Lindsay-Rae Weitzel1, Dayalan Sampath2, Kaori Shimizu1, Andrew M White2, Paco S Herson3, Yogendra H Raol4. 1. Department of Anesthesiology, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. 2. Department of Pediatrics, Division of Neurology, School of Medicine, Translational Epilepsy Research Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. 3. Department of Anesthesiology, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA; Department of Pharmacology, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. 4. Department of Pediatrics, Division of Neurology, School of Medicine, Translational Epilepsy Research Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045, USA. Electronic address: Yogendra.Raol@ucdenver.edu.
Abstract
AIMS: Cardiac arrest (CA) is a major cause of mortality and survivors often develop neurologic deficits. The objective of this study was to determine the effect of CA and cardiopulmonary resuscitation (CPR) in mice on the EEG and neurologic outcomes, and identify biomarkers that can prognosticate poor outcomes. MAIN METHODS: Video-EEG records were obtained at various periods following CA-CPR and examined manually to determine the presence of spikes and sharp-waves, and seizures. EEG power was calculated using a fast Fourier transform (FFT) algorithm. KEY FINDINGS: Fifty percent mice died within 72h following CA and successful CPR. Universal suppression of the background EEG was observed in all mice following CA-CPR, however, a more severe and sustained reduction in EEG power occurred in the mice that did not survive beyond 72h than those that survived until sacrificed. Spikes and sharp wave activity appeared in the cortex and hippocampus of all mice, but only one out of eight mice developed a purely electrographic seizure in the acute period after CA-CPR. Interestingly, none of the mice that died experienced any acute seizures. At 10days after the CA-CPR, 25% of the mice developed spontaneous convulsive and nonconvulsive seizures that remained restricted to the hippocampus. The frequency of nonconvulsive seizures was higher than that of convulsive seizures. SIGNIFICANCE: A strong association between changes in EEG power and mortality following CA-CPR were observed in our study. Therefore, we suggest that the EEG power can be used to prognosticate mortality following CA-CPR induced global ischemia.
AIMS: Cardiac arrest (CA) is a major cause of mortality and survivors often develop neurologic deficits. The objective of this study was to determine the effect of CA and cardiopulmonary resuscitation (CPR) in mice on the EEG and neurologic outcomes, and identify biomarkers that can prognosticate poor outcomes. MAIN METHODS: Video-EEG records were obtained at various periods following CA-CPR and examined manually to determine the presence of spikes and sharp-waves, and seizures. EEG power was calculated using a fast Fourier transform (FFT) algorithm. KEY FINDINGS: Fifty percent mice died within 72h following CA and successful CPR. Universal suppression of the background EEG was observed in all mice following CA-CPR, however, a more severe and sustained reduction in EEG power occurred in the mice that did not survive beyond 72h than those that survived until sacrificed. Spikes and sharp wave activity appeared in the cortex and hippocampus of all mice, but only one out of eight mice developed a purely electrographic seizure in the acute period after CA-CPR. Interestingly, none of the mice that died experienced any acute seizures. At 10days after the CA-CPR, 25% of the mice developed spontaneous convulsive and nonconvulsive seizures that remained restricted to the hippocampus. The frequency of nonconvulsive seizures was higher than that of convulsive seizures. SIGNIFICANCE: A strong association between changes in EEG power and mortality following CA-CPR were observed in our study. Therefore, we suggest that the EEG power can be used to prognosticate mortality following CA-CPR induced global ischemia.
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