Aldosterone secretion (part of hpa axis dysregulation in RRMS) increases sodium retention and upregulates sodium channels.http://registration.akm.ch/einsicht.php ... KEN_ID=900
Brain sodium accumulation and spreading correlate with disability in multiple sclerosis
W. Zaaraoui, B. Audoin, S. Konstandin, A.M. Nagel, E. Soulier, I. Malikova, A. Rico, F. Reuter, P. Viout, S. Confort-Gouny, P.J. Cozzone, J. Pelletier, L.R. Schad, J.-P. Ranjeva (Marseille, FR; Mannheim, Heidelberg, DE)
Purpose: Recent histopathological studies have highlighted the potential key role of sodium accumulation that leads to neuronal injury in multiple sclerosis (MS). We aimed to quantify brain sodium accumulation and characterize for the first time the spatial location of sodium abnormalities at different stages of relapsing remitting multiple sclerosis (RRMS) using sodium MRI.
Materials and Methods: MR explorations were performed at 3T (Verio, Siemens) in two groups of RRMS patients, 14 early RRMS (disease duration<5years) and 12 advanced RRMS (>5years) and 15 controls. Sodium 23Na MRI was acquired using a double-tuned 23Na-1H volume head coil (RapidBiomed) and a density-adapted 3D radial projection reconstruction pulse sequence (Nagel et al 2009) (TE=200µs, TR=120ms, 17000 projections, resolution 3.6x3.6x3.6 mm3) with two external references. Proton MRI 3D-MPRAGE (resolution 1x1x1mm3) and T2-weighted were also obtained. The post-processing included reconstruction of the quantitative 3D radial sodium images (q23Na-MRI); coregistration of the q23Na-MRI with 1H-3D-MPRAGE; normalization and segmentation of the 1H-3D-MPRAGE (VBM8); application of the resulting grey matter (GM), white matter (WM) and T2-lesions masks to the normalized q23Na-MRI; smoothing of the resulting q23Na-MRI maps and statistical mapping analysis (SPM8) to locate total sodium concentration (TSC) abnormalities.
Results: For the two groups of MS patients, TSC was increased inside demyelinating lesions while increased TSC was observed in normal appearing WM and GM only in advanced RRMS. In patients, increased TSC inside GM was correlated to disability (EDSS) (p=0.046) and T2 lesion load (p=0.003) but not to disease duration (p=0.089). Statistical mapping analysis (SPM8, Anova, p<0.001) showed that abnormal TSC are already present at the early stage of RRMS in limited regions (brainstem, cerebellum and temporal poles) and are widespread, affecting the whole brain parenchyma, at the advanced stage of RRMS. EDSS was correlated to TSC increases inside a coherent motor network including bilateral cerebellum, primary motor area and bilateral prefrontal cortices (SPM8, simple regression, p<0.001).
Conclusions: Total sodium accumulation dramatically increases in advanced stage of RRMS especially in the normal appearing brain tissues concomitantly to disability. Further brain sodium MRI longitudinal studies with more patients are required to help monitoring the occurrence of tissue injury and disability.