Abstracts

Rationale: Ictal asystole (IA) is a well-known but poorly understood complication of epilepsy. Previous studies have found IA to be associated with long-standing, refractory focal epilepsy1. Pacemaker insertion in patients with IA not responding to medical or surgical treatment is common practice, given the assumed risks of sudden unexpected death in epilepsy (SUDEP) and fall related trauma. The aim of this case report was to search for specific patterns of seizures associated with risk of IA. Methods: We present the case of a 63-year-old male with epilepsy who was admitted to the Department of Neurology at Rigshospitalet, Copenhagen, Denmark for epilepsy surgery evaluation. The patient’s EEG, ECG and video recordings were reviewed in detail. Results: The patient was diagnosed with epilepsy in 2008 after a first bilateral tonic-clonic seizure. Since 1980 he had had episodes starting with a metallic taste and epigastric aura, sometimes progressing to déja-vu and subsequent loss of consciousness with oromandibular automatisms, without seeking medical care. EEG showed spikes in the right mid-temporal region and MRI showed mesial temporal sclerosis and parietal cortical dysplasia, both on the right side. Since the diagnosis he continued to have five to six monthly focal seizures despite polytherapy. In 2019, he was admitted for video-EEG monitoring to determine epilepsy surgery eligibility. Upon admittance, he was treated with lacosamide 450 mg, eslicarbazepine acetate 1600 mg and topiramate 200 mg per day.  During a four-day long admittance, with gradual tapering of the AEDs, the patient had 18 focal seizures, 17 of which showed clear EEG correlate over the right pre-mid-(post)-temporal region. The first 16 seizures lasted between 30 to 50 seconds. The 17th and 18th seizures lasted 97 and 113 seconds, respectively, and towards the end of these seizuress the ECG showed bradycardia progressing to asystolic periods lasting 10.3 (5.2+5.1) seconds in the 17th seizure and 10.0 (3.6+6.4) seconds in the 18th seizure. Epileptiform activity terminated around the start of asystole in both seizures. The patient was unresponsive during the asystolic periods and had myoclonic movements in the extremities which were not observed during the seizures without asystole. At that time, the AED treatment had been tapered off to eslicarbazepine acetate 400 mg per day. Conclusions: This case report of 18 successive focal seizures showed an evolvement of the seizures throughout the four days of video-EEG monitoring, as AEDs were gradually tapered, with longer duration of the seizures towards the end of the observation period and finally with four episodes of IA in the two last seizures. The increased seizure frequency, and indeed the increased duration of the two last seizures, possibly allowing for propagation to areas critical to autonomic control, might explain why this patient without a history of cardiac disease suddenly had seizures with IA. Whether IA serves as a way of seizure-termination2 or could lead to SUDEP needs further investigation. However, our observation of asystole co-occurring with the end of electrographical seizure activity might raise the question of whether pacemaker insertion could prolong seizure activity. References 1. Tényi, D., Gyimesi, C., Kupó, P., Horváth, R., Bóné, B., Barsi, P., Kovács, N., Simor, T., Siegler, Z., Környei, L., Fogarasi, A. and Janszky, J. (2019). Ictal asystole: A systematic review. 2. Benditt, D., van Dijk, G. and Thijs, R. (2015). Ictal Asystole. Circulation: Arrhythmia and Electrophysiology, 8(1), pp.11-14. Funding: No funding