J Psychiatry Neurosci 2017;42(6):414-423
Li Wang, PhD, MD*; Qing-Mei Kong, PhD, MD*; Ke Li, PhD, MD*; Xue-Ni Li, PhD, MD; Ya-Wei Zeng, MD; Chao Chen, PhD, MD; Ying Qian, PhD, MD; Shi-Jie Feng, MD; Ji-Tao Li, PhD, MD; Yun’Ai Su, PhD, MD; Christoph U. Correll, PhD, MD; Philip B. Mitchell, PhD, MD; Chao-Gan Yan, PhD; Da-Rong Zhang, PhD, MD; Tian-Mei Si, PhD, MD
Background: Bulimia nervosa is a severe psychiatric syndrome with uncertain pathogenesis. Neural systems involved in sensorimotor and visual processing, reward and impulsive control may contribute to the binge eating and purging behaviours characterizing bulimia nervosa. However, little is known about the alterations of functional organization of whole brain networks in individuals with this disorder.
Methods: We used resting- state functional MRI and graph theory to characterize functional brain networks of unmedicated women with bulimia nervosa and healthy women.
Results: We included 44 unmedicated women with bulimia nervosa and 44 healthy women in our analyses. Women with bulimia nervosa showed increased clustering coefficient and path length compared with control women. The nodal strength in patients with the disorder was higher in the sensorimotor and visual regions as well as the precuneus, but lower in several subcortical regions, such as the hippocampus, parahippocampal gyrus and orbitofrontal cortex. Patients also showed hyperconnectivity primarily involving sensorimotor and unimodal visual association regions, but hypoconnectivity involving subcortical (striatum, thalamus), limbic (amygdala, hippocampus) and paralimbic (orbitofrontal cortex, parahippocampal gyrus) regions. The topological aberrations correlated significantly with scores of bulimia and drive for thinness and with body mass index.
Limitations: We reruited patients with only acute bulimia nervosa, so it is unclear whether the topological abnormalities comprise vulnerability markers for the disorder developing or the changes associated with illness state.
Conclusion: Our findings show altered intrinsic functional brain architecture, specifically abnormal global and local efficiency, as well as nodal- and network-level connectivity across sensorimotor, visual, subcortical and limbic systems in women with bulimia nervosa, suggesting that it is a disorder of dysfunctional integration among large-scale distributed brain regions. These abnormalities contribute to more comprehensive understanding of the neural mechanism underlying pathological eating and body perception in women with bulimia nervosa.
Submitted Sept. 13, 2016; Revised Nov. 7, 2016; Revised Feb. 6, 2017; Accepted Mar. 8, 2017; Early-released Sept. 26, 2017
*These authors contributed equally to this work.
Acknowledgements: The authors are grateful for funding from the National Key Technology R&D Program (2015BAI13B01), Beijing Municipal Science and Technology Commission (D121100005012002 and Z161100000216152), Doctoral Program of Higher Education of China (20130001110106), National Key Basic Research Program of China (973 Program) (2013CB531305), National Natural Science Foundation of China (81671774), and the Hundred Talents Program of the Chinese Academy of Sciences.
Affiliations: From Peking University Sixth Hospital, Institute of Mental Health, Beijing, China (Wang, Kong, Li Xue-Ni, Chen, Qian, Li Ji-Tao, Su, Zhang, Si); the National Clinical Research Center for Mental Health Disorders & Key Laboratory of Mental Health, Ministry of Health, Peking University, Beijing, China (Wang, Kong, Li Xue-Ni, Chen, Qian, Li Ji-Tao, Su, Zhang, Si); the Department of Radiology, 306 Hospital of People’s Liberation Army, Beijing, China (Li Ke, Zeng); the Shanxi Mental Health Center, Shanxi, China (Feng); the Zucker Hillside Hospital, Psychiatry Research, North Shore — Long Island Jewish Health System, Glen Oaks, NY (Correll); the Hofstra Northwell School of Medicine, Hempstead, NY (Correll); the Feinstein Institute for Medical Research, Manhasset, NY (Correll); the School of Psychiatry, University of New South Wales and Black Dog Institute, Sydney, Australia ( Mitchell); the CAS Key Laboratory of Behavioral Science, Institute of Psychology, Beijing, China (Yan); the Magnetic Resonance Imaging Research Center, Institute of Psychology, Chinese Academy of Sciences, Beijing, China (Yan); and the Department of Psychology, University of Chinese Academy of Sciences, Beijing (Yan).
Competing interests: C. Correll is on the boards of Alkermes, Intra- Cellular Therapies, Janssen, Johnson & Johnson, Lundbeck, Neurocrine, Otsuka, Pfizer, Sunovion and Teva; a consultant for Alkermes, Allergan, the Gerson Lehrman Group, IntraCellular Therapies, Janssen, Johnson & Johnson, LB Pharma, Lundbeck, Medscape, Otsuka, Pfizer, Sunovion, Takeda and Teva; has been paid by Bristol-Myers Squibb, Janssen, and Otsuka for expert testimony; has received speaker fees from Alkermes, Allergan, the Gerson Lehrman Group, IntraCellular Therapies, Janssen, Johnson & Johnson, LB Pharma, Lundbeck, Medscape, Otsuka, Pfizer, Sunovion, Takeda and Teva; and has received payment from Medscape for manuscript preparation. No other competing interests declared.
Contributors: Q. Kong, K. Li, X. Li, D. Zhang and T. Si designed the study. L.Wang, Y. Zeng, C. Chen, Y. Qian, S. Feng, J. Li and Y. Su acquired the data, which C. Correll, P. Mitchell and C. Yan analyzed. L. Wang wrote the article, which all authors reviewed and approved for publication.
Correspondence to: T. Si, Clinical Psychopharmacology Division, Institute of Mental Health, Peking University, No. 51 Hua Yuan Bei Road, Hai Dian District 100191, Beijing, China; firstname.lastname@example.org; or C. Yan, CAS Key Laboratory of Behavioral Science, Institute of Psychology, Chinese Academy of Sciences, 16 Lincui Road, Chaoyang District 100101, Beijing, China; email@example.com