INCYT   25562
INSTITUTO DE NEUROCIENCIA COGNITIVA Y TRASLACIONAL
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Functional connectivity changes in the cognitive-affective network in MS
Autor/es:
COUTO B; ESTEVES S; ROCA M; PAGANI F; SEDEÑO L; IBAÑEZ A; SINAY V; BRUNO D; MANES F
Reunión:
Encuentro; 68th AAN Annual Meeting; 2016
Resumen:
BACKGROUND and OBJECTIVE: Functional connectivity analyses allow the characterization of cortical networks. Multiple sclerosis pathology can be posited as a disconnection disease. Furthermore, salience network is anattentional network involved in cognitive-affective domains and its integration. Previous research evidenced MS impairment in those emotional-cognitive tasks and its related atrophy of the salience network´s nodes.METHODS: 21 RRMS patients and 18 healthy controls were scanned for 10 min resting state functional MRI. Functional connectivity (as the Spearman timeseries correlation) between voxels of 6 regions of interest (ROIs) ofthe salience network: right and left anterior cingulate cortex (ACC), right and left primary somatosensory (S1) cortex, right and left insular cortex (IC).RESULTS: Increments in functional connectivity between ROIs of the salience network were found for MS patients. Right anterior cingulate showed hiperconnectivity with right S1 (t=2.53;p=.01), with left insular cortex (r=2.36;p=.02) and with right insular cortex (r=2.11;p=.04). Meanwhile, left anterior cingulate showed hiperconnectivity in MS patients with left insular cortex (r=2.51;p=.01) left anterior cingulate (r=2.21;p=.03).CONCLUSIONS: The functional connectivity of MS showed hiperconnectivity between nodes of the salience network. Specifically, these areas included the right ACC and IC widely known as major hubs for the integration of higher cognitive functions (i.e. executive functions) and affective-driven behavior (i.e. social cognition). Although unexpected, functional hiperconnectivity in MS might refex a compensatory hiperfunction reactive to the already known atrophy of IC and ACC in this disease, a phenomena evidenced for FC of other neurologic diseases.