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Seizure-induced asystole
  1. David Steckman,
  2. David Katz,
  3. William Sauer,
  4. Duy Nguyen
  1. Cardiac Electrophysiology, Cardiology Division, University of Colorado, Denver, Colorado, USA
  1. Correspondence to Dr Duy Nguyen, 12401 E 17th Ave, Leprino Bldg., 5th Floor, Mailstop B-132, Aurora, CO 80045-2548, USA; duy.t.nguyen{at}ucdenver.edu

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A 48-year-old woman with pharmacologically intractable epilepsy was admitted for continuous electroencephalography for seizure characterisation and surgery. She had a long history of generalised tonic-type seizures for which a vagal nerve stimulator (VNS) was implanted. During electroencephalography monitoring, she experienced her typical visual aura with seizure onset, which was then followed by 45 s of asystole (panel A). A right-sided single chamber pacemaker was implanted, avoiding the left pectoral VNS. Testing of the VNS at high output revealed no detection by the pacemaker. Repeat electroencephalography monitoring during seizure activity resulted in pacing prevention of asystole allowing for further neurological mapping (panel B).

Panel A

Pre-pacemaker implantation continuous EEG with single-lead telemetry displaying right temporal lobe epileptic activity triggering an asystolic rhythm. The black solid arrow signifies asystolic telemetry lead recording. Electrocardiogram (EKG), Oxygen saturation (OSAT).

Panel B

Continuous EEG with single-lead telemetry displaying seizure activity onset with sinus rhythm followed by bradycardia with pacemaker initiation at 50 beats per minute. The black solid arrow refers to normal sinus beat. The open arrow refers to beginning of pacemaker activity. Electrocardiogram (EKG), Oxygen saturation (OSAT).

Ictal asystole is a rare but life-threatening consequence of epileptic seizures and may be a cause of sudden unexpected death in epilepsy (SUDEP). Asystole is probably caused by a dysautonomic mechanism independent of neurocardiogenic syncope.1 SUDEP is thought to cause 7–17% of all deaths in epilepsy and is 24 times more common in patients with epilepsy than the normal population.2

In this case, seizure mapping and treatment were possible with the use of pacing to prevent ictal asystole. There was no interaction with a previously implanted contralateral vagal stimulator. Those patients similar to the one described in our case requiring seizure provocation may be considered for pacemaker implantation as a bridge to epilepsy surgery and for the prevention of SUDEP.

References

Footnotes

  • Competing interests None.

  • Provenance and peer review Not commissioned; internally peer reviewed.

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