Obstructive sleep apnea and respiratory complications associated with vagus nerve stimulators

Abstract

Intermittent vagus nerve stimulation can reduce the frequency of seizures in patients with refractory epilepsy. Stimulation of vagus nerve afferent fibers can also cause vocal cord dysfunction, laryngeal spasm, cough, dyspnea, nausea, and vomiting. Vagus nerve stimulation causes an increase in respiratory rate, decrease in respiratory amplitude, decrease in tidal volume, and decrease in oxygen saturation during periods of device activation. It usually does not cause an arousal, or a change in heart rate or blood pressure. Most patients have an increase in their apnea-hypopnea index (AHI). Patients with VNS can have central apneas, obstructive hypopneas, and obstructive apneas. These respiratory events can be reduced with changes in the vagus nerve stimulator operational parameters or with the use of CPAP. In summary, there are complex relationships between epilepsy and obstructive sleep apneas. In particular, patients with refractory epilepsy need assessment for undiagnosed and untreated obstructive sleep apnea before implantation of vagus nerve stimulator devices. Patients with vagus nerve stimulators often have an increase in apneic events after implantation, and these patients need screening for sleep apnea both before and after implantation.

Keywords: Vagus nerve stimulator; dysphonia; seizure disorder; sleep apnea.

Figure 1

A 300-second representative epoch from a patient with a vagus nerve stimulator Chin EMG (green) shows artifacts corresponding to the VNS activation (labeled “VNS On”). VNS activation corresponds to an increase in respiratory rate, decrease in airflow, decrease in chest and abdominal excursion, and a variable decrease in oxygen saturation.