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Pathophysiology of MS damage and repair: Linking cerebral hypoperfusion to the development of irreversible tissue loss in MS using MRI

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Lipp,  Ilona       
Department Neurophysics (Weiskopf), MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Brain Research Imaging Centre, School of Psychology, Cardiff University, United Kingdom;

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Citation

Mascali, D., Villani, A., Chiarelli, A. M., Biondetti, E., Lipp, I., Digiovanni, A., et al. (2023). Pathophysiology of MS damage and repair: Linking cerebral hypoperfusion to the development of irreversible tissue loss in MS using MRI. European Journal of Neurology. doi:10.1111/ene.15827.


Cite as: https://hdl.handle.net/21.11116/0000-000D-1581-9
Abstract
Background: Reduced cerebral perfusion has been observed in Multiple Sclerosis and may contribute to tissue loss both acutely and chronically. Here, we test the hypothesis that hypoperfusion occurs in MS and relates to the presence of irreversible tissue damage.

Methods: In 91 patients with relapsing MS and 26 healthy controls (HC), GM CBF was assessed using pulsed arterial spin labelling (pASL). GM volume, T1 hypointense and T2 hyperintense lesion volumes (T1LV and T2LV, respectively) and the proportion of T2-hyperintense lesion volume that appears hypointense on T1-weighted MRI (T1LV/T2LV) were quantified. GM CBF and GM volume were evaluated globally, as well as regionally, using an atlas-based approach.

Results: Global GM CBF was lower in patients (56.9±12.3 ml/100g/min) than in HC (67.7±10.0 ml/100g/min) (p<0.001), a difference that was widespread across brain regions. While total GM volume was comparable between groups, significant reductions were observed in a subset of subcortical structures. GM CBF negatively correlated with T1LV (r=-0.43, p=0.0002) and T1LV/T2LV (r=-0.37, p=0.0004), but not with T2LV.

Conclusions: GM hypoperfusion occurs in MS and is associated with irreversible WM damage, thus suggesting that cerebral hypoperfusion may actively contribute and possibly precede neurodegeneration by hampering tissue repair abilities in MS.