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April 18, 2017; 88 (16 Supplement) April 26, 2017

Axonal degeneration is present in benign multiple sclerosis. (P4.403)

Adil Maarouf, Soraya Gherib, Fanelly Pariollaud, Maxime GUYE, Audrey Rico Lamy, Bertrand Audoin, Jean Philippe Ranjeva, Wafaa Zaaraoui, Jean Pelletier
First published April 17, 2017,
Adil Maarouf
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Soraya Gherib
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Fanelly Pariollaud
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Maxime GUYE
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Audrey Rico Lamy
2Hospital Timone Adultes Marseille, Cedex 5 France
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Bertrand Audoin
2Hospital Timone Adultes Marseille, Cedex 5 France
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Jean Philippe Ranjeva
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Wafaa Zaaraoui
1CEMEREM, Aix Marseille Université CRMBM-CNRS-UMR7339 Marseille France
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Jean Pelletier
2Hospital Timone Adultes Marseille, Cedex 5 France
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Citation
Axonal degeneration is present in benign multiple sclerosis. (P4.403)
Adil Maarouf, Soraya Gherib, Fanelly Pariollaud, Maxime GUYE, Audrey Rico Lamy, Bertrand Audoin, Jean Philippe Ranjeva, Wafaa Zaaraoui, Jean Pelletier
Neurology Apr 2017, 88 (16 Supplement) P4.403;

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Abstract

Objective: To assess neuro-degenerative process in benign multiple sclerosis (BMS)

Background: The natural course of MS is highly variable between patients. Some of them are particularly notable by a relative smaller number of relapses followed by a good recovery and subsequently a lower disability after a long disease course (benign MS-BMS). We can hypothesize that this relative better evolution is related to a less irreversible neurodegenerative process. Recent studies have evidenced in vivo brain sodium accumulation in MS from the earliest stage to the progressive forms. These findings were related to ionic exchanges dysfunction known to lead to irreversible neuro-axonal loss in MS.

Design/Methods: 56 subjects were enrolled in the study (25 patients with a disease duration ≥ 15 years, without any DMT and EDSS < 3.0 and 31 matched controls). MRI was performed at 3T (Verio, Siemens) using sodium 3D-MRI and proton T1 and T2-weighted images to obtain total sodium concentration (TSC) of the brain compartments (lesions, NAWM and NAGM) and usual conventionnal MRI parameters. Comparisons of TSC between patients and controls were assessed using statistical mapping analysis with t-test for a p<0.001, FDR corrected.

Results: The mean disease duration of BMS patients was 19.2 years (SD=5.4) and the median EDSS was 1.5 [Range= 0–2.5]. TSC was significantly increased (p<0.05) in lesions, NAWM and NAGM in BMS patients compared to controls. Statistical mapping analysis showed that this sodium accumulation was located bilaterally in the thalami, the cerebellum and the right supramarginal gyrus.

Conclusions: This study demonstrates that BMS patients are affected by sodium accumulation in lesions, NAWM and NAGM that could be related to neuro-degeneration. Future studies are needed to evaluate the impact of sodium accumulation on others aspects of disability, such as cognitive impairment.

Disclosure: Dr. Maarouf has nothing to disclose. Dr. Gherib has nothing to disclose. Dr. Pariollaud has nothing to disclose. Dr. GUYE has nothing to disclose. Dr. Rico Lamy has nothing to disclose. Dr. Audoin has nothing to disclose. Dr. Ranjeva has nothing to disclose. Dr. Zaaraoui has nothing to disclose. Dr. Pelletier has nothing to disclose.

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