Rationale: Ictal asystole (IA) is a rare neurocardiac manifestation of focal epilepsy, particularly with temporal or insular onset, and may mimic intrinsic cardiac arrhythmias such as sick sinus syndrome (SSS). In older adults, distinguishing seizure-related cardiac pauses from primary conduction abnormalities is essential to prevent injury, guide treatment, and detrimental outcomes.
Methods: We report a unique case with possible concurrent IA and intrinsic SSS.
Results:
A 61-year-old woman with epilepsy since age 16, previously well-controlled on phenytoin, experienced infrequent focal impaired awareness seizures (FIAS), averaging 3–4 per year. Over the past decade, she developed new seizure semiology characterized by sudden atonia, falls, and transient loss of consciousness lasting 15–30 seconds. In the months leading up to her admission to the epilepsy monitoring unit (EMU), seizure frequency increased to twice weekly, resulting in frequent falls and injuries despite adjustments to her antiseizure medications.
During EMU evaluation, multiple habitual events were recorded and confirmed as FIAS, with electrographic onset localized to the right posterior temporal and parietal regions. Thirteen seizures were associated with prolonged asystole lasting 15 to 36 seconds (median 24 sec), and four additional events showed ictal bradycardia. Diffuse EEG background slow and diffuse cerebral suppression were seen when IA. The average latency from EEG seizure onset to asystole was 31.5 ± 10 seconds. Given the frequency, duration and severity of the cardiac pauses, along with the history of frequent falling/injuries, a dual-chamber (DDD) pacemaker was implanted. Post implantation telemetry subsequently revealed two pacing events in the absence of concurrent EEG ictal activity or seizure symptoms, raising concern for a coexisting diagnosis of SSS.
Conclusions:
IA is thought to result from seizure propagation to central autonomic structures—particularly the insula, amygdala, and medial prefrontal cortex—leading to heightened parasympathetic output and transient cardiac inhibition. IA typically manifests after electrographic seizure onset and resolves spontaneously. In contrast, SSS reflects intrinsic sinoatrial node dysfunction, causing spontaneous bradyarrhythmias or pauses independent of ictal activity.
This patient’s post-pacemaker pacing events without corresponding EEG seizure patterns raises concern for dural pathology of coexisting SSS besides the confirmed IA. The overlap complicates clinical interpretation. Accurate differentiation is critical, as treatment approaches differ. While pacemaker implantation remains debated in isolated IA, its utility is recommended for prolonged asystole or suspected concurrent arrhythmia. This case underscores the importance of integrated EEG-ECG monitoring in evaluating seizure-related syncope or falls, especially when recognized as new seizure semiology. Ongoing cardiac evaluation is warrant when pacing occurs independent of electrographic seizures, suggesting a dual neurocardiac pathology. Ultimately, optimizing seizure control remains essential for reducing morbidity, injury, and unexpected death risk in this vulnerable population.
Funding: none