Stimulation of the Internal Superior Laryngeal Nerve as a Potential Therapy for Obstructive Sleep Apnea in a Porcine Model.

Abstract

Impaired pharyngeal sensing of negative pressure can lead to a blunted response of the upper airway dilator muscles and contribute to the development of obstructive sleep apnea (OSA). This response is modulated by the nerve fibers in the internal branch of the superior laryngeal nerve (iSLN), mediating negative pressure sensation. Artificial excitation of these fibers could be a potential treatment target for OSA. To evaluate this, electrostimulation of the iSLN was performed in a porcine isolated upper airway model. Artificial obstructions were induced by varying levels of negative pressure and the ability of the animal to resolve these obstructions was evaluated. The pressure at which the animal was still able to resolve the obstruction was quantified as 'Resolvable Pressure'. Thereby, the effects on pharyngeal patency (n=35) and the duration of the therapeutic effect outlasting the stimulation (n=6) were quantified. Electrostimulation prior to the introduction of an artificial obstruction improved the median resolvable pressure from -28.3 cmH2O [IQR: -45.9; -26.1] to -92.6 cmH2O [IQR: -105.1; -78.6]. The median therapeutic effect was found to outlast the last stimulation burst applied by 163 s when five stimulation bursts were applied in short succession [IQR: 58; 231], 58 s when two were applied [IQR: 7; 65], and 6 s when one was applied [IQR: 0; 51]. Stimulation of the iSLN increased EMG in the genioglossus. The proposed treatment concept can improve pharyngeal patency in the model. Transfer of the results to clinical application could enable the development of a new neuromodulation therapy for OSA.