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ID 300 – Cortical excitability and connectivity in early RRMS using TMS-EEG

Objective Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system frequently affecting the corpus callosum, the largest interhemispheric fiber bundle, at an early stage of the disease. Here, we employed transcranial magnetic stimulation (TMS) combined with high...

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Bibliographic Details
Published in:Clinical neurophysiology 2016-03, Vol.127 (3), p.e122-e122
Main Authors: Zipser, C, Premoli, I, Castellanos, N, Rivolta, D, Belardinelli, P, Heidegger, T, Müller-Dahlhaus, F, Ziemann, U
Format: Article
Language:English
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Summary:Objective Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system frequently affecting the corpus callosum, the largest interhemispheric fiber bundle, at an early stage of the disease. Here, we employed transcranial magnetic stimulation (TMS) combined with high-density 64-channel electroencephalography (EEG) to investigate cortical excitability and interhemispheric connectivity in 13 patients with early relapsing-remitting MS (RRMS) with mean EDSS 1 ± 1 compared to 16 age- and gender-matched healthy controls. Methods TMS was applied to the left and right M1 separately. Latencies and amplitudes of TMS-evoked EEG potential (TEP) components N45, N100, P180, N280 in the stimulated and non-stimulated hemisphere were analyzed using two different approaches: a cluster-based permutation analysis and an automated extraction of maximum and minimum values. Results Compared to healthy control subjects, RRMS patients did not show any significant differences in TEP latencies or amplitudes in the stimulated or non-stimulated hemisphere, neither for left nor for right M1 stimulation (all p > 0.05). Conclusion and key message We conclude that basic excitability and connectivity measures of TMS-EEG data are unaltered in early RRMS patients, which may indicate a high level of functional compensation for structural deficits in these patients, e.g. by activation of alternate routes of TEP propagation.
ISSN:1388-2457
1872-8952
DOI:10.1016/j.clinph.2015.11.414