Automated quantification of spike-wave activity may be used to predict the development of electrical status epilepticus in sleep (ESES) in children with perinatal stroke.


Journal

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
ISSN: 1872-8952
Titre abrégé: Clin Neurophysiol
Pays: Netherlands
ID NLM: 100883319

Informations de publication

Date de publication:
01 2021
Historique:
received: 14 01 2020
revised: 30 10 2020
accepted: 06 11 2020
pubmed: 6 12 2020
medline: 17 7 2021
entrez: 5 12 2020
Statut: ppublish

Résumé

Continuous spike and wave in slow-wave sleep (CSWS), an epileptic encephalopathy, occurs after perinatal stroke where it is associated with cognitive decline. CSWS features a distinct EEG pattern, electrical status epilepticus in sleep (ESES). Biomarkers for the prediction of ESES have not been identified but will facilitate earlier diagnosis and treatment. We hypothesized that spike-frequency and differences in power spectra would be predictive of subsequent ESES. A cross-sectional study comparing EEG spike-frequency and Power before the development of ESES in patients with perinatal stroke, patients with focal epilepsy, and appropriate controls. 43 patients met the inclusion criteria; 11 stroke-ESES, 10 stroke controls, 14 epilepsy-ESES, 8 epilepsy controls. ESES patients had higher pre-diagnosis mean spike-frequency (24.0 ± 24 versus 6.6 ± 9.1 SW/min, p = 0.002) than patients that did not develop ESES; these differences present ~ 3 years before ESES diagnosis. Pre-diagnosis, normalized delta power (1-4 Hz) was higher in the stroke-ESES group (105.7 ± 58 dB/Hz) compared to stroke controls (57.4 ± 45 dB/Hz, p = 0.036). Spike-frequency and delta power may represent EEG biomarkers of the risk of developing ESES in children with perinatal stroke. EEG biomarkers may be used by clinicians to assess which patients are more at-risk for ESES. Using spike-frequency, clinicians may be able to identify patients at risk of developing ESES.

Identifiants

pubmed: 33278667
pii: S1388-2457(20)30539-3
doi: 10.1016/j.clinph.2020.11.003
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

146-153

Informations de copyright

Copyright © 2020 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

Auteurs

Abdullah Azeem (A)

Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada.

Adam Kirton (A)

Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Department of Pediatrics, Section of Neurology, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Alberta Children's Hospital, Calgary AB T3B 6A8, Canada.

Juan Pablo Appendino (JP)

Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Department of Pediatrics, Section of Neurology, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Alberta Children's Hospital, Calgary AB T3B 6A8, Canada.

Silvia Kozlik (S)

Alberta Children's Hospital, Calgary AB T3B 6A8, Canada.

Aleksandra Mineyko (A)

Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Department of Pediatrics, Section of Neurology, Cumming School of Medicine, University of Calgary, Calgary AB T2N 1N4, Canada; Alberta Children's Hospital, Calgary AB T3B 6A8, Canada. Electronic address: aleksandra.mineyko@ahs.ca.

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