Abstract
The disturbance of cortical communication has been hypothesized as an important factor in the appearance of cognitive impairment in (MS). Cortical communication is quantified here in control subjects and patients with relapsing-remitting multiple sclerosis (RRMS) on the basis of mean coherence in theδ,θ,α,βandγbands and using mutual information computed between pairs of bipolar EEG signals recorded during resting condition. Each patient received also a cognitive assessment using a battery of neuropsychological tests specific to cognitive deficits in MS.No difference was observed for the coherence indices whereas inter-hemispheric and right hemisphere mutual information is significantly lower in patients with MS than in control subjects. Moreover, inter-hemispheric mutual information decrease significantly with illness duration and right mutual information differentiate cognitively deficient and non-deficient patients.Mutual information allows to quantify the cortical communication in patients with RRMS and is related to clinical characteristics.Cortical communication quantified in a resting state might be a potential marker for the neurological damage induced by RRMS.
Highlights
Multiple sclerosis (MS) is an autoimmune disorder characterized by multiple lesions of the central myelin and accumulating clinical signs due to demyelination and progressive axonal damage [1]
Once significant clusters of pairs of bipolar signals were selected according to the procedure described above, we explored the comparison between clinical data which characterizes patients, scores to neuropsychological tests and electrophysiological indices
Functional information about interand intra-hemispheric cortical communication was obtained using standard EEG data obtained from patients with RMMS in resting eyes closed condition
Summary
Multiple sclerosis (MS) is an autoimmune disorder characterized by multiple lesions of the central myelin and accumulating clinical signs due to demyelination and progressive axonal damage [1]. Widespread demyelination and axonal damage in MS impairs the conduction of neural impulses which leads to physical and cognitive disability [2]. Cognitive impairment affects approximately 30 to 70% of MS patients and strongly affects their quality of life [3,4]. MS impairs several cognitive functions, including attention [5,6],information processing efficiency [5], executive functioning [7] and long term memory [8]. Cognitive functions that are supported by brain networks are highly dependent upon the integrity of long white matter tracts which mediate information flow between distant cortical areas [9]. Increased risk for cognitive decline in MS patients has been associated with the extent of diffuse tissue damage, lesion localisation, deficiency in neural connectivity and cortical reorganization [10]. Slower neural conduction induced by white matter pathology [11], grey matter pathology and cortical atrophy [12,13] and inter-hemispheric transfer perturbation due to callosal
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