Functional correlate of visual working memory impairment in newly diagnosed patients with relapsing remitting Multiple Sclerosis.

Resumen

Introduction: Impairments in working memory (WM) are common and disabling symptoms of multiple sclerosis (MS), frequently manifesting in the early stages of the disease. However, the nature oftheir interplay on the WM components, particularly within visual WM, is still questioned. Objectives/Aims: This study aimed to identify brain functional correlates underlying visual short-term WMperformance for recently diagnosed patients with relapsing-remitting (RMMS),facilitatingunderstanding of neural mechanisms that promoteencoding of information into visual workingmemory (WM).Methods: Thirty-one newly diagnosed patients with RRMS and nineteen healthy controls (HC), matchedin aged, gender and yearsof schooling, were recruited. Visual WM was evaluated throughthe Sternberg task and by manipulating stimuli congruency andcognitive load. Event relatedpotentials (ERPs) and neural sourceanalysis can be applied to disentangle the the dynamicmodulations of large-scale cortical network activity involved in WMencoding and theirrelationship with performance. Cortical EEGsource imaging and reconstructions wereperformed usingBrainstorm and SPM12 software by cortical reconstructions ofindividualcortical current source density map estimations performed on each condition.Results: MS patients were slower and less accurate than HC,especially under lower cognitive load. Moreover, WM encodingelicited both a larger P300 amplitude in HC than in RRMSpatientswhen task also was less demanding, and also exhibitedenhanced activations over bilateralmedial and inferior frontalgyrus and over right posterior temporal areas. Interestedly,WMaccuracy was associated with both increased P300 amplitudes and cortical activations for all participants.Conclusion: These results highlight the spatiotemporal dynamicsof prefrontal and temporal sourcesunderlying impaired visualWM encoding in RRMS patients, and shows that these deficitsappear to be related to lower level WM encoding. Our findingsprovide updated functional evidence that supports critical frontaltemporal network interactions during WM impairments in newlydiagnosed MS patients.Disclosure of interest: Esteban Sarrias Arrabal and ConstantinoMendez Bertolo were supported by 2 postdoctoral fellowshipfrom the Spain Government (Juan de la Cierva) A.J. CruzGomez and F. Sanmatino were supported by 2postdoctoral fellowships from the Department of Health (grants: PI-0025-2017and PI-0034-2019). L Forero received speaker fees and travelsupport from Biogen, Merck Serono, Novartis, Sanofi, Teva, andRoche. E Lozano-Soto was supported by a research contractform the Andalusian General Secretariat of Universities,Research and Technology (grant: ProyExcel-01041). R. RashidLopez received speaker fees and travel support from Teva,AbbVie, Zambon, BIAL, and Italfarmaco. J. Paz-Esposito hadnothing to disclose. Espinosa-Rosso received speaker fees andtravel support from Teva, AbbVie, Zambon, BIAL,Italfarmaco,Biogen, Merck Serono, Novartis, Sanofi, and Roche. J.J.Gonzalez-Rosa was supported by the University of Cadiz and atenure-track “Ramon y Cajal” research fellowship/grant(RYC-2015-18467).