# Severe, Non‐apneic Respiratory Dysfunction and Hypoxia following Generalized Convulsive Seizures

## TL;DR

This study shows that seizures can cause dangerous breathing and heart issues, even without stopping breathing, which may contribute to sudden deaths in epilepsy patients.

## Contribution

The study identifies non-apneic respiratory dysfunction as a novel and significant risk factor for SUDEP.

## Key findings

- Severe non-apneic respiratory dysfunction occurs frequently after generalized convulsive seizures.
- Shallow or irregular breathing is linked to severe oxygen drops and slower heart rates.
- Breathing and heart issues are closely connected after seizures.

## Abstract

Sudden unexpected death in epilepsy (SUDEP) is a devastating consequence of some generalized convulsive seizures (GCS). Recent work has focused on seizure related apnea as a biomarker of SUDEP risk, frequently without characterizing the adequacy of non‐apneic ventilation or identifying other dysfunctional breathing patterns. We hypothesized that GCS frequently induce immediate, severe, non‐apneic respiratory dysfunction that can induce critical hypoxia and bradycardia and sought to characterize breathing patterns after GCS.

Adult patients admitted to an epilepsy monitoring unit were studied. The effects of GCS on breathing and heart rate were analyzed using nasal pressure transducers, chest and abdominal respiratory inductance plethysmography, capillary oxygen saturation, transcutaneous CO2, electrocardiogram, electroencephalogram, and expert audiovisual analysis. Correlation analyses, the Mann–Whitney test, and an unpaired t test were used to analyze relationships between dysfunctional breathing patterns and both the severity of postictal hypoxemia and the heart rate.

Thirty‐two GCS from 22 patients were analyzed and 31 exhibited 1 or more of the following breathing patterns: disordered rhythmicity (n = 28/32, 87.5%), shallow breathing (n = 12/32, 37.5%), thoracoabdominal asynchrony (n = 24/30, 80.0%), and upper airway obstruction (n = 30/32, 93.8%). Oxygen desaturation was more severe when postictal breathing was shallow or irregular in amplitude. The latter was associated with absolute or relative bradycardia.

Nonfatal GCS frequently induce immediate, severe, non‐apneic respiratory dysfunction temporally associated with severe hypoxia and bradycardia. Our study suggests that postictal respiratory and cardiac function are tightly coupled and highlights the importance of including all the relevant pathologic variables in studies of SUDEP pathogenesis. ANN NEUROL 2026;99:1263–1276