ECTRIMS eLearning

Structural connectivity in multiple sclerosis and simulation of disconnection
Author(s): ,
E De Meo
Affiliations:
San Raffaele Scientific Institute
,
M.A Rocca
Affiliations:
Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience
,
E Pagani
Affiliations:
Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience
,
B Colombo
Affiliations:
Department of Neurology
,
M Rodegher
Affiliations:
Department of Neurology
,
P Preziosa
Affiliations:
Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience
,
G Comi
Affiliations:
Department of Neurology
,
A Falini
Affiliations:
Department of Neuroradiology, S. Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy
M Filippi
Affiliations:
Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience
ECTRIMS Learn. De Meo E. 09/15/16; 146384; P544
Ermelinda De Meo
Ermelinda De Meo
Contributions
Abstract

Abstract: P544

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Imaging

Background and aims: Several functional magnetic resonance imaging (fMRI) studies demonstrated the presence of disconnection across brain networks in multiple sclerosis (MS) patients and its relationship with clinical manifestations. Starting from this backgroung the aim of our study is to quantify structural connectivity integrity in multiple sclerosis (MS) patients with different clinical phenotypes and to simulate a disconnection due to T2 visible lesions and to verify the effect of macroscopic tissue damage on network-based measures.

Methods: Diffusion tensor (DT) and dual-echo MRI scans were obtained from 239 MS patients (12 with a clinically isolated syndrome [CIS], 111 relapsing-remitting [RR] MS, 45 benign MS and 71 secondary progressive [SP] MS) and 131 healthy controls (HC). Structural connectivity matrices were produced and then artificially disconnected based on T2 lesion distribution. Global and nodal network metrics were calculated for both cases.

Results: Compared to HC, MS patients showed decreased (p< 0.001) strength, assortativity, transitivity, global efficiency and increased average path length of the whole network. Similar hubs were identified in patients and controls. The postcentral, superior parietal, precuneus and cerebellar crus 1 e 2 hubs had reduced strength in SPMS versus RRMS patients. The analysis of the disconnected matrices identified more nodes with decreased strength in SPMS compared to RRMS and BMS patients.

Conclusions: Global measures of structural connectivity were significantly different in MS patients compared with HC, showing an extended disruption of structural integrity in MS. The pattern of hub distribution was preserved in MS patients, with a preserved architecture of brain structural networks but a reduced strength of connections of nodes identified as hubs. The simulation of disconnection allowed us to identify the role of lesions in determining abnormalities in structural connectivity in MS patients and to better characterize the main disease clinical phenotypes.

This work has been partially supported by grants from Fondazione Italiana Sclerosi Multipla (FISM/2011/R/19) and Italian Ministry of Health (GR-2009-1529671).

Disclosure:

Drs De Meo, Pagani, Colombo, Rodegher, Preziosa, and Falini have nothing to disclose.

Dr Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.

Prof. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.

Prof. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory boards for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

Abstract: P544

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Imaging

Background and aims: Several functional magnetic resonance imaging (fMRI) studies demonstrated the presence of disconnection across brain networks in multiple sclerosis (MS) patients and its relationship with clinical manifestations. Starting from this backgroung the aim of our study is to quantify structural connectivity integrity in multiple sclerosis (MS) patients with different clinical phenotypes and to simulate a disconnection due to T2 visible lesions and to verify the effect of macroscopic tissue damage on network-based measures.

Methods: Diffusion tensor (DT) and dual-echo MRI scans were obtained from 239 MS patients (12 with a clinically isolated syndrome [CIS], 111 relapsing-remitting [RR] MS, 45 benign MS and 71 secondary progressive [SP] MS) and 131 healthy controls (HC). Structural connectivity matrices were produced and then artificially disconnected based on T2 lesion distribution. Global and nodal network metrics were calculated for both cases.

Results: Compared to HC, MS patients showed decreased (p< 0.001) strength, assortativity, transitivity, global efficiency and increased average path length of the whole network. Similar hubs were identified in patients and controls. The postcentral, superior parietal, precuneus and cerebellar crus 1 e 2 hubs had reduced strength in SPMS versus RRMS patients. The analysis of the disconnected matrices identified more nodes with decreased strength in SPMS compared to RRMS and BMS patients.

Conclusions: Global measures of structural connectivity were significantly different in MS patients compared with HC, showing an extended disruption of structural integrity in MS. The pattern of hub distribution was preserved in MS patients, with a preserved architecture of brain structural networks but a reduced strength of connections of nodes identified as hubs. The simulation of disconnection allowed us to identify the role of lesions in determining abnormalities in structural connectivity in MS patients and to better characterize the main disease clinical phenotypes.

This work has been partially supported by grants from Fondazione Italiana Sclerosi Multipla (FISM/2011/R/19) and Italian Ministry of Health (GR-2009-1529671).

Disclosure:

Drs De Meo, Pagani, Colombo, Rodegher, Preziosa, and Falini have nothing to disclose.

Dr Rocca received speakers honoraria from Biogen Idec, Novartis and ExceMed and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.

Prof. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, Excemed.

Prof. Filippi is Editor-in-Chief of the Journal of Neurology; serves on scientific advisory boards for Teva Pharmaceutical Industries; has received compensation for consulting services and/or speaking activities from Biogen Idec, Excemed, Novartis, and Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Teva Pharmaceutical Industries, Novartis, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, Cure PSP, Alzheimer´s Drug Discovery Foundation (ADDF), the Jacques and Gloria Gossweiler Foundation (Switzerland), and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

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