Recent animal work and limited clinical data have suggested that laryngospasm may be involved in the cardiorespiratory collapse seen in sudden unexpected death in epilepsy (SUDEP). In previous work, we demonstrated in an animal model of seizures that laryngospasm and sudden death were always preceded by acid reflux into the esophagus. Here, we expand on that work by testing several techniques to prevent the acid reflux or the subsequent laryngospasm.
In urethane anesthetized Long Evans rats, we used systemic kainic acid to acutely induce seizure activity. We recorded pH in the esophagus, respiration, electrocorticography activity, and measured the liquid volume in the stomach postmortem. We performed the following three interventions to attempt to prevent acid reflux or laryngospasm and gain insights into mechanisms: fasting animals for 12 h, severing the gastric nerve, and electrical stimulation of either the gastric nerve or the recurrent laryngeal nerve.
Seizing animals had significantly more liquid in their stomach. Severing the gastric nerve and fasting animals significantly reduced stomach liquid volume, subsequent acid reflux, and sudden death. Laryngeal nerve stimulation can reverse laryngospasm on demand. Seizing animals are more susceptible to death from stomach acid-induced laryngospasm than nonseizing animals are to artificial acid-induced laryngospasm.
These results provide insight into the mechanism of acid production and sudden obstructive apnea in this model. These techniques may have clinical relevance if this model is shown to be similar to human SUDEP.

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