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Τετάρτη 27 Σεπτεμβρίου 2017

Remission of encephalopathy with status epilepticus (ESES) during sleep renormalizes regulation of slow wave sleep

Summary

Objective

In previous studies, we showed an altered overnight decrease of non–rapid-eye-movement (NREM) sleep slow waves in children with encephalopathy related to status epilepticus during sleep (ESES). Here, we test the hypothesis that these alterations renormalize after remission of ESES. Because overnight decrease of slow waves has been linked to brain recovery and cognition, we investigate whether cognitive outcome is related to overnight changes of slow waves.

Methods

We performed a retrospective analysis of longitudinal overnight electroencephalography (EEG) in 10 patients with idiopathic ESES. Automated slow wave detection and calculation of slope of slow waves during the first and last hour of NREM sleep were employed. Intraindividual comparisons were undertaken of the slope during active phase and after remission of ESES, and between patients after remission of ESES and healthy controls. Explorative analysis of the relationship between slow wave slope and cognitive outcome was performed.

Results

The slope of slow waves did not decrease significantly across the night during active ESES, particularly at the spike focus. After remission of ESES, the slope decreased significantly overnight. Compared to controls, there was no difference in overnight slope decrease. Association between slope and neuropsychological outcome showed best cognitive outcome after remission in those children (n = 3) who showed some degree of slope decline during active ESES.

Significance

This study provides evidence that alterations of overnight changes of NREM-sleep slow waves during active ESES are reversible when ESES resolves, and that the severity of neuropsychological compromise might be related to the extent of slow wave impairment during ESES. Our findings suggest that analysis of slow waves might serve as a prognostic factor regarding cognitive outcome. ESES may serve as disease model of pathologic slow wave sleep and our results might be expanded to epilepsies with spike wave activation in slow wave sleep not only in children but also in adults.



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