Intracranial Electrophysiological Investigation during Cardiac Arrest: A Case Study
Abstract number :
3.208
Submission category :
3. Neurophysiology / 3C. Other Clinical EEG
Year :
2025
Submission ID :
743
Source :
www.aesnet.org
Presentation date :
12/8/2025 12:00:00 AM
Published date :
Authors :
Presenting Author: Serdar Akkol, MD PhD – University of Alabama at Birmingham
Ashley Thomas, MD – University of Alabama at Birmingham
Zeenat Jaisani, MD – University of Alabama at Birmingham
Benjamin Cox, MD – University of Alabama at Birmingham
Rachel Smith, PhD, MS, BS – University of Alabama at Birmingham
Nicole Bentley, MD – University of Alabama at Birmingham
Jasmine Thum, MD – University of Alabama at Birmingham
Rationale: Cerebral electrophysiological recordings at the time of cardiac arrest are rare due to the sudden nature of these events. Certain populations, like people with epilepsy, especially those with drug-resistant epilepsy, face higher mortality. Proposed pathophysiological mechanisms include brainstem, autonomic or cardiorespiratory failure due to epileptogenic activity or altered cerebral connectivity. Current understanding is limited to post-mortem analyses, case reports, and animal models. We report a rare case of stereo-electroencephalography (sEEG) recording during cardiac arrest and eventual brain death due to global cerebral edema of unknown etiology, showing neural dynamics during this transition.
Methods: A 46-year-old woman with a 15-year history of drug-resistant epilepsy was admitted to the epilepsy monitoring unit after sEEG implantation. After an unremarkable surgery and hospital course, she had a witnessed cardiac arrest on postoperative day (POD) 3. We analyzed four epochs of sEEG: interictal (POD 1), interictal (POD 3), 15 min pre-cardiac arrest, and 5 min post-arrest. Analyses included spectral decomposition using Morlet wavelets, power spectrum density (PSD), and functional connectivity by correlating the low frequency fluctuations (0.1-1 Hz) of high-frequency activity (HFA, 70-200 Hz).
Results: Admission medications included Oxcarbazepine, Levetiracetam and Lacosamide. On POD 3, patient was arousable but obtunded, presumed to be postictal due to prior seizures. Non-contrast head CT showed mild global cerebral edema. Despite escalating ASMs, patient continued to have frequent focal seizures. On that night, she desaturated and had a witnessed cardiac arrest. Resuscitation was achieved after one round of CPR and she was moved to the intensive care unit. A repeat exam two hours later showed no brainstem reflexes with fixed, dilated pupils. A head CT angiogram showed bilateral uncal and cerebellar tonsillar herniation with absent cerebral blood flow. Clinical analyses showed seizures arising from bilateral anterior hippocampi, predominantly right-lateralized, and independent epileptiform discharges in bilateral hippocampi and right lateral temporal cortex. PSD showed progressively decreased power in the seizure onset zone from POD 1 to post-arrest, with a shift from higher frequencies ( >30 Hz) to low frequencies (< 14 Hz) prior to arrest, and diffuse suppression following cardiac arrest (Fig1 & 2, rmANOVA). Functional connectivity showed an increase in brain-wide connectivity from POD 1 to POD 3, with abrupt loss post-arrest (Fig 3). Post-mortem workup was negative. The cause of cerebral edema remains unknown, but is assumed to have led to mental and respiratory depression, causing cardiac arrest and brain death.
Conclusions: Intracranial EEG during the transition to brain death due to cerebral edema showed progressive slowing, increased functional connectivity, and eventual network collapse. The findings may support future biomarker development for improved risk assessment and intervention strategies. This is the first intracranial EEG study to analyze the spectral and network level changes during cardiac arrest and brain death.
Funding: No funding to disclose.
Neurophysiology