Respiratory acidosis caused by spontaneous focal seizures in the EMU
Abstract number :
1.024
Submission category :
3. Neurophysiology
Year :
2015
Submission ID :
2327420
Source :
www.aesnet.org
Presentation date :
12/5/2015 12:00:00 AM
Published date :
Nov 13, 2015, 12:43 PM
Authors :
Mirasol Forcadela, Patrick W. Carney, Annie Roten, Saul Mullen
Rationale: Hypoventilation leading to respiratory acidosis is ubiquitous in convulsive seizures. In focal seizures, reduced oxygen saturation has been reported in around a third. This reduced respiration has been proposed as part of the mechanism of Sudden Unexpected Death in Epilepsy (SUDEP). Conversely, animal models suggest that acute respiratory acidosis may be anti-epileptic, meaning this acidosis may form part of the homeostatic mechanism bringing seizures to an end. Saturation of O2 changes late in hypoventilation, however, so that a more sensitive measure of ventilation is needed. Here we use transcutaneous CO2 (tcCO2); an accurate, real time, non-invasive measure of arterial CO2Methods: 30 patients admitted to the Epilepsy Monitoring Unit at Austin Health, Melbourne for focal epilepsy were recruited and underwent transcutaneous monitoring of arterial carbon dioxide (tcCO2) using the TOSCA 500 (Radiometer, Basel, Switzerland). Data was recorded using Compumedics Profusion 4 software allowing time-synchronised review of EEG, video and tcCO2. Seizures were recorded in 10 patients.Results: Five patients with brief (<2 minute) self-limiting temporal lobe seizures demonstrated a rapid increase in tcCO2 of 6-10mmHg. Return to baseline tcCO2 was slow, taking up to an hour despite complete clinical and EEG recovery. Peak tcCO2 occurred within two minutes of seizure onset. Four temporal lobe seizures progressing to convulsion showed a lesser rise in tcCO2 during the focal phase (mean 2mmHg vs 7.6mmHg, p<0.05). Two patients with multiple brief, hypermotor frontal seizures (<30s) showed no increase in tcCO2 associated with these seizures.Conclusions: Brief temporal lobe seizures result in rapid hypoventilation that is sustained long past apparent clinical recovery. In temporal seizures that instead progress to convulsion, this hypoventilation appears significantly less pronounced. This suggests that hypoventilation may contribute to the homeostatic mechanisms that bring temporal lobe seizures to an end. There is also evidence of remarkably prolonged alteration of central respiratory drive after even brief temporal seizures; a phenomenon that may be of importance to the proposed respiratory mechanism of sudden unexpected death in epilepsy.
Neurophysiology