Abstract

Obstructive sleep apnea (OSA) in patients with epilepsy can be magnified when they are treated with a Vagus Nerve Stimulator (VNS). Studies have shown that patients with a VNS have reduced airflow and respiratory effort [1]. These changes in respiratory mechanics during sleep can predispose patients to develop OSA. We describe a 12-year-old female with medically intractable epilepsy who had a VNS implanted as additional therapy. She was referred for snoring, excessive tiredness, and frequent movements during sleep. The Pediatric Daytime Sleepiness Scale was 11. During the overnight PSG, there was evidence of obstructive apneas and hypopneas associated with VNS firing. (30 seconds on and 180 seconds off). The patient had an obstructive AHI of 13.5/hr.; oxygen nadir of 77% and pCO2 of 41. BPAP was initiated and titrated to 11/7 cm H20 with a backup rate of 12. BPAP with the VNS “on” resulted in an obstructive AHI of 0.0 and oxygen nadir of 94%. VNS usage can be effective in treating patients with refractory epilepsy. During activation, narrowing of the pharynx and larynx is a result of stimulation of motor efferents in the dorsal motor nucleus of the vagus nerve and nucleus ambigus that leads to airflow limitation. VNS associated respiratory events may be treated with PAP therapy in cases where adjustment of the VNS is not helpful or cannot be turned “off” in order to maintain seizure control. In our experience, three patterns of events from firing of the VNS impact breathing during sleep. In this report, firing of the VNS was associated with airflow limitation, arousal and/or 3% oxygen desaturation. Firing of the VNS with flow limitation but no arousal or 3% oxygen desaturation- an unscorable event. A mixed pattern of scorable and unscorable events associated with VNS firing.

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