Wenbin Guo1,2,3,4,5, Feng Liu6, Jindong Chen1,2,3,4,5, Renrong Wu1,2,4,5,6, Lehua Li1,2,3,4,5, Zhikun Zhang7, Huafu Chen6, Jingping Zhao1,2,3,4,5,8. 1. a Department of Psychiatry , The Second Xiangya Hospital, Central South University , Changsha , Hunan , China. 2. b Mental Health Institute of the Second Xiangya Hospital , Central South University , Changsha , Hunan , China. 3. c National Clinical Research Center on Mental Disorders , Changsha , Hunan , China. 4. d National Technology Institute on Mental Disorders , Changsha , Hunan , China. 5. e Hunan Key Laboratory of Psychiatry and Mental Health , Changsha , Hunan , China. 6. f Key Laboratory for NeuroInformation of Ministry of Education, School of Life Science and Technology , University of Electronic Science and Technology of China , Chengdu , Sichuan , China. 7. g Mental Health Center , The First Affiliated Hospital, Guangxi Medical University , Nanning , Guangxi , China. 8. h Guangzhou Hui Ai Hospital , Affliated Brain Hospital of Guangzhou Medical University , Guangzhou , Guangdong , China.
Abstract
OBJECTIVES: Deficits in homotopic connectivity have been implicated in schizophrenia. However, alterations in homotopic connectivity associated with antipsychotic treatments in schizophrenia remain unclear due to lack of longitudinal studies. METHODS: Seventeen drug-free patients with recurrent schizophrenia and 24 healthy controls underwent resting-state functional magnetic resonance imaging scans. The patients were scanned at three time points (baseline, at 6 weeks of treatment, and at 6 months of treatment). Voxel-mirrored homotopic connectivity (VMHC) was applied to analyse the imaging data to examine alterations in VMHC associated with antipsychotic treatment. RESULTS: The results showed that patients with schizophrenia exhibited decreased VMHC in the default-mode network (such as the precuneus and inferior parietal lobule) and the motor and sensory processing regions (such as the lingual gyrus, fusiform gyrus and cerebellum lobule VI), which could be normalised or denormalised by olanzapine treatment. In addition, negative correlations were found between decreased VMHC and symptom severity in the patients at baseline. CONCLUSIONS: The present study shows that olanzapine treatment can normalise or denormalise decreased homotopic connectivity in schizophrenia. The findings also provide a new perspective to understand treatment effects of antipsychotic drugs on homotopic connectivity in schizophrenia that contribute to the disconnection hypothesis of this disease.
OBJECTIVES: Deficits in homotopic connectivity have been implicated in schizophrenia. However, alterations in homotopic connectivity associated with antipsychotic treatments in schizophrenia remain unclear due to lack of longitudinal studies. METHODS: Seventeen drug-free patients with recurrent schizophrenia and 24 healthy controls underwent resting-state functional magnetic resonance imaging scans. The patients were scanned at three time points (baseline, at 6 weeks of treatment, and at 6 months of treatment). Voxel-mirrored homotopic connectivity (VMHC) was applied to analyse the imaging data to examine alterations in VMHC associated with antipsychotic treatment. RESULTS: The results showed that patients with schizophrenia exhibited decreased VMHC in the default-mode network (such as the precuneus and inferior parietal lobule) and the motor and sensory processing regions (such as the lingual gyrus, fusiform gyrus and cerebellum lobule VI), which could be normalised or denormalised by olanzapine treatment. In addition, negative correlations were found between decreased VMHC and symptom severity in the patients at baseline. CONCLUSIONS: The present study shows that olanzapine treatment can normalise or denormalise decreased homotopic connectivity in schizophrenia. The findings also provide a new perspective to understand treatment effects of antipsychotic drugs on homotopic connectivity in schizophrenia that contribute to the disconnection hypothesis of this disease.