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Mult Scler. 2017 Oct 1:1352458517736146. doi: 10.1177/1352458517736146. [Epub ahead of print]

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

Author information

1
Aix-Marseille University, CNRS, CRMBM, APHM, Marseille, France/Timone University Hospital, CEMEREM, Marseille, France/Siemens Healthineers, Saint-Denis, France.
2
Aix-Marseille University, CNRS, CRMBM, APHM, Marseille, France/Timone University Hospital, CEMEREM, Marseille, France.
3
Aix-Marseille University, CNRS, CRMBM, APHM, Marseille, France/Timone University Hospital, CEMEREM, Marseille, France/APHM, Timone University Hospital, Department of Neurology, Marseille, FranceCNRS, CRMBM UMR 7339, Medical School of Marseille, Aix-Marseille University, Marseille, France/AP-HM, CHU Timone, Department of Imaging, CEMEREM, Marseille, France/AP-HM, CHU Timone, Pole de Neurosciences Cliniques, Department of Neurology, Marseille, France.
4
Computer Assisted Clinical Medicine, Mannheim University Hospital, Heidelberg University, Mannheim, Germany.
5
Department of Radiology, University of Miami School of Medicine, Miami, FL, USA.

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 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.

KEYWORDS:

23Na-MRI; MRSI; demyelination; multiple sclerosis; neurodegeneration; stepwise regression

PMID:
29064346
DOI:
10.1177/1352458517736146

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