Zhizheng Zhuo1, Yunyun Duan1, Decai Tian2, Xinli Wang3, Chenyang Gao4, Jinli Ding5, Fenglian Zheng5, Tian Zhang6, Xinghu Zhang4, Frederik Barkhof7, Fu-Dong Shi8, Yaou Liu1. 1. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China/Tiantan Image Research Center, China National Clinical Research Center for Neurological Diseases, Beijing, P.R. China. 2. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China/China National Clinical Research Center for Neurological Diseases, Beijing, P.R. China/Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing, P.R. China. 3. Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, P.R. China. 4. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China. 5. Department of Radiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China. 6. Department of Radiology, Beijing Bo'ai Hospital, China Rehabilitation Research Center, Beijing, P.R. China. 7. Department of Radiology and Nuclear Medicine, Amsterdam University Medical Center, Amsterdam, The Netherlands/Queen Square Institute of Neurology and Center for Medical Image Computing, University College London, London, UK. 8. Center for Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, P.R. China/China National Clinical Research Center for Neurological Diseases, Beijing, P.R. China/Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, P.R. China.
Abstract
BACKGROUND: The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function is unknown. OBJECTIVES: The aim of this study was to study the multimodal brain MRI alterations in MOGAD and to investigate their clinical significance. METHODS: A total of 17 MOGAD, 20 aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4 + NMOSD), and 28 healthy controls (HC) were prospectively recruited. Voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) were compared between groups. Clinical associations and differential diagnosis were determined using partial correlation and stepwise logistic regression. RESULTS: In comparison with HC, MOGAD had GM atrophy in frontal and temporal lobe, insula, thalamus, and hippocampus, and WM fiber disruption in optic radiation and anterior/posterior corona radiata; DC decreased in cerebellum and increased in temporal lobe. Compared to AQP4 + NMOSD, MOGAD presented lower GM volume in postcentral gyrus and decreased DC in cerebellum. Hippocampus/parahippocampus atrophy associated with Expanded Disability Status Scale (R = -0.55, p = 0.04) and California Verbal Learning Test (R = 0.62, p = 0.031). The differentiation of MOGAD from AQP4 + NMOSD achieved an accuracy of 95% using FA in splenium of corpus callosum and DC in occipital gyrus. CONCLUSION: Distinct structural and functional alterations were identified in MOGAD. Hippocampus/parahippocampus atrophy associated with clinical disability and cognitive impairment.
BACKGROUND: The impact of myelin oligodendrocyte glycoprotein antibody disease (MOGAD) on brain structure and function is unknown. OBJECTIVES: The aim of this study was to study the multimodal brain MRI alterations in MOGAD and to investigate their clinical significance. METHODS: A total of 17 MOGAD, 20 aquaporin-4 antibody seropositive neuromyelitis optica spectrum disorders (AQP4 + NMOSD), and 28 healthy controls (HC) were prospectively recruited. Voxel-wise gray matter (GM) volume, fractional anisotropy (FA), mean diffusivity (MD), and degree centrality (DC) were compared between groups. Clinical associations and differential diagnosis were determined using partial correlation and stepwise logistic regression. RESULTS: In comparison with HC, MOGAD had GM atrophy in frontal and temporal lobe, insula, thalamus, and hippocampus, and WM fiber disruption in optic radiation and anterior/posterior corona radiata; DC decreased in cerebellum and increased in temporal lobe. Compared to AQP4 + NMOSD, MOGAD presented lower GM volume in postcentral gyrus and decreased DC in cerebellum. Hippocampus/parahippocampus atrophy associated with Expanded Disability Status Scale (R = -0.55, p = 0.04) and California Verbal Learning Test (R = 0.62, p = 0.031). The differentiation of MOGAD from AQP4 + NMOSD achieved an accuracy of 95% using FA in splenium of corpus callosum and DC in occipital gyrus. CONCLUSION: Distinct structural and functional alterations were identified in MOGAD. Hippocampus/parahippocampus atrophy associated with clinical disability and cognitive impairment.