Core Unit for recruitment and diagnostics of the Clinical Research Unit 256: A. Spohn, S. Cackowski, K. Haeussler, Dr. D. Gescher and Dr. F. Mancke.
Affiliations: From the Department of General Psychiatry, Center for Psychosocial Medicine, University of Heidelberg, Heidelberg, Germany (Bertsch, Herpertz); the Donders Institute for Brain, Cognition and Behaviour, Nijmegen, the Netherlands (Roelofs); Division of Experimental Radiology, University of Heidelberg, Heidelberg, Germany (Ma); the Department of Psychosomatic Medicine, Central Institute of Mental Health Mannheim, Medical Faculty Mannheim/Heidelberg University, Heidelberg, Germany (Hensel); and the Sobell Department of Motor Neuroscience and Movement Disorders, UCL Institute of Neurology, London, UK (Volman).
Competing interests: None declared.
Contributors: K. Bertsch, K. Roelofs, S. Herpertz and I. Volman designed the study. K. Bertsch, K. Roelofs, P. Roch, B. Ma and S. Hensel acquired the data, which K. Bertsch, K. Roelofs, S. Herpertz and I. Volman analyzed. K. Bertsch, K. Roelofs and I. Volman wrote the article which all authors reviewed. All authors approved the final version to be published and can certify that no other individuals not listed as authors have made substantial contributions to the paper.
Correspondence to: K. Bertsch, Department for General Psychiatry, Center of Psychosocial Medicine, University of Heidelberg Voßstr. 269115 Heidelberg, Germany; email@example.com