Catamenial Temporal Lobe Epilepsy Presenting with Ictal Asystole: A Case of Hormonal Modulation and Cardiac Pacing
Objective:
To describe a unique case of catamenial temporal lobe epilepsy presenting with ictal bradycardia(IB)/ictal asystole(IA) and to highlight the role of hormonal modulation in management.
Background:
IA/IB is a rare but serious cardiac complication of focal epilepsy, occurring in approximately 0.27% to 0.40% of patients undergoing long-term video-EEG monitoring.Temporal lobe onset is predominant in IA, accounting for ~80–90% of cases, often lateralized to the left hemisphere. Seizure frequency can align with menstrual cycle in women which is designated as catamenial epilepsy. Hormonal fluctuations play a key role: progesterone exerts anticonvulsant effects through GABA_A receptor modulation, whereas estrogen promotes neuronal excitability. Abrupt progesterone withdrawal and relatively elevated estrogen levels during the perimenstrual phase reduce seizure threshold and may precipitate severe complications.
Design/Methods:
A 41-year-old woman with a longstanding history of perimenstrual syncopal episodes underwent continuous video-EEG and ECG monitoring in the epilepsy monitoring unit. Clinical, electrographic, and hormonal correlations were analyzed, and treatment outcomes were followed over two years.
Results:
Multiple habitual seizures were recorded, each beginning with intrusive thought auras followed by loss of consciousness and generalized jerking. Ictal EEG showed rhythmic theta activity over the left temporal region evolving into generalized delta and background suppression. ECG revealed sinus arrest lasting 11 seconds following seizure onset. Interictal EEG demonstrated left temporal sharp waves and slowing. A loop recorder confirmed recurrent asystole, prompting pacemaker implantation. Syncope resolved, but perimenstrual seizure clustering persisted. Initiation of elagolix, a gonadotropin-releasing hormone (GnRH) antagonist, eliminated both seizures and syncopal events. The patient remained event-free for two years.
Conclusions:
This is the first reported case of IA triggered by hormonal fluctuations during the perimenstrual phase. Seizure onset in the left frontotemporal region likely induced excessive vagal activation, compounded by progesterone withdrawal. Combined therapy with cardiac pacing and hormonal suppression successfully prevented both ictal systole and seizure clustering.
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