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Updated: May 12, 2026
Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
Peak width of skeletonized mean diffusivity: a novel biomarker for white matter damage in spinocerebellar ataxia type
Nan Chen1,2,3, Juan Peng4, Fei Xiong5
1Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Purpose:
Peak width of skeletonized mean diffusivity (PSMD) is a robust and fully automated imaging marker employed to detect microstructural damage in white matter. This study aimed to evaluate whether PSMD reflects the severity of white matter damage and tracks disease progression in patients with spinocerebellar ataxia type 2 (SCA2).
Methods:
Nine patients with SCA2 and sixteen age- and gender-matched healthy controls were enrolled. Clinical and imaging data were collected at baseline and after 3.5 years. Each participant underwent MRI scans twice to obtain diffusion tensor imaging data, from which PSMD were automatically calculated. Differences in PSMD between SCA2 patients and healthy controls were analyzed using a linear mixed model. Additionally, Spearman's rank correlations were employed to assess associations between PSMD values and clinical variables.
Results:
Patients with SCA2 exhibited higher PSMD values at baseline and follow-up compared to HCs, indicating more severe white matter damage. Longitudinal data revealed a continual increase in PSMD values in SCA2 patients over time. The mixed-effects model confirmed significant differences in PSMD values between the two groups, as well as an interaction effect suggesting different progression rates. These findings suggest that SCA2 associates with progressive deterioration of white matter. No significant correlations were observed between PSMD values and clinical variables in this study.
Conclusion:
This study underscores the potential of PSMD as a neuroimaging biomarker for detecting microstructural white matter damage and monitoring disease progression in patients with SCA2.
