P 125
Investigation of the Value of Sodium (23Na) MRI in Multiple Sclerosis: Focus on Microscopic
Tissue Changes
Philipp Eisele1, Simon Konstandin2, Martin Griebe1, Kristina Szabo1, Marc E. Wolf1, Angelika Alonso1,
Christopher J. Schwarzbach1, Anne Ebert1, Christina Roßmanith1, Christel Weiß3, Melissa Ong4,
Stefan Schönberg4, Lothar R. Schad5, Achim Gass1
1Universität
Heidelberg, Universitätsmedizin Mannheim, Neurologie, Mannheim, Germany
2Universität
Bremen, Faculty 01 (Physics/Electrical Engineering), MR-Imaging and Spectroscopy,
Bremen, Germany
3Universität
Heidelberg, Universitätsmedizin Mannheim, Department for Statistical Analysis,
Mannheim, Germany
4Universität
Heidelberg, Universitätsmedizin Mannheim, Institute of Clinical Radiology and Nuclear
Medicine, Mannheim, Germany
5Universität
Heidelberg, Universitätsmedizin Mannheim, Computer Assisted Clinical Medicine,
Mannheim, Germany
Background: Conventional magnetic resonance imaging (MRI) is currently the most applied
biomarker in multiple sclerosis (MS), but not all MRI parameters correlate with clinical impairment.
Microscopic tissue damage causing diffuse axonal damage seems to play a major pathogenetic role in
MS. Recent studies using sodium (23Na) imaging suggested that increased sodium concentrations are
likely to reflect neuroaxonal damage leading to disease progression and disability.
Objective: To detect and quantify different degrees of disease-related tissue changes in the
microstructure outside macroscopically visible lesions using a multiparametric MRI protocol including
1H, 23Na and diffusion MRI in a large cohort of MS patients.
Methods: We performed 23Na, 1H and diffusion MRI in 14 healthy controls (HC), 18 patients with a
clinically isolated syndrome (CIS), 47 patients with early relapsing-remitting multiple sclerosis (RRMS,
< 5 years disease duration), 20 patients with advanced RRMS and 10 patients with secondary
progressive multiple sclerosis (SPMS).
Results: Sodium concentrations of the grey and white matter (GM, WM) were significantly higher in
advanced RRMS (GM: 46.7 ± 3.1 mM, WM: 40.5 ± 2.7 mM) and SPMS (GM: 52.5 ± 5.4 mM, WM:
46.2 ± 5.0 mM) compared to HC (GM: 40.1 ± 3.3 mM, WM: 34.9 ± 2.4 mM), CIS (GM: 41.5 ± 2.7 mM,
WM: 35.6 ± 2.2 mM) and early RRMS (GM: 43.8 ± 2.5 mM, WM: 38.1 ± 2.6 mM; p < 0.05). Total brain
volume (TBV) and brain volume of the grey (GMBV) and white matter (WMBV) was significantly lower
in advanced RRMS (TBV: 1396 ± 68 ml; GMBV: 706 ± 44 ml; WMBV: 690 ± 34 ml) and SPMS (TBV:
1352 ± 69 ml; GMBV: 684 ± 38 ml; WMBV: 668 ± 37 ml) compared to controls (TBV: 1477 ± 52 ml;
GMBV: 744 ± 28 ml; WMBV: 732 ± 37 ml), CIS (TBV: 1472 ± 67 ml, GMBV: 748 ± 41 ml; WMBV: 724
± 34 ml) and early RRMS (TBV: 1454 ± 56 ml; GMBV: 748 ± 35 ml; WMBV: 706 ± 33 ml; p < 0.05).
Apparent diffusion coefficient values of the white matter were significantly higher in SPMS (0.79 ± 0.07
x 10-3 mm/s2) compared to HC (0.66 ± 0.04), CIS (0.71 ± 0.04) and early RRMS (0.72 ± 0.06, p <
0.05). Strong correlations between MRI parameters and EDSS were observed for brain volume and
sodium concentrations of the grey and white matter (p < 0.001). Figure 1 shows representative MRI
images of all subgroups.
Conclusion: Sodium accumulation, decreased brain volume and increased diffusion were already
present in patients with CIS and progressed dramatically throughout the disease course. These
findings could possibly better identify patients early in the disease to improve effective treatment
choices in order to achieve favourable long-term outcomes. Loss of brain volume and sodium
concentrations showed strong correlation with disability indicating that these parameters are highly
sensitive to demonstrate irreversible damage.