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Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine logoLink to Journal of Clinical Sleep Medicine : JCSM : Official Publication of the American Academy of Sleep Medicine
. 2023 Feb 1;19(2):403–408. doi: 10.5664/jcsm.10296

Personalized multimodal management for severe obstructive sleep apnea in a patient intolerant of positive airway pressure with hypoglossal nerve stimulator and mandibular advancement device

Megan M Lowery 1,✉, Jessica Vensel Rundo 2, Harneet K Walia 3, Vaishal Shah 2
PMCID: PMC9892739  PMID: 36117433

Abstract

Treatment of moderate to severe obstructive sleep apnea poses clinical challenges in persons with intolerance or inadequate response to traditional treatment modalities, including positive airway pressure and mandibular advancement devices. Hypoglossal nerve stimulation is a new treatment option, but few management guidelines exist when it is intolerable or ineffective. Combining several treatment modalities has been an effective strategy for improving symptoms, tolerance, and efficacy. We describe a patient intolerant to positive airway pressure therapy who had continued sleepiness, morning headaches, and snoring with a mandibular advancement device. He underwent hypoglossal nerve stimulation implantation but was intolerant of the voltages required to adequately control his obstructive sleep apnea. Multimodal management with hypoglossal nerve stimulation, mandibular advancement device, and positional therapy was successfully implemented to improve sleepiness, nocturnal symptoms, and the apnea-hypopnea index. This case highlights the personalization and adaptability of combination therapy to suit patient needs while effectively controlling obstructive sleep apnea.

Citation:

Lowery MM, Rundo JV, Walia HK, Shah V. Personalized multimodal management for severe obstructive sleep apnea in a patient intolerant of positive airway pressure with hypoglossal nerve stimulator and mandibular advancement device. J Clin Sleep Med. 2023;19(2):403–408.

Keywords: personalized medicine, multimodal treatment, OSA, obstructive sleep apnea, hypoglossal nerve stimulation, HGNS, CPAP, positive airway pressure, MAD, mandibular advancement device, oral appliance therapy, positional therapy

INTRODUCTION

Moderate to severe obstructive sleep apnea (OSA), an apnea-hypopnea index (AHI) ≥ 15 events/h, has been associated with hypertension, ischemic cerebrovascular disease, cancer mortality, and all-cause mortality.1,2,3 OSA treatment serves to mitigate these comorbid conditions but has been dependent on patient adherence to therapy. While positive airway pressure (PAP) remains the mainstay of therapy for OSA, mandibular advancement device and upper airway stimulation therapy are options for patients intolerant of PAP. Oral appliance therapy via mandibular advancement has been shown to significantly reduce the AHI but is less effective in achieving an AHI < 10 compared to CPAP in patients with moderate-severe OSA.4–6

Satisfying patients’ preferences while effectively treating OSA to mitigate cardiovascular complications is a common conundrum in sleep medicine. The emergence of hypoglossal nerve stimulation (HGNS) has offered a treatment option for patients with moderate-severe OSA who have had inadequate response to CPAP.7 Like CPAP and mandibular advancement device (MAD) therapy, HGNS requires consistent use to maintain adequate control of apneas, hypopneas, and oxygenation. HGNS compared to PAP therapy has been associated with improved Epworth Sleepiness Scores (ESS), Functional Outcomes of Sleep Questionnaire (FOSQ) scores, and Insomnia Severity Index (ISI).8 Withdrawal of HGNS has demonstrated return of AHI to baseline levels and return of sleepiness symptoms as determined by elevated ESS and FOSQ scores.9 HGNS was approved by the Food and Drug Administration in 2014 and consists of a sensing lead implanted between intercostal muscles to sense respiratory effort, the implantable pulse generator (neurostimulator device), typically placed in the right midclavicular, delto-pectoral groove, and a stimulation electrode lead with cuffs placed on the hypoglossal nerve for tongue and genioglossus recruitment.7,9–11 Eligible patients include: those who failed first-line therapy of CPAP and are over 18 years of age (22 years for Centers of Medicare & Medicaid), an AHI of 15–65 events/h, < 25% of central or mixed events, no palatal complete concentric collapse on drug-induced sleep endoscopy, and body mass index < 35 kg/m2 (weight guidelines may vary by insurance coverage).7,10,12 After implantation, the neurostimulator’s electrode configuration, stimulation amplitude voltage, and pulse width/rate can be modified to obtain the optimal configuration for tongue and genioglossal recruitment.

