Contributions
Abstract: P1058
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
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 total sodium concentrations (TSC) 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.
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: Normal appearing grey and white matter (GM, WM) TSC 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, WM: 46.2 ± 5.0) vs. HC (GM: 40.1 ± 3.3, WM: 34.9 ± 2.4), CIS (GM: 41.5 ± 2.7, WM: 35.6 ± 2.2) and early RRMS (GM: 43.8 ± 2.5, WM: 38.1 ± 2.6). Total brain volume (TBV) and grey matter volume (GMV) and white matter (WMV) was significantly lower in advanced RRMS (TBV: 1396 ± 68 ml; GMV: 706 ± 44 ml; WMV: 690 ± 34 ml) and SPMS (TBV: 1352 ± 69; GMV: 684 ± 38; WMV: 668 ± 37) vs. HC (TBV: 1477 ± 52; GMV: 744 ± 28; WMV: 732 ± 37), CIS (TBV: 1472 ± 67, GMV: 748 ± 41; WMV: 724 ± 34) and early RRMS (TBV: 1454 ± 56; GMV: 748 ± 35; WMV: 706 ± 33). Apparent diffusion coefficients of the NAWM were significantly higher in SPMS (0.79 ± 0.07 x 10-3 mm/s2) vs. 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 TBV and TSC of the NAGM and NAWM.
Conclusion: TSC increase, loss of TBV, GMV, WMV and increased diffusion were already present in patients with CIS and progress in later stages of MS and SPMS. The loss of TBV, GMV, WMV and increase of TSC in NAGM and NAWM showed strong correlation with EDSS suggesting that these parameters are highly sensitive to irreversible tissue damage. Our findings indicate that increased sodium tissue concentrations are closely reflecting tissue damage in MS.
Disclosure: P. Eisele - travel expenses from Bayer Health Care.
S. Konstandin - Nothing to disclose.
M. Griebe - lecturing fees from Biogen.
K. Szabo - financial support for research from Merck Serono.
M. Wolf - lecturing fees from Biogen.
A. Alonso - is on the editorial board for Advances in Neuroscience and Cerebrovascular Diseases.
C.J. Schwarzbach - Nothing to disclose.
A. Ebert - Nothing to disclose.
C. Roßmanith - Nothing to disclose.
C. Weiß - Nothing to disclose.
M. Ong - Nothing to disclose.
S. O. Schoenberg - the institute of clinical radiology and nuclear medicine has research agreements with Siemens Healthcare GmbH.
L. R. Schad - Nothing to disclose.
A. Gass - honoraria for lecturing, travel expenses for attending meetings, and financial support for research from Bayer Schering, Biogen Idec, Merck Serono, Novartis and TEVA Neurosciences. All other authors report no disclosures.
Abstract: P1058
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
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 total sodium concentrations (TSC) 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.
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: Normal appearing grey and white matter (GM, WM) TSC 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, WM: 46.2 ± 5.0) vs. HC (GM: 40.1 ± 3.3, WM: 34.9 ± 2.4), CIS (GM: 41.5 ± 2.7, WM: 35.6 ± 2.2) and early RRMS (GM: 43.8 ± 2.5, WM: 38.1 ± 2.6). Total brain volume (TBV) and grey matter volume (GMV) and white matter (WMV) was significantly lower in advanced RRMS (TBV: 1396 ± 68 ml; GMV: 706 ± 44 ml; WMV: 690 ± 34 ml) and SPMS (TBV: 1352 ± 69; GMV: 684 ± 38; WMV: 668 ± 37) vs. HC (TBV: 1477 ± 52; GMV: 744 ± 28; WMV: 732 ± 37), CIS (TBV: 1472 ± 67, GMV: 748 ± 41; WMV: 724 ± 34) and early RRMS (TBV: 1454 ± 56; GMV: 748 ± 35; WMV: 706 ± 33). Apparent diffusion coefficients of the NAWM were significantly higher in SPMS (0.79 ± 0.07 x 10-3 mm/s2) vs. 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 TBV and TSC of the NAGM and NAWM.
Conclusion: TSC increase, loss of TBV, GMV, WMV and increased diffusion were already present in patients with CIS and progress in later stages of MS and SPMS. The loss of TBV, GMV, WMV and increase of TSC in NAGM and NAWM showed strong correlation with EDSS suggesting that these parameters are highly sensitive to irreversible tissue damage. Our findings indicate that increased sodium tissue concentrations are closely reflecting tissue damage in MS.
Disclosure: P. Eisele - travel expenses from Bayer Health Care.
S. Konstandin - Nothing to disclose.
M. Griebe - lecturing fees from Biogen.
K. Szabo - financial support for research from Merck Serono.
M. Wolf - lecturing fees from Biogen.
A. Alonso - is on the editorial board for Advances in Neuroscience and Cerebrovascular Diseases.
C.J. Schwarzbach - Nothing to disclose.
A. Ebert - Nothing to disclose.
C. Roßmanith - Nothing to disclose.
C. Weiß - Nothing to disclose.
M. Ong - Nothing to disclose.
S. O. Schoenberg - the institute of clinical radiology and nuclear medicine has research agreements with Siemens Healthcare GmbH.
L. R. Schad - Nothing to disclose.
A. Gass - honoraria for lecturing, travel expenses for attending meetings, and financial support for research from Bayer Schering, Biogen Idec, Merck Serono, Novartis and TEVA Neurosciences. All other authors report no disclosures.