Neural signature of behavioural inhibition in women with bulimia nervosa

• Published in: Journal of psychiatry & neuroscience 2016-09, Vol.41 (5), p.E69-E78
• Main Authors: Skunde, Mandy, PhD, Herzog, Wolfgang, MD, Walther, Stephan, PhD, Simon, Joe J., PhD, Wu, Mudan, PhD, Friederich, Hans-Christoph, MD, Bendszus, Martin, MD
• Format: Article
• Language: English
• Subjects: Adult; Anorexia; Attention deficit hyperactivity disorder; Behavior; Brain - diagnostic imaging; Brain - physiopathology; Brain Mapping; Bulimia; Bulimia Nervosa - diagnostic imaging; Bulimia Nervosa - physiopathology; Bulimia Nervosa - psychology; Development and progression; Female; Food; Health aspects; Humans; Inhibition; Inhibition (Psychology); Magnetic Resonance Imaging; Medical Education; Neuropsychological Tests; Psychiatry; Psychomotor Performance - physiology; Research Paper; Studies; Visual Perception - physiology
• ISSN: 1180-4882; 1488-2434
• DOI: 10.1503/jpn.150335

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.