Electroclinical features and cardiorespiratory dysfunction in generalized convulsive seizures

Abstract

Generalized convulsive seizures (GCS) have been consistently associated with Sudden Unexpected Death in Epilepsy (SUDEP) in case-control studies. Animal studies have shown that GCS may produce cardiorespiratory collapse through seizure-induced brainstem dysfunction, affecting crucial structures for cardiorespiratory homeostasis. Moreover, semiology observed during GCS in humans can resemble the decerebrate and decorticate posturing seen in comatose patients, suggesting varying degrees of cerebral and brainstem compromise. We hypothesized that peri-ictal brainstem semiology might predict the severity of a GCS, based on cardiorespiratory dysfunction and postictal generalized electroencephalographic suppression (PGES). To test our hypothesis, we conducted a multicentric and prospective analysis of GCS-induced cardiorespiratory dysfunction and PGES and their relationship with peri-ictal brainstem semiology in adult patients admitted for VEEG monitoring. The results of our study show that peri-ictal brainstem semiology is a biomarker of GCS severity defined by PGES and variables of respiratory dysfunction but not of cardiac arrhythmias of interest (exaggerated sinus arrhythmia with bradycardia [ESAWB], asystole, bradycardia, atrioventricular block [AVB], supraventricular tachycardia [SVT], atrial fibrillation [Afib], non-sustained ventricular tachycardia [NSVT] and, ventricular fibrillation [VF]). Specifically, any ictal brainstem semiology (decerebration, decortication, or hemi-decerebration) during GCS increases the risk of PGES and is associated with larger SpO2 desaturations. Moreover, ictal decerebration is associated with longer PGES. Regarding postictal brainstem semiology, this is associated with a sixfold increased risk of PCCA and longer hypoxemia and SpO2 recovery after GCS. Potentially fatal cardiac arrhythmias such as asystole, bradycardia, AVB, SVT, Afib, NSVT, and VF are rare, and along with ESAWB, are unrelated to peri-ictal brainstem semiology, PGES, and respiratory dysfunction. This suggests that arrhythmias caused by GCS are unrelated to cortical suppression or hypoxia and may be due to underlying cardiac occult abnormalities.

Date of Award	16 Dec 2024
Original language	English
Supervisor	Samdem Dorjee Lhatoo (Director) & Nuria Lacuey Lecumberri (Director)