While HGNS can be an option for patients intolerant to PAP/MAD, little information is available regarding management of patients who exhibit intolerance to HGNS. Additionally, the role of multimodal therapy, such as the simultaneous use of HGNS with PAP, MAD, or positional therapy, is not systematically studied. A previous case report has been described utilizing HGNS with MAD.13 We describe a patient with severe OSA, intolerance to CPAP, and partial response to MAD who developed intolerance of HGNS and required a personalized approach to treat his sleep apnea and associated symptoms with the combination of HGNS, MAD, and positional therapy.

REPORT OF CASE

A 71-year-old man with osteoarthritis of the knees, a pancreatic neck cyst, former smoker (44 pack years) presented with a history of OSA since childhood. He underwent a tonsillectomy at 7 years old. At age 60, a diagnostic polysomnogram (PSG) performed with a body mass index of 30.1 kg/m2 showed overall mild OSA with an overall AHI of 8.5 events/h (hypopnea defined as ≥ 30% drop in peak signal excursion from pre-event baseline for ≥ 10 seconds with a ≥ 4% oxygen desaturation from pre-event baseline)14 exacerbated to the severe range when supine with an AHI of 56.6 events/h (Table 1). The patient was snoring, choking at night, having daytime sleepiness (characterized by falling asleep when reading), cognitive dysfunction, memory issues, and severe morning headaches 4–5 times per week. He trialed CPAP but was intolerant due to claustrophobia and significant discomfort with the mask interface and unintentional removal at night.

Table 1.

Summary polysomnogram variables and patient characteristics.

PSG 1 PSG 2 PSG 3 PSG 4
Type of study Diagnostic PSG Diagnostic PSG HGNS titration HGNS titration with MAD
Age at time of study 60 65 69 70
BMI (kg/m2) 30.1 32.7 23.6 25.9
Weight (kg) 103.4 112.5 81.3 88.9
Total sleep time (min) 326.5 291.5 380 380
Sleep efficiency (%) 78.2 80.3 85.4 88.0
REM sleep (%) 22.7 17.5 23.7 19.3
% Supine – – 32.1 21.8
Arousal index 5.9 3.0 51.0 22.3
Total AHI (events/h)a 8.5 34.0 – –
Respiratory disturbance index (events/h)b 10.8 34.0 – –
Supine AHI (events/h)a 56.6 30.7 – –
REM AHI (events/h)a 18.6 36.0 – –
Mean SpO2 (%) – 89.5 95 93
SpO2 nadir (%) 85 82 84 87
ETCO2 (wake, baseline, mmHg) – – 36 39
Max ETCO2 (mmHg) – – 43 48
Electrode configuration [+, −, +, off] [+, −, +, off]
Amplitudes tested (min, max, volts) – – 1.8, 2.5 1.0, 1.3
Functional Threshold (volts) – – 1.5
Minimum therapeutic amplitude in REM, off-supine sleep (volts) – – 2.0 1.2
Residual AHI at minimum therapeutic amplitude – – 1.0 2.5
Tested amplitude, supine NREM sleep (volts) – – 2.2 1.1
Residual AHI with supine NREM sleep – – 11.8 13.0
Tested amplitude during REM, supine sleep (volts) – – 2.4 1.3c
Residual AHI with REM, supine amplitude – – 17.8 5.1
Highest tested therapeutic amplitude (volts) – – 2.5 1.3
Residual AHI at highest tested therapeutic amplitude – – 34.3 5.1
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aHypopnea defined as ≥ 30% drop in peak signal excursion from pre-event baseline for ≥ 10 seconds with a ≥ 4% oxygen desaturation from pre-event baseline. bHypopnea defined as ≥ 30% drop in peak signal excursion from pre-event baseline for ≥ 10 seconds with an arousal or a ≥ 3% oxygen desaturation from pre-event baseline. c39% supine sleep. AHI = apnea-hypopnea index, BMI = body mass index, ETCO2 = end tidal carbon dioxide, HGNS = hypoglossal nerve stimulator, MAD = mandibular advancement device, NREM = nonrapid eye movement, PSG = polysomnogram, REM = rapid eye movement. Empty table boxes represent missing or uncollected data for that sleep study (ie, amplitudes are not collected for non-HGNS sleep studies).

