Contributions
Abstract: 259
Type: Oral
Sodium accumulation occurs in the first steps of the pathologic pathway leading to neuronal death and traduces early dysfunction of neuronal energy metabolism (Waxman et al. Nat Rev Neurosc 2006). Recently, several in vivo magnetic resonance imaging studies have applied 23Na MRI in MS and reported significant and diffuse accumulations of brain total sodium —predominantly in the GM—that correlate with physical disability (Inglese et al. Brain 2010, Zaaraoui et al. Radiology 2012, Paling et al. Brain 2013, Maarouf et al. Magn Res Mat & Phys 2014) and cognitive impairment (Maarouf et al. Neurology 2017) . The use of new MR contrasts such as Triple Quantum Filtering (Petracca et al. Brain 2016), and/or inversion recovery at high (3T) and ultra-high field (7T) (Madelin et al. Plos One 2015), demonstrate the decreases in intracellular volume fraction and increase in intracellular sodium concentrations in MS patients (Petracca et al. Brain 2016). Nevertheless, as noted in a recent review (Thulborn Neuroimage 2016)., the metabolic substrates of such accumulations of brain total sodium observed by 23Na MRI are not known yet. Complementary information on physiological and pathological processes can be obtained from metabolites detected using proton MR spectroscopic imaging, but the brain is generally partially sampled.
This talk will aim at presenting the last advances in the in vivo characterization of metabolic and ionic abnormalities associated to the pathophysiological processes accompanying MS through combined measurements of optimized fast volumic echo planar spectroscopic imaging (3D-EPSI) (Donadieu et al. JMRI 2016) and 23Na MRI within the same subjects over the entire human brain. Perspective to relate these parameter to new specific MR markers of myelin such as inhomogenous magnetization transfer (ihMT) (Varma et al. JMR 2015) will be discussed.
Disclosure: NA
Abstract: 259
Type: Oral
Sodium accumulation occurs in the first steps of the pathologic pathway leading to neuronal death and traduces early dysfunction of neuronal energy metabolism (Waxman et al. Nat Rev Neurosc 2006). Recently, several in vivo magnetic resonance imaging studies have applied 23Na MRI in MS and reported significant and diffuse accumulations of brain total sodium —predominantly in the GM—that correlate with physical disability (Inglese et al. Brain 2010, Zaaraoui et al. Radiology 2012, Paling et al. Brain 2013, Maarouf et al. Magn Res Mat & Phys 2014) and cognitive impairment (Maarouf et al. Neurology 2017) . The use of new MR contrasts such as Triple Quantum Filtering (Petracca et al. Brain 2016), and/or inversion recovery at high (3T) and ultra-high field (7T) (Madelin et al. Plos One 2015), demonstrate the decreases in intracellular volume fraction and increase in intracellular sodium concentrations in MS patients (Petracca et al. Brain 2016). Nevertheless, as noted in a recent review (Thulborn Neuroimage 2016)., the metabolic substrates of such accumulations of brain total sodium observed by 23Na MRI are not known yet. Complementary information on physiological and pathological processes can be obtained from metabolites detected using proton MR spectroscopic imaging, but the brain is generally partially sampled.
This talk will aim at presenting the last advances in the in vivo characterization of metabolic and ionic abnormalities associated to the pathophysiological processes accompanying MS through combined measurements of optimized fast volumic echo planar spectroscopic imaging (3D-EPSI) (Donadieu et al. JMRI 2016) and 23Na MRI within the same subjects over the entire human brain. Perspective to relate these parameter to new specific MR markers of myelin such as inhomogenous magnetization transfer (ihMT) (Varma et al. JMR 2015) will be discussed.
Disclosure: NA