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- Anna Lybeck, Hans Friberg, Niklas Nielsen, Malin Rundgren, Susann Ullén, Henrik Zetterberg, Kaj Blennow, Tobias Cronberg, and Erik Westhall.
- Lund University, Skane University Hospital, Department of Clinical Sciences, Anesthesia & Intensive Care, 221 85 Lund, Sweden. Electronic address: anna.lybeck@med.lu.se.
- Resuscitation. 2021 Jan 1; 158: 253-257.
AimTo explore if electrographic status epilepticus (ESE) after cardiac arrest causes additional secondary brain injury reflected by serum levels of two novel biomarkers of brain injury: neurofilament light chain (NfL) originating from neurons and glial fibrillary acidic protein (GFAP) from glial cells.MethodsSimplified continuous EEG (cEEG) and serum levels of NfL and GFAP, sampled at 24, 48 and 72 h after cardiac arrest, were collected during the Target Temperature Management (TTM)-trial. Two statistical methods were used: multivariable regresssion analysis; and a matched control group of patients without ESE matched for early predictors of poor neurological outcome.Results128 patients had available biomarkers and cEEG. Twenty-six (20%) patients developed ESE, the majority (69%) within 24 h. ESE was an independent predictor of elevated serum NfL (p < 0.001) but not of serum GFAP (p = 0.16) at 72 h after cardiac arrest. Compared to a control group matched for early predictors of poor neurological outcome, patients who developed ESE had higher levels of serum NfL (p = 0.03) and GFAP (p = 0.04) at 72 h after cardiac arrest.ConclusionESE after cardiac arrest is associated with higher levels of serum NfL which may suggest increased secondary neuronal injury compared to matched patients without ESE but similar initial brain injury. Associations with GFAP reflecting glial injury are less clear. The study design cannot exclude imperfect matching or other mechanisms of secondary brain injury contributing to the higher levels of biomarkers of brain injury seen in the patients with ESE.Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.
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