J Psychiatry Neurosci 2016;41(5):E69-E78
Mandy Skunde, PhD; Stephan Walther, PhD; Joe J. Simon, PhD; Mudan Wu, PhD; Martin Bendszus, MD; Wolfgang Herzog, MD; Hans-Christoph Friederich, MD
Background: Impaired inhibitory control is considered a behavioural phenotype in patients with bulimia nervosa. However, the underlying neural correlates of impaired general and food-specific behavioural inhibition are largely unknown. Therefore, we investigated brain activation during the performance of behavioural inhibition to general and food-related stimuli in adults with bulimia nervosa.
Methods: Women with bulimia and healthy control women underwent event-related fMRI while performing a general and a food-specific no-go task.
Results: We included 28 women with bulimia nervosa and 29 healthy control women in our study. On a neuronal level, we observed significant group differences in response to general no-go stimuli in women with bulimia nervosa with high symptom severity; compared with healthy controls, the patients showed reduced activation in the right sensorimotor area (postcentral gyrus, precentral gyrus) and right dorsal striatum (caudate nucleus, putamen).
Limitations: The present results are limited to adult women with bulimia nervosa. Furthermore, it remains unclear whether impaired behavioural inhibition in patients with this disorder are a cause or consequence of chronic illness.
Conclusion: Our findings suggest that diminished frontostriatal brain activation in patients with bulimia nervosa contribute to the severity of binge eating symptoms. Gaining further insight into the neural mechanisms of behavioural inhibition problems in individuals with this disorder may inform brain-directed treatment approaches and the development of response inhibition training approaches to improve inhibitory control in patients with bulimia nervosa. The present study does not support greater behavioural and neural impairments to food-specific behavioural inhibition in these patients.
Submitted Oct. 20, 2015; Revised Jan. 28, 2016; Revised Mar. 3, 2016; Revised Apr. 3, 2016; Accepted Apr. 3, 2016; Early-released June 28, 2016
Acknowledgements: The authors thank the individuals who participated in the study for their time and effort. This study was supported by the German Research Foundation (FR 2626/ 3-1).
Affiliations: From the Departments of General Internal Medicine and Psychosomatics (Skunde, Walther, Simon, Wu, Herzog, Friederich) and General Adult Psychiatry (Walther), Centre for Psychosocial Medicine, University Hospital Heidelberg, Heidelberg, Germany; the Department of Psychosomatic Medicine and Psychotherapy, Medical Faculty, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany (Friederich, Simon); the Department of Psychology, College of Education, Shanghai Normal University, Shanghai, China (Wu); and the Department of Neuroradiology, University Hospital Heidelberg, Heidelberg, Germany (Bendszus).
Competing interests: M. Bendszus has received grants from DFG, Guerbet, Novartis, Hopp Foundation, Stryker, Medtronic and Siemens and personal fees from Guerbet, Novartis, Roche, Bayer, Teva and Vascular Dynamics. No other competing interests declared.
Contributors: M. Wu, M. Bendszus and H.-C. Friederich designed the study. M. Skunde, M. Wu and W. Herzog acquired the data, which M. Skunde, S. Walther, J. Simon and H.-C. Friederich analyzed. M. Skunde and H.-C. Friederich wrote the article, which all authors reviewed and approved for publication.
Correspondence to: M. Skunde, Centre for Psychosocial Medicine, General Internal Medicine and Psychosomatics, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg; email@example.com