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Updated: Dec 6, 2025
A Standardized Pipeline for Examining Human Cerebellar Grey Matter Morphometry using Structural Magnetic Resonance Imaging
Published on: February 4, 2022
Gray matter atrophy patterns within the cerebellum-neostriatum-cortical network in SCA3
Jing Guo1, Hui Chen2, Bharat B Biswal1
1From The Clinical Hospital of Chengdu Brain Science Institute, MOE Key Lab for Neuroinformation (J.G., B.B.B., X.G., H.Z., L.L., Y.F., S.H., Huafu Chen), School of Medicine (J.G.), and School of Life Science and Technology, Center for Information in Medicine (X.G., H.Z., L.L., Y.F., S.H.), University of Electronic Science and Technology of China, Chengdu; Departments of Radiology (Hui Chen, Y.Z., J.L, J.W., C.L., Huafu Chen) and Laboratory Medicine (L.F.), Southwest Hospital, Department of Medical Genetics, College of Basic Medical Science (L.D.), and Department of Biomedical Engineering & Imaging Medicine (Q.W.), Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China; and Department of Biomedical Engineering (B.B.B.), New Jersey Institute of Technology, Newark.
Objective:
To investigate the spatial patterns and the probable sequences of gray matter atrophy in spinocerebellar ataxia type 3 (SCA3).
Methods:
A total of 47 patients with SCA3 and 49 age- and sex-matched healthy controls participated in the study. High-resolution T1-weighted MRI were examined in all participants. We used the causal network of structural covariance (CasCN) to identify the sequence of gray matter atrophy patterns. This was achieved by applying Granger causality analysis to a gray matter atrophy staging scheme performed by voxel-based morphometry from the network level.
Results:
Participants in the premanifest stage of the disease showed the presence of focal gray matter atrophy in the vermis. As the disease duration increased, there was progressive gray matter atrophy in the cerebellar, neostriatum, frontal lobe, and parietal lobe. The patients with SCA3 also showed proximal and distal cortical atrophy sequences exerting from the vermis to the regions mainly located in the cerebellum-neostriatum-cortical network.
Conclusion:
Our results, although preliminary in nature, indicate that the gray matter atrophy in SCA3 lies and extends to involve more regions according to distinct anatomical patterns, mainly in the cerebellum-neostriatum-cortical network. These findings advance our understanding on the natural history of structural damage in SCA3, while confirming known clinical features. This could provide unique insight into the ordered sequential process of regional brain atrophy that targets a particular network.
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