Effect of Novel Hypoglossal Stimulation on Airflow and Airway Collapsibility in OSA

Hypoglossal nerve stimulation (HNS) to treat OSA currently requires placement of a cuff or "saddle" electrode around or adjacent to the hypoglossal nerve or nerves. Limitations for this therapy include cost, invasiveness, and variable efficacy.

Can HNS applied via percutaneous implantation of a linear, multipair electrode array restore airflow to airway narrowing, obstruction, or both and improve airway collapsibility in people with OSA?

Participants with OSA undergoing drug-induced sleep endoscopy with propofol were instrumented with an epiglottic pressure catheter, nasal mask, and pneumotachograph. Ultrasound was used to identify the hypoglossal nerve and to guide percutaneous electrode array placement. Transient CPAP reductions induced airflow limitation or obstruction for ≥ 9 breaths/efforts with HNS applied during breaths 4 through 6. A range of HNS amplitudes (0.5-5 mA) and electrode array combinations were tested to determine optimal airflow responses. Time-permitting, active critical closing pressure (P_crit) also was quantified with and without HNS.

Fourteen people with moderate to severe OSA (mean [SD] apnea-hypopnea index, 30 [16] events/h) were studied. HNS increased airflow in 13 participants. Mean (SD) peak inspiratory flow on therapeutic CPAP was 0.43 (0.09) L/s. During transient CPAP reductions, mean (SD) peak inspiratory flow reduced to 0.10 (0.07) L/s for breaths 1 through 3, increased to therapeutic CPAP levels with HNS for breaths 4 through 6 (0.41 (0.18) L/s), and returned to 0.14 (0.14) L/s for breaths 7 through 9 after HNS (P < .001). Mean (SD) active P_crit with HNS vs without HNS was -7.2 (1.6) cm H₂O vs 0.1 (2.4) cm H₂O, respectively (P < .01).

Our results show that acute HNS via a minimally invasive, percutaneous, ultrasound-guided approach increases airflow to levels equivalent to therapeutic CPAP and improves airway collapsibility in people with OSA.