Stephane Lehéricy and Bruno Stankoff contributed equally to the work.
Brain networks disconnection in early multiple sclerosis cognitive deficits: An anatomofunctional study
Article first published online: 31 MAR 2014
Copyright © 2014 Wiley Periodicals, Inc.
Human Brain Mapping
Volume 35, Issue 9, pages 4706–4717, September 2014
How to Cite
Louapre, C., Perlbarg, V., García-Lorenzo, D., Urbanski, M., Benali, H., Assouad, R., Galanaud, D., Freeman, L., Bodini, B., Papeix, C., Tourbah, A., Lubetzki, C., Lehéricy, S. and Stankoff, B. (2014), Brain networks disconnection in early multiple sclerosis cognitive deficits: An anatomofunctional study. Hum. Brain Mapp., 35: 4706–4717. doi: 10.1002/hbm.22505
Celine Louapre has received lecture fees from Novartis. Rana Assouad report consulting fees from Biogen-Idec and Teva. Damien Galanaud reports consulting fees from Olea Médical (La Ciotat, France), Sanofi Aventis (Paris, France), and Biogen (Cambridge, MA). Caroline Papeix reports receiving consulting fees from Biogen Idec, Novartis, Merck Serono, Sanofi-Aventis, Teva-Pharma Bayer-schering, Genzyme, and Roche. Ayman Tourbah reports receiving consulting and lecture fees from Sanofi-Aventis-Genzyme, Teva-Pharma and research support from Biogen Idec, Novartis, Merck Serono Sanofi Aventis, participating in clinical trials for Biogen Idec, Novartis, Merck Serono, Bayer, and Roche. Catherine Lubetzki reports consulting fees from Roche, Novartis, Sanofi Aventis, and Teva Pharma, lecture fees from Merck-Serono, Biogen-Idec, Sanofi Aventis, and Teva, participating in clinical trials for Biogen Idec, Novartis, Merck Serono, Bayer-schering, Sanofi Aventis, Teva Pharma, Genzyme, and Roche. Bruno Stankoff reports receiving consulting and lecture fees from Biogen Idec, Novartis, Merck Serono, Sanofi-Aventis, Genzyme, Teva-Pharma, and Bayer and research support from Biogen Idec, Sanofi Aventis. Vincent Perlbarg, Daniel Garcia-Lorenzo, Marika Urbanski, Habib Benali, Leorah Freeman report no disclosure.
- Issue published online: 18 JUL 2014
- Article first published online: 31 MAR 2014
- Manuscript Accepted: 25 FEB 2014
- Manuscript Revised: 22 FEB 2014
- Manuscript Received: 1 MAY 2013
- ARSEP Foundation
- JNLF. Grant Number: ANR-10-IAIHU-06
- multiple sclerosis;
- resting state;
- default mode network
Severe cognitive impairment involving multiple cognitive domains can occur early during the course of multiple sclerosis (MS). We investigated resting state functional connectivity changes in large-scale brain networks and related structural damage underlying cognitive dysfunction in patients with early MS. Patients with relapsing MS (3–5 years disease duration) were prospectively assigned to two groups based on a standardized neuropsychological evaluation: (1) cognitively impaired group (CI group, n = 15), with abnormal performances in at least 3 tests; (2) cognitively preserved group (CP group, n = 20) with normal performances in all tests. Patients and age-matched healthy controls underwent a multimodal 3T magnetic resonance imaging (MRI) including anatomical T1 and T2 images, diffusion imaging and resting state functional MRI. Structural MRI analysis revealed that CI patients had a higher white matter lesion load compared to CP and a more severe atrophy in gray matter regions highly connected to networks involved in cognition. Functional connectivity measured by integration was increased in CP patients versus controls in attentional networks (ATT), while integration was decreased in CI patients compared to CP both in the default mode network (DMN) and ATT. An anatomofunctional study within the DMN revealed that functional connectivity was mostly altered between the medial prefrontal cortex (MPFC) and the posterior cingulate cortex (PCC) in CI patients compared to CP and controls. In a multilinear regression model, functional correlation between MPFC and PCC was best predicted by PCC atrophy. Disconnection in the DMN and ATT networks may deprive the brain of compensatory mechanisms required to face widespread structural damage. Hum Brain Mapp 35:4706–4717, 2014. © 2014 Wiley Periodicals, Inc.