1200 Overstimulated: A Case of Hypoglossal Nerve Stimulator Over-titration

Abstract Introduction Hypoglossal nerve stimulation (HNS) is an effective treatment for obstructive sleep apnea (OSA) that stimulates nerves that protrude the tongue and move the hyoid bone anteriorly to restore airway patency during sleep. After implantation, the stimulator voltage is titrated to an optimal therapeutic level. We describe the case of a patient whose OSA was effectively treated at a lower voltage and then demonstrated worsening sleep apnea after over-titration to a higher voltage. Report of case(s) A 37-year-old healthy man with a body mass index of 32 kg/m2 presented with snoring. A polysomnogram revealed an apnea hypopnea index (AHI) of 53.9 events per an hour consistent with severe OSA. He was intolerant of continuous positive airway pressure (CPAP) and trial of a mandibular advancement device (MAD) was ineffective. The patient subsequently underwent hypoglossal nerve stimulator implantation without complications. After an appropriate healing period, his device was activated with a noted functional amplitude of 0.8V and an allowed range of 0.8V to 1.8V. During self-titration, the patient noted improvement of snoring and apneas at an amplitude of 1.6V. However when he increased the amplitude further he noted recurrence of his OSA symptoms. He underwent an attend polysomnography titration study that revealed an estimated AHI of less than 10 with his HNS set to 1.6V representing an appropriate treatment response. However, when his HNS was titrated up to 1.7V, his estimated AHI increased to 26.4 consistent with moderate OSA. The patient’s device was set to a voltage of 1.6V. Conclusion HNS is an important treatment option for patients with OSA who are intolerant of CPAP. After implantation, attention must be given to careful titration of the stimulation voltage during an attended polysomnogram to avoid over titration which can lead to an increased number of obstructive events in some patients. While the mechanism of this phenomenon is currently unknown, theoretical mechanisms include stimulation of the lateral division of the hypoglossal nerve triggering tongue retraction at higher voltages and genioglossus muscle fatigue. Support (if any)