A repeat PSG at age 65 showed an overall AHI in the severe range, 34.0 events/h, with a rapid eye movement (REM) sleep supine AHI of 31.5 events/h, oxygen nadir of 82% SpO2, and body mass index of 32.7 kg/m2 (Table 1). The patient again was intolerant of CPAP and ultimately began using a mandibular advancement device (MAD), the Thornton Adjustable Positioner (TAP3; Airway Management, Dallas, TX).15 He did not have PSG testing with use of his MAD. While nocturnal snoring improved with the use of the MAD, he continued to have regular morning headaches, nocturnal awakenings to urinate, and daytime sleepiness. The patient sought evaluation for a hypoglossal nerve stimulator (HGNS) at age 69.

A drug-induced sleep endoscopy showed complete posterior collapse of the plate and near total anterior-posterior collapse of the base of the tongue and lingual tonsils with intermittent independent collapse of the epiglottis. He subsequently underwent implantation of an Inspire HGNS (Inspire Medical Systems, Maple Grove, MN) without complications. The initial neurostimulator electrode configuration was the default configuration of the stimulation lead ([+, −, +, Off]). The patient’s sensation threshold was 1.1 V and functional threshold was 1.5 V; he was configured with a range of 1.5–2.5 V for the device titration. Initial HGNS titration PSG tested amplitudes from 1.8 V to 2.5 V with the default electrode configuration ([+, −, +, Off]). During nonsupine REM sleep, the AHI was well controlled with 1.8–2.0 V with an AHI of 1.0 events/h. However, during supine REM sleep with an amplitude of 2.3–2.5 V the AHI only improved to 17.8 events/h (Table 1).

The patient was unable to tolerate sleeping with higher voltage settings (2.3–2.5 V) required to control REM supine OSA and was having nocturnal awakenings characterized by panic and dyspnea with inability to return to sleep. He stopped using HGNS by himself and began again wearing his MAD without use of the HGNS but continued to have nocturnal awakenings and unrefreshing sleep. The patient was lost to follow up for 15 months, and then returned to clinic to retrial HGNS due to persistent symptoms. A gradual increase in settings to improve tolerance was attempted upon his return, and the patient desired to use MAD with HGNS. After detailed discussion with the patient, both therapies were continued to improve adherence. With the same default electrode configuration (+, –, +, Off), his sensation threshold was 0.7 V with a functional threshold of 0.8 V, and he began on a slow titration starting at 0.8 V. The patient was able to tolerate titrating up to 1.4 V and reported that symptoms of snoring, nocturnal awakenings, feeling refreshed, morning headaches, and daytime sleepiness were significantly better with voltages between 1.2 and 1.4 V in combination of MAD. He noted no interference from the MAD with tongue stimulation. Despite a slow titration, he was unable to titrate to his prior higher settings (1.8–2.5 V) required for normalization of AHI during nonsupine sleep without MAD. He began to utilize positional therapy adhering to nonsupine sleep while combining MAD and HGNS.

