Background Chronic active MS lesions with paramagnetic rim can be identified by high-pass filtered (HPF) phase imaging or quantitative susceptibility mapping (QSM). Purpose The objective was to compare the ability of HPF and QSM to identify MS lesions with greater myelin damage and to distinguish MS patients with increased clinical disability. Material and Methods Eighty-six patients were scanned with gradient echo sequence for lesion rim detection and FAST-T2 sequence for myelin water fraction (MWF) mapping. Chronic lesions were classified based on the presence/absence of rim on HPF and QSM images (HPF rim+/QSM rim+, HPF rim+/QSM rim-, HPF rim-/QSM rim+, HPF rim-/QSM rim-). A lesion-level linear mixed-effects model with MWF as outcome was used to compare myelin damage among the lesion groups. A multivariate patient-level linear regression model was fit to establish the association between Expanded Disease Status Scale (EDSS) and the number of rim lesions (zero vs. one or more). Results Of 2229 lesions, 96 (8.8%) were HPF rim+/QSM rim+, 211 (9.5%) were HPF rim+/QSM rim-, and the remainder had no rim. Adjusting for other factors, HPF rim+/QSM rim+ lesions had on average significantly lower MWF than both HPF rim+/QSM rim- (p<0.001) and HPF rim-/QSM rim- (p<0.001) lesions, while the MWF difference between HPF rim+/QSM rim- and HPF rim-/QSM rim- lesions was not statistically significant (p=0.309). Having at least one QSM rim+ lesion was associated with an increase in EDSS compared to having no QSM rim+ lesions, holding all other factors constant (p=0.026). The relationship between having one or more HPF rim+ lesions vs. having no HPF rim+ lesions and EDSS was not statistically significant. Conclusion QSM identifies chronic MS lesions with paramagnetic rim that on average have greater myelin damage. QSM may be a valuable tool for studying the impact of rim lesions on clinical disability in MS.
Motor recovery following ischemic stroke is contingent on the ability of surviving brain networks to compensate for damaged tissue. In rodent models, sensory and motor cortical representations have been shown to remap onto intact tissue around the lesion site, but remapping to more distal sites (e.g. in the contralesional hemisphere) has also been observed. Resting state functional connectivity (FC) analysis has been employed to study compensatory network adaptations in humans, but mechanisms and time course of motor recovery are not well understood. Here, we examine longitudinal FC in 23 first-episode ischemic pontine stroke patients (34-74 years old; 8 female, 15 male) and utilize a graph matching approach to identify patterns of regional functional connectivity reorganization during recovery. We quantified functional reorganization between several intervals ranging from 1 week to 6 months following stroke, and demonstrated that the areas that undergo functional reorganization most frequently are in cerebellar/subcortical networks. Brain regions with more structural connectome disruption due to the stroke also had more functional remapping over time. Finally, we show that the amount of functional reorganization between time points is correlated with the extent of motor recovery observed between those time points in the early to late subacute phases, and, furthermore, individuals with greater baseline motor impairment demonstrate more extensive early subacute functional reorganization (from one to two weeks post-stroke) and this reorganization correlates with better motor recovery at 6 months. Taken together, these results suggest that our graph matching approach can quantify recovery-relevant, whole-brain functional connectivity network reorganization after stroke.
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