Hypoglossal nerve stimulation(HNS)is an increasingly popular CPAP-alternative treatment for select patients with obstructive sleep apnea(OSA) .It displaces the tongue, dilating the pharyngeal airway at multiple levels by elastically pulling other airway structures anteriorly via palatoglossal coupling.Nevertheless, only a portion of treated patients respond sufficiently to HNS, indicating that additional respiratory neurostimulation strategies are needed.Pharyngeal patency is intimately linked to changes in pulmonary volume.Lung volume increases induce caudal pharyngeal traction via tracheal attachments, decreasing pharyngeal collapsibility.Putative mechanisms include unfolding and longitudinal stretching of the pharyngeal walls, decompressing peripharyngeal tissues, and displacing the hyoid bone anteriorly and inferiorly.The infrahyoid strap muscles can also pull the pharynx caudally.Available data document that ansa cervicalis stimulation(ACS)of the infrahyoid muscles increases airflow and retropalatal cross-sectional area and decreases pharyngeal collapsibility during flow-limited breathing.The stylopharyngeus muscle originates from the styloid process of the temporal bone and inserts medially into the oropharyngeal lateral wall between the superior and middle constrictor muscles.It is innervated by the glossopharyngeal nerve, which also contributes to the pharyngeal plexus motor branches innervating the constrictor muscles.Glossopharyngeal nerve stimulation(GNS)is hypothesized to generate coactivation of the stylopharyngeus muscle and pharyngeal constrictor muscles to stiffen the oropharyngeal wall and pulls it laterally to stabilize it during inspiration.Here we review the pathophysiologic mechanisms of pharyngeal collapse and available data regarding the mechanical effects of HNS, ACS, and GNS on pharyngeal patency.
Hara et al. (Mon,) studied this question.