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

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, Jean Philippe Ranjeva

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish (US)
JournalMultiple Sclerosis Journal
DOIs
StateAccepted/In press - Oct 1 2017

Fingerprint

Multiple Sclerosis
Sodium
Brain
Inositol
Relapsing-Remitting Multiple Sclerosis
Creatine
Choline
Neuroglia
Volunteers
White Matter
Gray Matter
N-acetylaspartate

Keywords

  • Na-MRI
  • demyelination
  • MRSI
  • multiple sclerosis
  • neurodegeneration
  • stepwise regression

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Metabolic counterparts of sodium accumulation in multiple sclerosis : A whole brain 23Na-MRI and fast 1H-MRSI study. / Donadieu, Maxime; Le Fur, Yann; Maarouf, Adil; Gherib, Soraya; Ridley, Ben; Pini, Lauriane; Rapacchi, Stanislas; Confort-Gouny, Sylviane; Guye, Maxime; Schad, Lothar R.; Maudsley, Andrew A; Pelletier, Jean; Audoin, Bertrand; Zaaraoui, Wafaa; Ranjeva, Jean Philippe.

In: Multiple Sclerosis Journal, 01.10.2017.

Research output: Contribution to journalArticle

Donadieu, M, Le Fur, Y, Maarouf, A, Gherib, S, Ridley, B, Pini, L, Rapacchi, S, Confort-Gouny, S, Guye, M, Schad, LR, Maudsley, AA, Pelletier, J, Audoin, B, Zaaraoui, W & Ranjeva, JP 2017, 'Metabolic counterparts of sodium accumulation in multiple sclerosis: A whole brain 23Na-MRI and fast 1H-MRSI study', Multiple Sclerosis Journal. https://doi.org/10.1177/1352458517736146
Donadieu, Maxime ; Le Fur, Yann ; Maarouf, Adil ; Gherib, Soraya ; Ridley, Ben ; Pini, Lauriane ; Rapacchi, Stanislas ; Confort-Gouny, Sylviane ; Guye, Maxime ; Schad, Lothar R. ; Maudsley, Andrew A ; Pelletier, Jean ; Audoin, Bertrand ; Zaaraoui, Wafaa ; Ranjeva, Jean Philippe. / Metabolic counterparts of sodium accumulation in multiple sclerosis : A whole brain 23Na-MRI and fast 1H-MRSI study. In: Multiple Sclerosis Journal. 2017.
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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.",
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T1 - Metabolic counterparts of sodium accumulation in multiple sclerosis

T2 - A whole brain 23Na-MRI and fast 1H-MRSI study

AU - Donadieu, Maxime

AU - Le Fur, Yann

AU - Maarouf, Adil

AU - Gherib, Soraya

AU - Ridley, Ben

AU - Pini, Lauriane

AU - Rapacchi, Stanislas

AU - Confort-Gouny, Sylviane

AU - Guye, Maxime

AU - Schad, Lothar R.

AU - Maudsley, Andrew A

AU - Pelletier, Jean

AU - Audoin, Bertrand

AU - Zaaraoui, Wafaa

AU - Ranjeva, Jean Philippe

PY - 2017/10/1

Y1 - 2017/10/1

N2 - 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.

AB - 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.

KW - Na-MRI

KW - demyelination

KW - MRSI

KW - multiple sclerosis

KW - neurodegeneration

KW - stepwise regression

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