Treating Obstructive Sleep Apnea With Hypoglossal Nerve Stimulation

Arie Oliven


Curr Opin Pulm Med. 2011;17(6):419-424. 

In This Article

Hypoglossus Nerve Stimulation in Obstructive Sleep Apnea Patients

The major breakthrough for this new OSA treatment modality occurred when investigators from Johns Hopkins University initiated a series of well designed studies leading ultimately to an implantable hypoglossus nerve stimulation system. In a preliminary acute study, five OSA patients were implanted with hypoglossus nerve cuff electrodes and were transferred, after arousal from anesthesia, to the sleep laboratory. Electrodes were activated by an external stimulator, and measurements performed during sleep showed an improvement in inspiratory airflow ranging between 50 and 200 ml/s, without arousal.[36] The success of this preliminary study led to approval and initiation of a phase I, hypoglossus nerve stimulation, multicenter feasibility study undertaken to investigate the efficacy of a fully implantable hypoglossus nerve stimulation system. The system (Inspire I; Medtronic, Minneapolis, Minnesota, USA) consisted of three components: an implantable pacemaker-like pulse generator, a tri-polar, half-cuff peripheral nerve-stimulation electrode, and a pressure sensor designed to recognize intrathoracic pressure deflection and initiate hypoglossus nerve stimulation during inspiration. Limiting stimulation to inspiration was physiologically logical and considered necessary to prevent neuromuscular fatigue. The system was implanted under general anesthesia through three surgical incisions: the stimulation electrode was placed on the peripheral main branch of the hypoglossus nerve close to its entrance into the tongue muscle. The pulse generator was placed subcutaneously into an infraclavicular pocket. The pressure transducer was inserted into a hole drilled through the manubrium sterni, thereby allowing the measurement of intrathoracic pressure. The system contained a microprocessor that could be reprogrammed via transcutaneous instructions, enabling the physician to adjust stimulus frequency, duration, and amplitude. A remote control unit allowed the patient to turn the stimulator on at bedtime, and a preset delay enabled patients to fall asleep before the start of electrical stimulation.

The results of the study were published in 2001[36] and in several later reviews, including a recent comprehensive description of the same study.[37•] A substantial reduction in the apnea–hypopnea index (AHI) was observed in all but one of the eight patients implanted. The improvement was already appreciable in the first postimplantation sleep study performed after 1 month, and the same response was maintained over a follow-up period of 6 months. On average, the AHI in the seven successfully implanted OSA patients decreased from 53.4±22.2 to 21.4±9.8 events/h (mean±SD) and fell as low as 13.3±6.6 events/h if nonsynchronized stimulations were excluded. Unfortunately, technical faults that included lead rupture and sensor malfunctioning due to cardiac artifacts precluded prolonged assessment.[37•] Nevertheless, all patients tolerated the long-term stimulation and did not experience any adverse effects, and the three patients who remained free from stimulator malfunction continued to use the device as primary treatment until the lifetime of the internal power supply was reached.[37•]


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