Philipp Eisele1, Simon Konstandin2, Kristina Szabo3, Anne Ebert4, Christina Roßmanith5, Nadia Paschke6, Martin Kerschensteiner7, Michael Platten8, Stefan O Schoenberg9, Lothar R Schad10, Achim Gass11. 1. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: philipp.eisele@medma.uni-heidelberg.de. 2. Fraunhofer MEVIS, Am Fallturm 1, 28359 Bremen, Germany; Computer Assisted Clinical Medicine, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: simon.konstandin@mevis.fraunhofer.de. 3. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: kristina.szabo@umm.de. 4. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: anne.ebert@umm.de. 5. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: christina.rossmanith@umm.de. 6. Computer Assisted Clinical Medicine, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: nadia.paschke@medma.uni-heidelberg.de. 7. Institute of Clinical Neuroimmunology, University Hospital and Biomedical Center, Ludwig-Maximilians University Munich, 81377 Munich, Germany; Munich Cluster of Systems Neurology (SyNergy), 81377 Munich, Germany. Electronic address: Martin.Kerschensteiner@med.uni-muenchen.de. 8. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: michael.platten@umm.de. 9. Institute of Clinical Radiology and Nuclear Medicine, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: stefan.schoenberg@umm.de. 10. Computer Assisted Clinical Medicine, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: lothar.schad@medma.uni-heidelberg.de. 11. Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Electronic address: achim.gass@medma.uni-heidelberg.de.
Abstract
BACKGROUND: Several studies have reported the characteristics of acute multiple sclerosis (MS) lesions on diffusion-weighted magnetic resonance imaging (DWI MRI). Current publications reported a transient reduction of the apparent diffusion coefficient (ADC) delineating an early phase of lesion evolution, before increased diffusion occurs in parallel to blood-brain-barrier (BBB) breakdown. Sodium MRI might provide another perspective on lesion development, but clinical applications have been limited to high field MR systems. The objective in this study was to investigate the temporal evolution of acute MS lesions using conventional (T2-fluid-attenuated inversion recovery (T2-FLAIR) images, post-contrast T1-weighted images), diffusion and sodium MRI. METHODS: Initial and follow-up MRI (23Na and 1H MRI) were performed on a 3T scanner. Quantitative assessment of total sodium concentration (TSC) and ADC was performed. The study was designed for frequent follow-up MRI examinations during 4 weeks after the initial presentation. RESULTS: Thirty-one acute MS lesions (7 lesions with reduced diffusion) in eleven MS patients were included. On initial MRI, TSC in contrast-enhancing lesions was increased when compared to the normal-appearing white matter (NAWM), while lesions with an initial reduced diffusion showed a TSC comparable to the NAWM. On follow-up MRI, in lesions with reduced diffusion subsequent increase of ADC and TSC values occurred along with signs of the development of vasogenic edema and contrast-enhancement. After four weeks, TSC values decreased along with regression of vasogenic edema and contrast-enhancement. CONCLUSIONS: In lesions with a reduction of the ADC sodium levels are near normal and precede signs of BBB breakdown. These findings suggest a relatively preserved tissue structure in this early phase of lesion evolution.
BACKGROUND: Several studies have reported the characteristics of acute multiple sclerosis (MS) lesions on diffusion-weighted magnetic resonance imaging (DWI MRI). Current publications reported a transient reduction of the apparent diffusion coefficient (ADC) delineating an early phase of lesion evolution, before increased diffusion occurs in parallel to blood-brain-barrier (BBB) breakdown. Sodium MRI might provide another perspective on lesion development, but clinical applications have been limited to high field MR systems. The objective in this study was to investigate the temporal evolution of acute MS lesions using conventional (T2-fluid-attenuated inversion recovery (T2-FLAIR) images, post-contrast T1-weighted images), diffusion and sodium MRI. METHODS: Initial and follow-up MRI (23Na and 1H MRI) were performed on a 3T scanner. Quantitative assessment of total sodium concentration (TSC) and ADC was performed. The study was designed for frequent follow-up MRI examinations during 4 weeks after the initial presentation. RESULTS: Thirty-one acute MS lesions (7 lesions with reduced diffusion) in eleven MS patients were included. On initial MRI, TSC in contrast-enhancing lesions was increased when compared to the normal-appearing white matter (NAWM), while lesions with an initial reduced diffusion showed a TSC comparable to the NAWM. On follow-up MRI, in lesions with reduced diffusion subsequent increase of ADC and TSC values occurred along with signs of the development of vasogenic edema and contrast-enhancement. After four weeks, TSC values decreased along with regression of vasogenic edema and contrast-enhancement. CONCLUSIONS: In lesions with a reduction of the ADC sodium levels are near normal and precede signs of BBB breakdown. These findings suggest a relatively preserved tissue structure in this early phase of lesion evolution.
Authors: Sherif A Mohamed; Katrin Herrmann; Anne Adlung; Nadia Paschke; Lucrezia Hausner; Lutz FrÖlich; Lothar Schad; Christoph Groden; Hans Ulrich Kerl Journal: In Vivo Date: 2021 Jan-Feb Impact factor: 2.155