Association between postictal EEG suppression, postictal autonomic dysfunction, and sudden unexpected death in epilepsy: Evidence from intracranial EEG.
Heart rate variability
Intracranial EEG
Postictal EEG suppression
SUDEP
Scalp EEG
Sudden Unexpected Death in Epilepsy
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:
Feb 2023
Feb 2023
Historique:
received:
26
05
2022
revised:
18
11
2022
accepted:
02
12
2022
pubmed:
7
1
2023
medline:
25
1
2023
entrez:
6
1
2023
Statut:
ppublish
Résumé
The association between postictal electroencephalogram (EEG) suppression (PES), autonomic dysfunction, and Sudden Unexpected Death in Epilepsy (SUDEP) remains poorly understood. We compared PES on simultaneous intracranial and scalp-EEG and evaluated the association of PES with postictal heart rate variability (HRV) and SUDEP outcome. Convulsive seizures were analyzed in patients with drug-resistant epilepsy at 5 centers. Intracranial PES was quantified using the Hilbert transform. HRV was quantified using root mean square of successive differences of interbeat intervals, low-frequency to high-frequency power ratio, and RR-intervals. There were 64 seizures from 63 patients without SUDEP and 11 seizures from 6 SUDEP patients. PES occurred in 99% and 87% of seizures on intracranial-EEG and scalp-EEG, respectively. Mean PES duration in intracranial and scalp-EEG was similar. Intracranial PES was regional (<90% of channels) in 46% of seizures; scalp PES was generalized in all seizures. Generalized PES showed greater decrease in postictal parasympathetic activity than regional PES. PES duration and extent were similar between patients with and without SUDEP. Regional intracranial PES can be present despite scalp-EEG demonstrating generalized or no PES. Postictal autonomic dysfunction correlates with the extent of PES. Intracranial-EEG demonstrates changes in autonomic regulatory networks not seen on scalp-EEG.
Identifiants
pubmed: 36608528
pii: S1388-2457(22)00965-8
doi: 10.1016/j.clinph.2022.12.002
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
109-117Informations de copyright
Copyright © 2022 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Conflict of interest B. Esmaeili, D. Weisholtz, S. Tobochnik, F. Kaffashi, S. Cash, B. Cha, J. Laze, D. Reich, P. Farooque, T. Gholipour, M. Singleton, K. Loparo, and M. Koubeissi report no disclosures relevant to the manuscript. B. Dworetzky has received support from the A.J. Trustey Research Fund and royalties from Oxford University Press. D. Friedman has received salary support for consulting and clinical trial related activities performed on behalf of The Epilepsy Study Consortium, a non-profit organization. D. Friedman receives no personal income for these activities. NYU receives a fixed amount from the Epilepsy Study Consortium towards D. Friedman’s salary. Within the past two years, The Epilepsy Study Consortium received payments for research services performed by D. Friedman from: Alterity, Baergic, Biogen, BioXcell, Cerevel, Cerebral, Jannsen, Lundbeck, Neurocrine, SK Life Science, and Xenon. He has also served as a paid consultant for Neurelis Pharmaceuticals and Receptor Life Sciences. He has received travel support from the Epilepsy Foundation. He has received research support from NINDS, CDC, Epitel, and Neuropace unrelated to this study. He serves on the scientific advisory board for Receptor Life Sciences. He holds equity interests in Neuroview Technology. He received royalty income from Oxford University Press. S. Cash is supported by the National Institute of Neurological Disorders and Stroke (NINDS, K24NS088568 and R01NS062092). M. Singleton is supported by the National Center for Advancing Translational Sciences of the National Institutes of Health (UL1TR000423). O. Devinsky is supported by Finding a Cure for Epilepsy and Seizures (FACES), the National Institute of Neurological Disorders and Stroke (NINDS), National Institute of Mental Health (NIMH), Multidisciplinary University Research Initiatives (MURI), Centers for Disease Control and Prevention (CDC) and National Science Foundation (NSF). He has equity interests in Qstate Biosciences, Tevard Biosciences, Regel Therapeutics and Script Biosciences, Privateer Holdings, Tilray, Receptor Life Sciences, Empatica, Engage, Egg Rock/Papa & Barkley, Rettco, SilverSpike, and California Cannabis Enterprises (CCE). He is an investigator for PTC Therapeutics, Inc., Stoke Therapeutics, Marinus, Ovid and GW Pharmaceuticals. J.W. Lee has contract work with Bioserenity and Teladoc. He has served as a consultant for Biogen. He has received research funding from NINDS and Epilepsy Foundation. He is a co-founder of Soterya, Inc.