Xiang-Yun Yang1, Jing Sun2, Jia Luo3, Zhao-Xi Zhong4, Ping Li5, Shu-Min Yao6, Hong-Fang Xiong7, Fang-Fang Huang8, Zhan-Jiang Li9. 1. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: wysun828@126.com. 2. Menzies Health Institute Queensland and School of Medicine, Griffith University, Australia. Electronic address: j.sun@griffith.edu.au. 3. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: luojia529@aliyun.com. 4. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: zzxzzx9268@163.com. 5. Department of Psychiatry, Qiqihaer Medical University, Qiqihaer, Heilongjiang, China. Electronic address: lipingchxyy@163.com. 6. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. 7. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: xiongmaoxiehui@163.com. 8. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: hff87hff87@163.com. 9. Department of Clinical Psychology, Beijing Key Lab of Mental Disorders, Beijing Anding Hospital, Capital Medical University, and Center of Schizophrenia, Beijing Institute for Brain Disorders, Beijing, People's Republic of China. Electronic address: lizhj8@ccmu.edu.cn.
Abstract
BACKGROUND: Cognitive behavioural therapy (CBT) is an effective treatment for obsessive-compulsive disorder (OCD). Several neuroimaging studies have explored alterations of brain function in OCD patients as they performed tasks after CBT. However, the effects of CBT on the neural activityin OCD during rest remain unknown. Therefore, we investigated changes in regional homogeneity (ReHo) in OCD patients before and after CBT. METHODS: Twenty-two OCD patients and 22 well-matched healthy controls participated in the resting-state functional magnetic resonance imaging scans. We compared differences in ReHo between the OCD and control groups before treatment and investigated the changes of ReHo in 17 OCD patients who responded to CBT. RESULTS: Compared to healthy controls, OCD patients exhibited higher ReHo in the right orbitofrontal cortex (OFC), bilateral middle frontal cortex, right precuneus, left cerebellum, and vermis, as well as lower ReHo in the bilateral caudate, right calcarine, right posterior cingulate cortex, and right middle temporal cortex. Along with the clinical improvement in OCD patients after CBT, we found decreased ReHo in the right OFC, bilateral middle frontal cortex, left cerebellum and vermis, and increased ReHo in the left caudate. Improvement of OCD symptoms was significantly correlated with the changed ReHo in the right OFC and left cerebellum. CONCLUSIONS: Although these findings are preliminary and need to be replicated in larger samples, they indicate the presence of abnormal spontaneous brain activity of the prefrontal-striatal-cerebellar circuit in OCD patients, and provide evidence that CBT can selectively modulate the spontaneous brain activity of this circuit in OCD patients.
BACKGROUND: Cognitive behavioural therapy (CBT) is an effective treatment for obsessive-compulsive disorder (OCD). Several neuroimaging studies have explored alterations of brain function in OCDpatients as they performed tasks after CBT. However, the effects of CBT on the neural activityin OCD during rest remain unknown. Therefore, we investigated changes in regional homogeneity (ReHo) in OCDpatients before and after CBT. METHODS: Twenty-two OCDpatients and 22 well-matched healthy controls participated in the resting-state functional magnetic resonance imaging scans. We compared differences in ReHo between the OCD and control groups before treatment and investigated the changes of ReHo in 17 OCDpatients who responded to CBT. RESULTS: Compared to healthy controls, OCDpatients exhibited higher ReHo in the right orbitofrontal cortex (OFC), bilateral middle frontal cortex, right precuneus, left cerebellum, and vermis, as well as lower ReHo in the bilateral caudate, right calcarine, right posterior cingulate cortex, and right middle temporal cortex. Along with the clinical improvement in OCDpatients after CBT, we found decreased ReHo in the right OFC, bilateral middle frontal cortex, left cerebellum and vermis, and increased ReHo in the left caudate. Improvement of OCD symptoms was significantly correlated with the changed ReHo in the right OFC and left cerebellum. CONCLUSIONS: Although these findings are preliminary and need to be replicated in larger samples, they indicate the presence of abnormal spontaneous brain activity of the prefrontal-striatal-cerebellar circuit in OCDpatients, and provide evidence that CBT can selectively modulate the spontaneous brain activity of this circuit in OCDpatients.
Authors: Sarah W Feldstein Ewing; Tammy Chung; Justin D Caouette; Arielle Ketcherside; Karen A Hudson; Francesca M Filbey Journal: Neuroimage Date: 2016-12-28 Impact factor: 6.556