Abstracts

Rationale: Vagus nerve stimulation (VNS) has been widely used for treatment-resistant epilepsy in both adults and children since its FDA approval in 1997. Reported side effects include hoarse voice, dysphagia, cough, dyspnea, lower facial weakness, paresthesias, as well as cardiac arrhythmias. Although instances of cardiac side effects including brady-arrhythmias and even asystole have been reported, complications of arrhythmias associated with the removal or deactivation of VNS are not addressed in the literature. We report a case of a patient who suffered an episode of symptomatic supraventricular tachycardia (SVT) possibly associated with VNS deactivation.Methods: Case analysis with PUBMED literature review was employed.Results: The patient is a 30 year-old woman who had VNS implanted in 2006 for refractory epilepsy, and was being monitored in our epilepsy monitoring unit for pre-surgical evaluation. Her only comorbid medical diagnosis was nicotine dependence. Her outpatient medications included lamotrigine 400mg twice daily, zonisamide 100mg daily, imipramine 50mg daily, and folic acid 400mcg daily. During her admission all antiepileptic drugs were discontinued. Pertinent laboratories were normal. Her baseline pulse recorded prior to deactivation of VNS ranged from 72 to 107 beats per minute. Her vagus nerve stimulator was turned off on admission for monitoring prior to placement of intracranial leads. Following VNS deactivation, the patient displayed persistent sinus tachycardia into the 140s throughout her admission, which progressed to a clinically significant cardiac event that occurred on post-admission day 10. Within ten minutes of a GTC seizure, the patient had a 3-minute episode of aberrant SVT with heart rate into the 220s and respiratory decline prompting a hospital code. The patient subsequently recovered and metoprolol 25mg twice daily was initiated. Pulse returned to 80 to 100 beats per minute two weeks after her VNS was reactivated while on metoprolol. Risk factor analysis suggests that the precipitants for this patient s SVT were the combined effects of ictal tachyarrhythmia and reflex tachyarrhythmia due to the abrupt discontinuation of continual VNS. Conclusions: The severity of the cardiac event in this case and the associated risk of SUDEP (sudden unexpected death in epilepsy) suggest that when VNS is deactivated in epilepsy patients, closer cardiac monitoring and evaluation is warranted. If tachycardia develops following VNS deactivation, prophylactic treatment with beta-blockers may be indicated even if such tachycardia is asymptomatic. Further research addressing cardiac arrhythmias associated with deactivation of VNS is required.