In order to determine if combination therapy with MAD, HGNS, and nonsupine sleep was adequately controlling his OSA and to determine the optimal HGNS voltage for adequate control, a repeat PSG with HGNS default electrode configuration was performed in conjunction with the MAD and nonsupine sleep. This study demonstrated a residual AHI of 5.1 events/h with 1.3 V in nonsupine REM sleep. Very limited supine sleep was recorded (21% of sleep time) and supine non–rapid eye movement sleep showed an overall AHI of 13.0 events/h with 1.1 V (Table 1, Figure 1). Without HGNS, there were residual obstructive events with MAD use alone, though during the very limited, supine REM sleep. The HGNS was turned off only briefly to demonstrate proof-of-concept and efficacy of lower HGNS voltages with combination therapy. A PSG with MAD alone was not performed pre- or postoperatively and is a limitation in comparing efficacy of each modality individually. However with the patient’s intolerance to higher amplitude settings for HGNS, self-reported symptomatic improvement in snoring and improvement in AHI from 34.3 to 5.1 events/h with use of all 3 modalities, it was decided based on discussion with the patient to utilize these 3 modalities. A final range for HGNS was set to 1.1–2.1 V with treatment setting at 1.3 V to be used in conjunction with MAD and nonsupine sleeping. The patient’s ESS also decreased from 11 to 7. With this individualized approach utilizing triple therapy, HGNS, positional therapy and a MAD, the patient continued to report symptomatic improvement with refreshed morning awakenings and resolved daytime sleepiness on subsequent follow up visits and declined further changes in management given his satisfaction with triple therapy

Figure 1. Hypnogram of HGNS titration with MAD.

Figure 1

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PSG hypnogram with use of MAD while titrating voltages for HGNS. During NREM with part supine and nonsupine sleep, the AHI was > 10 events/h. The HGNS was briefly stopped (marked by a star) and coincided with an arousal and elevated AHI. Resumption of HGNS (marked by red arrow) with MAD showed adequate control of OSA even during REM sleep (AHI = 5.1 events/h) with superior control in nonsupine sleep (AHI = 2.5 events/h). APN = apnea, ADI = apnea desaturation index, AHI = apnea-hypopnea index, CA = central apnea, HYP = hypopnea, HDI = hypopnea desaturation index, HGNS = hypoglossal nerve stimulator, MA = mixed apnea, MAD = mandibular advancement device, OA = obstructive apnea, PSG = polysomnogram, R = REM, REM = rapid eye movement, W = wake. For body position graph: S = supine, R = right side, P = prone, L = left side. For sleep stages: R = REM sleep, N1 = Stage N1 sleep, N2 = Stage N2 sleep, N3 = Stage N3 sleep, W = wake.

DISCUSSION

This case highlights the adaptability of OSA treatment to best fit patients’ needs and preferences while optimizing AHI and nocturnal oxygenation and decreasing self-reported symptoms of snoring and sleepiness. While many patients respond favorably to HGNS, a proportion of patients is unable to achieve AHI < 10 events/h even after 5 years.16 There are others who have difficulty tolerating side effects of HGNS. Prior literature has shown that long-term utilization of HGNS for more than 12 months has resulted in up to 12%–13% of patients having tongue discomfort with stimulation.16–19 Postimplantation strategies include adjusting amplitudes and electrical configurations as well as utilizing additional OSA treatment modalities like positional therapy, MAD, and PAP to improve effectiveness and tolerability.20 Our case is the first demonstrating personalized therapy utilizing 3 modalities, HGNS, MAD, and positional therapy, in order to improve adherence, comfort, and effectiveness.

