Metabolic counterparts of sodium accumulation in multiple sclerosis: a whole brain 23Na-MRI and fast 1H-MRSI study

Background: Increase of brain total sodium concentrations (TSC) is present in multiple sclerosis (MS), but its pathological involvement has not been assessed yet. Objective: To determine in vivo the metabolic counterpart of brain sodium accumulation. Materials/methods: Whole brain 23Na-MR imaging an...

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Bibliographic Details
Main Authors: Donadieu, Maxime (Author) , Schad, Lothar R. (Author)
Format: Article (Journal)
Language:English
Published: 2019
In: Multiple sclerosis journal
Year: 2017, Volume: 25, Issue: 1, Pages: 39-47
ISSN:1477-0970
DOI:10.1177/1352458517736146
Online Access:Verlag, Volltext: http://dx.doi.org/10.1177/1352458517736146
Verlag, Volltext: http://journals.sagepub.com/doi/10.1177/1352458517736146
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Author Notes:Maxime Donadieu, Yann Le Fur, Adil Maarouf, Soraya Gherib, Ben Ridley, Lauriane Pini, Stanislas Rapacchi, Sylviane Confort-Gouny, Maxime Guye, Lothar R Schad, Andrew A Maudsley, Jean Pelletier, Bertrand Audoin, Wafaa Zaaraoui and Jean-Philippe Ranjeva
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Summary:Background: Increase of brain total sodium concentrations (TSC) is present in multiple sclerosis (MS), but its pathological involvement has not been assessed yet. Objective: To determine in vivo the metabolic counterpart of brain sodium accumulation. Materials/methods: Whole brain 23Na-MR imaging and 3D-1H-EPSI data were collected in 21 relapsing-remitting multiple sclerosis (RRMS) patients and 20 volunteers. Metabolites and sodium levels were extracted from several regions of grey matter (GM), normal-appearing white matter (NAWM) and white matter (WM) T2 lesions. Metabolic and ionic levels expressed as Z-scores have been averaged over the different compartments and used to explain sodium accumulations through stepwise regression models. Results: MS patients showed significant 23Na accumulations with lower choline and glutamate-glutamine (Glx) levels in GM; 23Na accumulations with lower N-acetyl aspartate (NAA), Glx levels and higher Myo-Inositol (m-Ins) in NAWM; and higher 23Na, m-Ins levels with lower NAA in WM T2 lesions. Regression models showed associations of TSC increase with reduced NAA in GM, NAWM and T2 lesions, as well as higher total-creatine, and smaller decrease of m-Ins in T2 lesions. GM Glx levels were associated with clinical scores. Conclusion: Increase of TSC in RRMS is mainly related to neuronal mitochondrial dysfunction while dysfunction of neuro-glial interactions within GM is linked to clinical scores.
Item Description:First Published October 24, 2017
Gesehen am 19.06.2019
Im Titelzusatz ist "23" und "1" hochgestellt
Physical Description:Online Resource
ISSN:1477-0970
DOI:10.1177/1352458517736146