Abstracts

Rationale: Peri-ictal asystole is uncommon. Ictal asystoles typically occur during focal seizures with impaired awareness, are self-limited in most cases, and in patients with refractory focal epilepsy admitted for video-EEG telemetry the mean prevalence of ictal asystole is 0.318% 1.  Postictal asystole occurs following bilateral tonic-clonic seizures and postictal generalized EEG suppression (PGES). Seven of 13 patients with postictal asystole died of probable SUDEP 1. Peri-ictal oxygen desaturation may be relevant in the pathophysiology of asystole with seizures. There are no published data on concurrent recording of respiratory parameters during ictal/postictal asystole. Methods: We report on two cases of patients with asystole recorded in the EMU where synchronized oxygenation data and EKG was available during video-EEG telemetry. Results: A 55-year-old woman with cortical migration anomaly involving the right parietal region had a history of seizures at times followed by sudden falls. A focal seizure over the right posterior quadrant without progression to bilateral tonic clonic seizure was captured (Figure 1). There was impaired awareness during the seizure that lasted 47 sec. The patient was sitting in bed and fell back abruptly 51 seconds after seizure onset, at which time the EEG showed generalized voltage attenuation. She was bradycardic (RR interval of 2480 msec) 39 seconds after seizure onset and then asystolic 3 seconds later. Asystole lasted 15 seconds. Oxygen saturation was 98-99% prior to seizure onset. A mild desaturation to a nadir of 89% occurred starting 65 seconds after seizure onset. There was a 10 second central apnea at seizure onset.A 43-year-old man with left temporal lobe focal epilepsy had a focal onset seizure with auditory aura progressing to a bilateral tonic clonic seizure 43 sec later. The seizure lasted 83 seconds followed by PGES for 37 seconds. Oxygen saturation was 100% at seizure onset. 106 sec after seizure onset saturation was below 90%, gradually reaching a nadir of below 50% at 186 sec after seizure onset (Figure 2). Oxygen saturation remained below 90% for 266 seconds. The patient was supine. Bradycardia (RR 2423 msec) occurred 163 sec after seizure onset followed by 8 sec asystole. The patient was bradycardic for another 20 seconds. He was apneic for 50 seconds with seizure generalization. Conclusions: In the patient with a focal seizure without generalization, there was ictal bradycardia and asystole with minimal oxygen desaturation. Oxygen desaturation in this case was not of a severity to cause asystole and other central mechanisms may have been causative. The second patient with a bilateral tonic clonic seizure had postictal asystole and severe oxygen desaturation. The severity of hypoxemia in this case likely contributed to the asystole. Different mechanisms may be involved in seizures with ictal asystole and those with postictal asystole. Severe hypoxemia may play a role in the causation of postictal bradycardia and asystole and sudden unexpected death in epilepsy.1. van der Lende M et al. J Neurol Neurosurg Psychiatry 2016;87:69-74 Funding: None.