EEG Synchronization—Parameters in Patients With Subcortical Arteriosclerotic Encephalopathy and Gait Disorder
- 25 May 2020
- journal article
- research article
- Published by Wolters Kluwer Health in Journal Of Clinical Neurophysiology
- Vol. 38 (4) , 331-339
- https://doi.org/10.1097/wnp.0000000000000701
Abstract
Purpose: Subcortical arteriosclerotic encephalopathy (SAE) is characterized by extensive white matter lesions in the MRI. Clinical symptoms are cognitive impairment, ranging from mild deficits to vascular dementia, impaired executive functioning, and gait disorders. In the EEG of SAE patients with vascular dementia, the lower frequencies are increased. However, it is unclear whether EEG changes also exist in SAE patients with gait disorders but without vascular dementia. Methods: The authors analyzed the EEGs of 50 nondemented patients with SAE and gait disorders and 50 healthy controls applying pointwise transinformation as a measure of synchronization. Results: Hundred seconds of waking EEG that appeared unaltered in visual analysis were sufficient to prove changes in synchronization. The authors found a decrease in the mean level of synchronization, combined with an elongation of synchronization time in all examined brain areas. These effects correlated slightly with the extent of subcortical lesions. Conclusions: Changes in EEG synchronization in patients with SAE and gait disorders seem to occur independently of cognitive function. The causal relationship of the changes in EEG synchronization and gait disorders remains to be clarified. The results of this study might point to a decrease in coupling efficiency in these patients, with the increase in synchronization duration as a possible compensatory mechanism. Because a time-efficient signal transmission particularly during gait execution is crucial, reduced efficiency might contribute to an impairment of postural stabilization. The study results might indicate a neuronal network for planning and execution of motor activity and particularly gait, extending from the frontal over the central to the parietal cortex.Keywords
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