Objective:
To describe a case of post-cardiac arrest refractory myoclonus and ventricular tachycardia responsive to high-dose levetiracetam.
Background:
Levetiracetam is a first-line agent for anoxic myoclonus. However, levetiracetam is not known to have anti-arrhythmia properties, particularly in persistent arrhythmias following cardiac arrest.
Design/Methods:
Case Description: A 17-month-old female presented in ventricular fibrillation arrest thought to be secondary to methamphetamine toxicity and a mitochondrial genetic mutation (discovered and confirmed later in her hospitalization). Return of spontaneous circulation was achieved after prolonged resuscitation. Seven days later, she demonstrated frequent (>40/minute), large-amplitude, non-stereotyped, brief movements involing the neck and all extremities consistent with myoclonus. Elecetroencephalogram (EEG) determined movements to be non-epileptic. Magnetic resonance imaging (MRI) on day 8 post-arrest was without evidence of diffusion restriction or T2-flair abnormalities and was thought to represent pseudonormalization in setting of hypoxic injury. Her movements were refractory to: ketamine, morphine, midazolam, dexmedetomidine, and cisatracurium. She developed frequent ectopy and intermittent ventricular tachycardia refractory to esmolol, sotalol, and lidocaine. After receiving 60 milligrams/kilogram (mg/kg) of intravenous levetiracetam, both the myoclonus and arrhythmia temporarily normalized, but returned on maintenance dosing of 30 mg/kg twice a day (BID). After increasing the maintenance dosing to 50 mg/kg BID, her myoclonus and arrhythmia both improved again with sustained benefit with higher dosing.
Conclusions:
A sustained improvement in post-cardiac arrest refractory myoclonus and tachyarrhythmia was achieved with high-dose levetiracetam. Peripheral overactive N-type calcium currents from sympathetic hyperactivation have been implicated in ventricular arrhythmogenesis. Hypoxic injury to the brainstem could cause a brainstem reticular reflex myoclonus as well as damage to the autonomic relay nuclei. Temporal lobe injury could cause subcortical myoclonus as well as increased sympathetic outflow. Levetiracetam’s blockade of calcium currents at any of these sites could be an explanation for its beneficial effect on both myoclonus and tachyarrhythmia in this patient.