Resident New York-Presbyterian Weill Cornell Medical Center New York, New York
Rationale: Ictal asystole is defined as the absence of ventricular complexes for more than four seconds following a seizure, and is a risk factor for sudden unexpected death in epilepsy (SUDEP), with reported incidence between 0.4 to 9 deaths per 1000 patient years and is often associated with temporal lobe epilepsy (TLE).1 We present a case report of ictal asystole captured during video EEG monitoring, treated with permanent pacemaker (PPM) placement and seizure control to reduce future SUDEP and fall risk. Methods: We present the case of a 70 year-old woman with idiopathic localization-related epilepsy characterized by impaired consciousness, poorly compliant on levetiracetam and lamotrigine, admitted to the epilepsy monitoring unit for seizure characterization and antiepileptic drug (AED) adjustment. Patient was monitored on long lead electrocardiogram, EEG montage, and cardiac telemetry. Results: A 40-second left temporal seizure was captured during sleep, with seizure onset accompanied by tachycardia progressing to bradycardia followed by 20 seconds of cardiac asystole captured on long lead ECG and cardiac telemetry. Post-ictal generalized EEG suppression (PGES) was seen. Patient spontaneously recovered cardiac activity in sinus rhythm and remained asleep with no event recollection upon interview. She completed comprehensive cardiac work up including ECG, troponin, and echocardiogram which showed no abnormalities. The patient underwent PPM and loop recorder placement on this admission. Lacosamide was discontinued and she was started on sodium valproate. Patient was counseled on AED compliance with close neurology and cardiology follow up. Conclusions: Ictal asystole is a rare but potentially fatal complication of TLE and a risk factor for SUDEP. Left TLE in particular is associated with autonomic-induced cardiorespiratory phenomena such as ictal bradycardia and ictal central apnea, due to the role of the left insular region in parasympathetic regulation demonstrated through cortical stimulation and lesional studies.2, 3. Genetic mutations causing cardiac arrhythmia syndromes such as Long-QT syndrome (KCNQ1, KCNH2), Brugada syndrome (SCN5A), and CHN channel mutations in (HCN1, 2, and 4) co-occurring with epilepsy are associated with an increased risk of SUDEP.4,5 AEDs such as lacosamide, carbamazepine, phenytoin, and lamotrigine have also been reported to cause bradyarrhythmias and cardiac arrest due to their effects on the sodium channel.6 Ictal asystole is a rare but potentially fatal complication of epilepsy, and these patients should undergo comprehensive cardiac work up. PPM placement and counseling on seizure control can mitigate fall risk and reduce overall morbidity and mortality in TLE patients.
References: 1. Tomson, T et al. “Sudden unexpected death in epilepsy: a review of incidence and risk factors.” Epilepsia. 2005 46(11):54-61. 2. Lanz, M et al “Seizure induced cardiac asystole in epilepsy patients undergoing long term video-EEG monitoring.” Seizure. 2011 20:167-72. 3. Britton, JW et al. “The ictal bradycardia syndrome: localization and lateralization.” Epilepsia. 2006 47(4):737-44. 4. Tu, E et al “Genetic analysis of hyperpolarization-activated cyclic nucleotide-gated cation channels in sudden unexpected death in epilepsy cases.” Brain Pathol. 2011. 21(6):692-8. 5. Bagnali, RD et al. “Genetic basis of sudden unexpected death in epilepsy.” Front Neurol. 2017 8:348. 6. Shah, RR et al. “Cardiac effects of antiepileptic drugs.” Atlas of Epilepsies. 1479-86. . Funding: Please list any funding that was received in support of this abstract.: No funding was received in support of this abstract. Click here to view image/table