Ansa Cervicalis and Hypoglossal Nerve Stimulation in a Patient With Obstructive Sleep Apnea

Hypoglossal nerve stimulation (HNS) is an alternative surgical therapy for individuals who are intolerant to positive airway pressure but have obstructive sleep apnea (OSA) that ventrally protrudes the tongue, although it may be insufficient in individuals with greater susceptibility to airway collapse.¹ The pharynx is also distensible axially. Evidence suggests that caudal tracheal traction physiologically supports pharyngeal patency, but modern surgical techniques for OSA, including HNS, do not modify the airway caudally.² Tracheal traction is primarily mediated by lung expansion, but infrahyoid cervical strap muscles, innervated by the ansa cervicalis, also exert a caudal pull on the pharynx. Physiologic experiments in animals have demonstrated substantial impacts on pharyngeal patency, especially with stimulation of the sternothyroid muscle.³

Ansa cervicalis stimulation (ACS) may engage caudal pharyngeal traction as a new surgical treatment strategy for OSA. Here we describe novel techniques for stimulating the ansa cervicalis with and without HNS in a sedated participant with OSA, generating substantial responses in maximum inspiratory airflow (V_Imax), inspiratory volume, and retropalatal cross-sectional area (CSA_RP).

Experimental Protocol

The Vanderbilt University Medical Center Institutional Review Board approved this study (181078). Hook-wire monopolar electrodes were placed under ultrasound guidance proximal to the medial branch of the right hypoglossal nerve and the branch of the ansa cervicalis, innervating the right sternothyroid muscle, and were then connected to a neurostimulation unit. Target muscle activation (right genioglossus and sternothyroid muscles) was confirmed via ultrasonography and clinical examination. A propofol infusion was titrated until the sedated participant achieved stable flow-limited inspirations. A pneumotachometer connected to an oronasal mask was placed on the participant. V_Imax was measured from airflow peaks during stimulation and compared with peak airflow values from unstimulated breaths immediately preceding and following stimulation. CSA_RP was measured in pixels from a single representative still image selected from contiguous flexible pharyngoscopy video of each experiment at end expiration, when the pharynx was most hypotonic.⁴

ACS and HNS were applied independently and simultaneously across 3 experiments in continuous 2-second bursts during flow-limited inspirations to evaluate the effect on V_Imax and CSA_RP as compared with unstimulated inspirations. If arousal was detected clinically or via bispectral index changes, the experimental trial data were discarded, and the propofol infusion was adjusted accordingly. Descriptive statistics are presented without inferential statistics since statistical significance could not be assessed from the limited number of observations in this single participant.

Results

The participant had a body mass index of 31.0 kg/m² and apnea-hypopnea index of 41.8 events/h. His standard clinical drug-induced sleep endoscopy evaluation demonstrated complete circumferential palatal and lateral pharyngeal wall collapse with partial tongue base collapse. ACS increased V_Imax by 405 ± 64 mL/s (mean ± SEM) from a baseline of 178 ± 94 mL/s (Figure 1A) over 5 pairs of stimulated and unstimulated breaths. ACS was not observed to activate tongue musculature. HNS increased V_Imax by 710 ± 253 mL/s from a baseline of 413 ± 253 mL/s over 2 pairs of breaths. Simultaneous ACS and HNS increased V_Imax by 1200 ± 208 mL/s from a baseline of 363 ± 173 over 4 pairs of breaths (Figure 1B). Inspiratory volume increased with stimulation during the ACS, HNS, and combined stimulation experiments by 269 ± 29 mL, 892 ± 128 mL, and 1015 ± 164 mL from baseline values of 137 ± 30 mL, 228 ± 128 mL, and 311 ± 123 mL, respectively. When compared with baseline, ACS increased CSA_RP 1.2-fold; HNS increased CSA_RP 2.5-fold; and ACS combined with HNS increased CSA_RP 4.3-fold (Figure 2).

Figure 1.

Inspiratory airflow (V_I) increased with 2-second stimulation from baseline (black vs open arrows). (A) Ansa cervicalis stimulation. (B) Hypoglossal nerve stimulation with ansa cervicalis stimulation. Isolated hypoglossal nerve stimulation (gray line and arrow) is overlaid.

Figure 2.

Stimulation increased retropalatal cross-sectional area (yellow lines). (A) Isolated ansa cervicalis stimulation (ACS). (B) Hypoglossal nerve stimulation (HNS) with and without ACS. ACS, HNS, and combined stimulation increased retropalatal cross-sectional area by 1.2-, 2.5-, and 4.3-fold, respectively.

Discussion

The results of this electrophysiology experiment in a single participant with OSA suggest that neurostimulation of the ansa cervicalis branch innervating the sternothyroid muscle is feasible and can increase V_Imax and CSA_RP with or without HNS.

Sternothyroid muscle innervation by the ansa cervicalis does not vary anatomically and can be reliably located 1 to 2 cm above the clavicle at the lateral border of the muscle.⁵ Contraction may stabilize the pharynx in the same fashion as tracheal traction by decreasing pharyngeal wall compliance and pulling the distal edge of the soft palate caudally, whereas tongue displacement with HNS dilates the pharynx radially.^2,3 Our results suggest that combining these 2 mechanisms can increase V_Imax and CSA_RP to a greater degree than with either modality alone.

This report describes an electrophysiologic experiment in a single participant with a limited number of observations. Further studies of ACS in larger, more diverse populations are required to quantify its precise anatomic, physiologic, and clinical effects.