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- Homotopic redistribution of functional connectivity in insula-centered diffuse low-grade glioma doi link

Auteur(s): Almairac Fabien, Deverdun J., Cochereau Jérôme, Coget Arthur, Lemaitre Anne-Laure, Moritz-Gasser Sylvie, Duffau Hugues, Herbet Guillaume

(Article) Publié: Neuroimage: Clinical, vol. 29 p.102571 (2021)
Texte intégral en Openaccess : openaccess


Ref HAL: hal-03130549_v1
PMID 33508623
DOI: 10.1016/j.nicl.2021.102571
Exporter : BibTex | endNote
Résumé:

Objective: In the event of neural injury, the homologous contralateral brain areas may play a compensatory role to avoid or limit the functional loss. However, this dynamic strategy of functional redistribution is not clearly established, especially in the pathophysiological context of diffuse low-grade glioma. Our aim here was to assess the extent to which unilateral tumor infiltration of the insula dynamically modulates the functional connectivity of the contralesional one.Methods: Using resting-state functional connectivity MRI, a seed-to-ROI approach was employed in 52 insula-centered glioma patients (n = 30 left and 22 right) compared with 19 age-matched healthy controls.Results: Unsurprisingly, a significant decrease of the inter-insular connectivity was observed in both patient groups. More importantly, the analyses revealed a significant increase of the contralesional insular connectivity towards both cerebral hemispheres, especially in cortical areas forming the visual and the sensorimotor networks. This functional redistribution was not identified when the analyses were performed on three control regions for which the homologous area was not impaired by the tumor. This overall pattern of results indicates that massive infiltration of the insular cortex causes a significant redeployment of the contralesional functional connectivity.Conclusion: This general finding suggests that the undamaged insula plays a role in the functional compensation usually observed in this patient population, and thus provides compelling support for the concept of homotopic functional plasticity in brain-damaged patients.