Different treatment modalities have previously been combined to help individualize OSA treatment for patient comfort and treatment success. For patients who are intolerant of high PAP pressures and experience an inadequate response to mandibular advancement, hybrid therapy can reduce the need for such high PAP levels and improve the patient experience. Liu and colleagues21 showed that hybrid therapy with MAD and CPAP lowered the residual AHI to < 5 events/h while reducing the required CPAP from 19 to 9.8 cm H2O. Similarly, MAD and HGNS have also been combined to achieve adequate control of OSA. In a case of a patient with severe OSA who had a residual AHI of 11.6 events/h and continued bothersome snoring after HGNS surgery, MAD successfully reduced the AHI to 2.1 events/h and resolved snoring.13 It is hypothesized that mandibular advancement added to genioglossus stimulation lowers the critical closing pressure of the upper airway thus dilating the oropharynx and improving airflow.22

Positional therapy has also been a popular addition to improving adherence to therapy and achieving treatment goals in patients with predominantly supine residual sleep apnea. Positional therapy has been an adjunct to PAP, MAD, and upper away surgery to achieve management goals. A study evaluating patients with moderate-severe OSA (AHI > 20 events/h) utilizing MAD with an elevated residual supine AHI ≥ 5 events/h found a higher therapeutic efficacy when patients used a chest-worn sleep trainer in addition to MAD therapy compared to either therapy alone.23 Additionally, in patients treated with PAP with a residual supine AHI > 10 events/h, positional therapy led to successful CPAP and bilevel PAP titrations in all patients who initially failed CPAP and bilevel PAP titrations in the supine position.24 Given these successes, positional therapy has been proposed as an adjunct for upper airway stimulation in those unable to tolerate the required voltage to achieve an adequate reduction in AHI. However, there are no prospective or retrospective studies evaluating the effectiveness of combination therapy of HGNS and positional therapy to determine effectiveness. Previously, positional therapy alone was only moderately successful at reducing the median AHI from 18.3 events/h to 12.5 events/h in patients with residual sleep apnea after upper airway surgery.25

Future studies are required to evaluate the mechanics and effectiveness of utilizing combination therapy with HGNS to achieve desired treatment outcomes. It is unknown if positional therapy or MAD will successfully reduce AHI when used in conjunction with HGNS in the majority of patients who are intolerant of the stimulation required to achieve therapeutic benefits. There may be a specific subset who may achieve AHI reduction with combination therapy who are unable to tolerate HGNS alone, but the clinical and physical characteristics of this subset should be explored in future studies. Further studies evaluating the relationship between the space the MAD occupies, tongue size, degree of tongue protrusion, and intramandibular area in conjunction with opening the posterior palate with HGNS may determine if this combination therapy with MAD and HGNS is a viable option. Just as drug-induced sleep endoscopy allows improved selection of patients predicted to have success with the mechanics of HGNS by determining that the patient does not have concentric airway collapse, we require more clinical information and prediction models to help determine which patients may be overly sensitive to stimulation.

As more information regarding postimplantation sensitivity issues is reported, we will be able to work toward early identification of clinical and physical characteristics that predict potential failures in tolerating HGNS. Future research will allow the development of more detailed pathways to optimize effectiveness and comfort with HGNS as well as identify those patients suited for a multimodal treatment approach. This case features the importance of personalizing therapy for each patient with multimodal approach and adds to the literature gap on utility of combination therapy with HGNS. The variability of treatments available for OSA permits adaptability to achieve treatment goals.

CONCLUSIONS

In patients intolerant of the voltage required for adequate reduction in AHI with treatment via HGNS, personalized therapy with positional therapy and/or MAD may be considered to alleviate symptoms of sleep-disordered breathing and provide effective control of OSA.

ABBREVIATIONS

AHI

apnea-hypopnea index

CPAP

continuous positive airway pressure

HGNS

hypoglossal nerve stimulator

MAD

mandibular advancement device

OSA

obstructive sleep apnea

PAP

positive airway pressure

PSG

polysomnogram

REM

rapid eye movement

DISCLOSURE STATEMENT

All authors have seen and approved the manuscript. This case is from the Cleveland Clinic Sleep Disorders Center in Cleveland, OH. Dr. Harneet K. Walia discloses that she previously served on the Advisory Board for ResMed and Idorsia but is not actively serving, and it is not a conflict of interest with this manuscript. The other authors report no conflicts of interest.

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