Abstract
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 23 Na-MR imaging and 3D- 1 H-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) T 2 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 23 Na accumulations with lower choline and glutamate–glutamine (Glx) levels in GM; 23 Na accumulations with lower N-acetyl aspartate (NAA), Glx levels and higher Myo-Inositol (m-Ins) in NAWM; and higher 23 Na, m-Ins levels with lower NAA in WM T 2 lesions. Regression models showed associations of TSC increase with reduced NAA in GM, NAWM and T 2 lesions, as well as higher total-creatine, and smaller decrease of m-Ins in T 2 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.
Original language | English (US) |
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Pages (from-to) | 39-47 |
Number of pages | 9 |
Journal | Multiple Sclerosis Journal |
Volume | 25 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2019 |
Keywords
- MRSI
- Na-MRI
- demyelination
- multiple sclerosis
- neurodegeneration
- stepwise regression
ASJC Scopus subject areas
- Neurology
- Clinical Neurology