Increase of brain total sodium concentrations (TSC) is present in multiple sclerosis (MS), but its pathological involvement has not been assessed yet.
To determine in vivo the metabolic counterpart of brain sodium accumulation.
Whole brain
Na-MR imaging and 3D-
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
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.
MS patients showed significant
Na accumulations with lower choline and glutamate-glutamine (Glx) levels in GM;
Na accumulations with lower N-acetyl aspartate (NAA), Glx levels and higher Myo-Inositol (m-Ins) in NAWM; and higher
Na, m-Ins levels with lower NAA in WM T
lesions. Regression models showed associations of TSC increase with reduced NAA in GM, NAWM and T
lesions, as well as higher total-creatine, and smaller decrease of m-Ins in T
lesions. GM Glx levels were associated with clinical scores.
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
