Determining, Treating, and Preventing Mechanisms of Sudden Death in Epilepsy using Medical Implantable Devices

Abstract

People with epilepsy have an increased risk of mortality when compared to the general population. These increased mortality risks include deaths related to status epilepticus and sudden unexpected death in epilepsy (SUDEP). Physiological data describing cardiac, respiratory, and brain function prior to sudden death in epilepsy is crucial to the studying the underlying mechanisms behind these deaths. Because it is unknown when sudden deaths in epilepsy may occur, continuous monitoring is necessary to guarantee the capture of physiological data prior to death. I have used custom designed implantable devices to continuously measure cardiac, respiratory, and neurological signals in freely behaving rats with chronically induced epilepsy. Due to the continuous respiration measurements, the resultant dataset is the first of its kind. This dataset indicates that respiratory abnormalities (reduced respiration and short apneas) occur during and after seizures. These abnormalities may indicate SUDEP onset because obstructive apneas due to laryngospasm have been indicated as possible causes of SUDEP in other studies. Laryngospasms can be caused by gastric acid coming into contact with the larynx. During a laryngospasm, intrinsic laryngeal muscles contract, resulting in the closure of the airway. Recently published research has indicated that acid reflux may be responsible for triggering fatal laryngospasms in rats with induced seizures. I have found that the larynx can be opened during a laryngospasm by electrically stimulating the recurrent laryngeal nerves. I have also found that performing gastric vagotomies leads to a statistically significant reduction in mortality due to fatal apneas in rats with induced seizures.