Contributions
Abstract: P838
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Neuropsychology
Background: Previous functional magnetic resonance imaging (fMRI) studies have indicated that alterations in connectivity of brain hubs are crucial in cognitive impairment (CI) in multiple sclerosis (MS). However, prodromal changes that potentially exist in cognitively preserved (CP) patients, have not been identified yet. Magnetoencephalography (MEG) is likely to shed new light on the behavior of brain hubs in different cognitive phenotypes, given its high temporal resolution.
Objective: To investigate alterations in brain hub connectivity patterns in CP and CI patients with MS, in order to identify possible mechanisms underlying both cognitive preservation and decline in MS.
Methods: MEG recordings of 145 MS patients and 65 healthy controls (HCs) were analyzed by calculating functional connectivity with the amplitude envelope correlation (AEC) between regions of the automated anatomical labeling (AAL) atlas using a beamformer approach. The minimum spanning tree (MST) was used to construct the backbone of the functional brain network, in which properties of hubs were studied. Hubs were defined as regions belonging to literature-based default-mode and fronto-parietal networks. Cognitive functioning was assessed with an expanded Brief Repeatable Battery of Neuropsychological tests (BRB-N). MS patients were classified as cognitively impaired (CI; < -2.0 (z-score) on at least 2 domains) or cognitively preserved (CP). Average connectivity was calculated between hubs, between hubs and non-hubs, and between non-hubs. Linear regression models assessed relations with cognition, as well as effects of deep gray matter volume and lesion volumes, both determined from MRI.
Results: Compared to HCs, CI patients (N=41) showed an increase in connectivity between hubs and non-hubs compared to HCs, whereas CP patients (N=104) showed increased connectivity between hubs. Furthermore, regression analyses showed that within the patient group, lower connectivity between hubs was an independent and significant predictor of cognitive impairment after structural measures were also added to the model.
Conclusions: These results could indicate an overload of brain hubs in MS which may start in CP patients between hubs and might then spread towards connections with non-hubs in CI patients. The level of communication between hub areas differentiated CI and CP patients beyond structural brain measures.
Disclosure: S.D. Kulik: nothing to disclose.
I.M. Nauta is supported by the Dutch MS Research Foundation, grant nr. 15-911.
L. Breedt: nothing to disclose.
B.A. de Jong has received speaker and consulting fees from Merck-Serono, Biogen, TEVA, Genzyme and Novartis.
P. Tewarie has received travel funding from Novartis.
A. Hillebrand serves as an editorial board member of Scientific Reports and Plos One.
E.M.M. Strijbis : nothing to disclose.
C.J. Stam: nothing to disclose.
J.J.G. Geurts is an editor of Multiple Sclerosis Journal. He serves on the editorial boards of Neurology and Frontiers in Neurology, and is president of the Netherlands Organization for Health Research and Innovation. He has served as a consultant for Merck-Serono, Biogen, Novartis, Genzyme, and Teva Pharmaceuticals.
L. Douw receives research support from Society in Science (Branco Weiss Fellowship).
M.M. Schoonheim serves as an editorial board member of Frontiers in Neurology, received research support from the Dutch MS Research Foundation and consulting or speaking fees from ExceMed, Genzyme, Novartis, and Biogen.
Abstract: P838
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Neuropsychology
Background: Previous functional magnetic resonance imaging (fMRI) studies have indicated that alterations in connectivity of brain hubs are crucial in cognitive impairment (CI) in multiple sclerosis (MS). However, prodromal changes that potentially exist in cognitively preserved (CP) patients, have not been identified yet. Magnetoencephalography (MEG) is likely to shed new light on the behavior of brain hubs in different cognitive phenotypes, given its high temporal resolution.
Objective: To investigate alterations in brain hub connectivity patterns in CP and CI patients with MS, in order to identify possible mechanisms underlying both cognitive preservation and decline in MS.
Methods: MEG recordings of 145 MS patients and 65 healthy controls (HCs) were analyzed by calculating functional connectivity with the amplitude envelope correlation (AEC) between regions of the automated anatomical labeling (AAL) atlas using a beamformer approach. The minimum spanning tree (MST) was used to construct the backbone of the functional brain network, in which properties of hubs were studied. Hubs were defined as regions belonging to literature-based default-mode and fronto-parietal networks. Cognitive functioning was assessed with an expanded Brief Repeatable Battery of Neuropsychological tests (BRB-N). MS patients were classified as cognitively impaired (CI; < -2.0 (z-score) on at least 2 domains) or cognitively preserved (CP). Average connectivity was calculated between hubs, between hubs and non-hubs, and between non-hubs. Linear regression models assessed relations with cognition, as well as effects of deep gray matter volume and lesion volumes, both determined from MRI.
Results: Compared to HCs, CI patients (N=41) showed an increase in connectivity between hubs and non-hubs compared to HCs, whereas CP patients (N=104) showed increased connectivity between hubs. Furthermore, regression analyses showed that within the patient group, lower connectivity between hubs was an independent and significant predictor of cognitive impairment after structural measures were also added to the model.
Conclusions: These results could indicate an overload of brain hubs in MS which may start in CP patients between hubs and might then spread towards connections with non-hubs in CI patients. The level of communication between hub areas differentiated CI and CP patients beyond structural brain measures.
Disclosure: S.D. Kulik: nothing to disclose.
I.M. Nauta is supported by the Dutch MS Research Foundation, grant nr. 15-911.
L. Breedt: nothing to disclose.
B.A. de Jong has received speaker and consulting fees from Merck-Serono, Biogen, TEVA, Genzyme and Novartis.
P. Tewarie has received travel funding from Novartis.
A. Hillebrand serves as an editorial board member of Scientific Reports and Plos One.
E.M.M. Strijbis : nothing to disclose.
C.J. Stam: nothing to disclose.
J.J.G. Geurts is an editor of Multiple Sclerosis Journal. He serves on the editorial boards of Neurology and Frontiers in Neurology, and is president of the Netherlands Organization for Health Research and Innovation. He has served as a consultant for Merck-Serono, Biogen, Novartis, Genzyme, and Teva Pharmaceuticals.
L. Douw receives research support from Society in Science (Branco Weiss Fellowship).
M.M. Schoonheim serves as an editorial board member of Frontiers in Neurology, received research support from the Dutch MS Research Foundation and consulting or speaking fees from ExceMed, Genzyme, Novartis, and Biogen.