Publication Type | Academic Article |
Authors | Tozlu C, Jamison K, Nguyen T, Zinger N, Kaunzner U, Pandya S, Wang Y, Gauthier S, Kuceyeski A |
Journal | Brain Behav |
Volume | 11 |
Issue | 10 |
Pagination | e2353 |
Date Published | 09/08/2021 |
ISSN | 2162-3279 |
Keywords | Multiple Sclerosis |
Abstract | BACKGROUND: In people with multiple sclerosis (pwMS), lesions with a hyperintense rim (rim+) on Quantitative Susceptibility Mapping (QSM) have been shown to have greater myelin damage compared to rim- lesions, but their association with disability has not yet been investigated. Furthermore, how QSM rim+ and rim- lesions differentially impact disability through their disruptions to structural connectivity has not been explored. We test the hypothesis that structural disconnectivity due to rim+ lesions is more predictive of disability compared to structural disconnectivity due to rim- lesions. METHODS: Ninety-six pwMS were included in our study. Individuals with Expanded Disability Status Scale (EDSS) <2 were considered to have lower disability (n = 59). For each gray matter region, a Change in Connectivity (ChaCo) score, that is, the percent of connecting streamlines also passing through a rim- or rim+ lesion, was computed. Adaptive Boosting was used to classify the pwMS into lower versus greater disability groups based on ChaCo scores from rim+ and rim- lesions. Classification performance was assessed using the area under ROC curve (AUC). RESULTS: The model based on ChaCo from rim+ lesions outperformed the model based on ChaCo from rim- lesions (AUC = 0.67 vs 0.63, p-value < .05). The left thalamus and left cerebellum were the most important regions in classifying pwMS into disability categories. CONCLUSION: rim+ lesions may be more influential on disability through their disruptions to the structural connectome than rim- lesions. This study provides a deeper understanding of how rim+ lesion location/size and resulting disruption to the structural connectome can contribute to MS-related disability. |
DOI | 10.1002/brb3.2353 |
PubMed ID | 34498432 |
PubMed Central ID | PMC8553317 |