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...
Gespeichert in:
| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
2019
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| In: |
Multiple sclerosis journal
Year: 2017, Jahrgang: 25, Heft: 1, Pages: 39-47 |
| ISSN: | 1477-0970 |
| DOI: | 10.1177/1352458517736146 |
| Online-Zugang: | Verlag, Volltext: http://dx.doi.org/10.1177/1352458517736146 Verlag, Volltext: http://journals.sagepub.com/doi/10.1177/1352458517736146 
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| Verfasserangaben: | 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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| 245 | 1 | 0 | |a Metabolic counterparts of sodium accumulation in multiple sclerosis |b a whole brain 23Na-MRI and fast 1H-MRSI study |c 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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| 520 | |a 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. | ||
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