Therapeutic Electrical Stimulation of the Hypoglossal Nerve in Obstructive Sleep Apnea

Schwartz, Alan R.; Bennett, Marc; Smith, Philip L.; Backer, Wilfried De; Hedner, Jan; Boudewyns, An; Heyning, Paul Van de; Ejnell, Hasse; Hochban, W; Knaack, Lennart; Podszus, T; Penzel, Thomas; Peter, J H; Goding, George S.; Erickson, Donald J.; Testerman, Roy; Ottenhoff, Frans; Eisele, David W.

doi:10.1001/archotol.127.10.1216

Cited by 265 publications

(207 citation statements)

References 36 publications

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“…The severity of upper airway obstruction during sleep is related to quantitative differences in pharyngeal collapsibility, as reflected by elevations in the critical closing pressure (Pcrit). Moreover, as Pcrit fell below a minimally negative threshold of approximately 25 cm H 2 O, sleep apnea remitted, suggesting that changes in Pcrit play a pivotal role in the pathogenesis of this disorder (see Figure 1, right) (25,(57)(58)(59)(60)(61). In further studies, investigators have demonstrated that Pcrit is determined by mechanical and neural factors that regulate pharyngeal collapsibility (62)(63)(64)(65)(66)(67).…”

Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 95%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

574

395

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Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

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Section: Obesity and Upper Airway Neuromechanical Control Modeling Upmentioning

confidence: 95%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

574

395

View full text Add to dashboard Cite

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“…Subsequently, investigators documented arousal thresholds during submental stimulation, which confounded assessment of airflow responses and limited clinical applicability of this technique during sleep (31,32). Investigators further refined the stimulation technique by inserting temporary fine-wire electrodes into lingual muscles, and demonstrated that protrusor muscle stimulation mitigated and retractor muscle stimulation worsened pharyngeal patency during sleep (13,16,18,19,33). In these prior studies, investigators scrutinized EEG and ECG signals to exclude responses associated with cortical or autonomic activation (13,18,19).…”

Section: Arousalsmentioning

confidence: 99%

“…Investigators further refined the stimulation technique by inserting temporary fine-wire electrodes into lingual muscles, and demonstrated that protrusor muscle stimulation mitigated and retractor muscle stimulation worsened pharyngeal patency during sleep (13,16,18,19,33). In these prior studies, investigators scrutinized EEG and ECG signals to exclude responses associated with cortical or autonomic activation (13,18,19). Additional studies with implantable nerve cuff (13) and fine-wire electrodes have demonstrated responses to selective lingual muscle stimulation during sleep and anesthesia (13)(14)(15)(16)(17).…”

Section: Arousalsmentioning

confidence: 99%

“…In these prior studies, investigators scrutinized EEG and ECG signals to exclude responses associated with cortical or autonomic activation (13,18,19). Additional studies with implantable nerve cuff (13) and fine-wire electrodes have demonstrated responses to selective lingual muscle stimulation during sleep and anesthesia (13)(14)(15)(16)(17). The present study also screened for evidence of cortical and autonomic activation, and further required strict temporal synchrony between the stimulus burst and airflow response to exclude arousal responses from the analysis.…”

Section: Arousalsmentioning

confidence: 99%

“…Hypoglossal nerve stimulation (HGNS) has been piloted as treatment for obstructive sleep apnea (13). Implantable HGNS systems have been developed to stimulate the hypoglossal nerve during inspiration, and recruit the lingual musculature, leading to decreases in pharyngeal collapsibility during sleep (14)(15)(16)(17).…”

mentioning

confidence: 99%

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Acute Upper Airway Responses to Hypoglossal Nerve Stimulation during Sleep in Obstructive Sleep Apnea

Schwartz

Barnes

Hillman

et al. 2012

Am J Respir Crit Care Med

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Rationale: Hypoglossal nerve stimulation (HGNS) recruits lingual muscles, reduces pharyngeal collapsibility, and treats sleep apnea. Objectives: We hypothesized that graded increases in HGNS relieve pharyngeal obstruction progressively during sleep. Methods: Responses were examined in 30 patients with sleep apnea who were implanted with an HGNS system. Current (milliampere) was increased stepwise during non-REM sleep. Frequency and pulse width were fixed. At each current level, stimulation was applied on alternating breaths, and responses in maximal inspiratory airflow (V I max) and inspiratory airflow limitation (IFL) were assessed. Pharyngeal responses to HGNS were characterized by the current levels at which V I max first increased and peaked (flow capture and peak flow thresholds), and by the V I max increase from flow capture to peak (DV I max). Measurements and Main Results: HGNS produced linear increases in V I max from unstimulated levels at flow capture to peak flow thresholds (215 6 21 to 509 6 37 ml/s; mean 6 SE; P , 0.001) with increasing current from 1.05 6 0.09 to 1.46 6 0.11 mA. V I max increased in all patients and IFL was abolished in 57% of patients (non-IFL subgroup). In the non-IFL compared with IFL subgroup, the flow response slope was greater (1241 6 199 vs. 674 6 166 ml/s/mA; P , 0.05) and the stimulation amplitude at peak flow was lower (1.23 6 0.10 vs. 1.80 6 0.20 mA; P , 0.05) without differences in peak flow. Conclusions: HGNS produced marked dose-related increases in airflow without arousing patients from sleep. Increases in airflow were of sufficient magnitude to eliminate IFL in most patients and IFL and non-IFL subgroups achieved normal or near-normal levels of flow, suggesting potential HGNS efficacy across a broad range of sleep apnea severity.Keywords: obstructive sleep apnea; electrical hypoglossal nerve stimulation; pharynx; upper airway; titration Obstructive sleep apnea is characterized by recurrent episodes of upper airway obstruction during sleep (1). Airflow obstruction is thought to result from decreases in pharyngeal neuromuscular activity at sleep onset (2). These episodes lead to intermittent hypoxemia and recurrent arousals from sleep, accounting for the long-term neurocognitive (3, 4), metabolic (5), and cardiovascular (6) sequelae of this disorder. Nasal continuous positive airway pressure remains the mainstay of treatment for moderate to severe obstructive sleep apnea (7). Difficulties adhering to therapy can limit its effectiveness in the home setting (8, 9), and alternatives have been generally less effective in relieving upper airway obstruction during sleep (10-12).Hypoglossal nerve stimulation (HGNS) has been piloted as treatment for obstructive sleep apnea (13). Implantable HGNS systems have been developed to stimulate the hypoglossal nerve during inspiration, and recruit the lingual musculature, leading to decreases in pharyngeal collapsibility during sleep (14-17). Motor activity protrudes the tongue, and mitigates airflow obstruction during sleep (18,19)....

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Hypoglossal Nerve Stimulation in Adolescents With Down Syndrome and Obstructive Sleep Apnea

Diercks

Wentland

Keamy

et al. 2017

JAMA Otolaryngol Head Neck Surg

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Therapeutic Electrical Stimulation of the Hypoglossal Nerve in Obstructive Sleep Apnea

Abstract: The findings demonstrate the feasibility and therapeutic potential for hypoglossal nerve stimulation in obstructive sleep apnea.

Cited by 265 publications

References 36 publications

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Acute Upper Airway Responses to Hypoglossal Nerve Stimulation during Sleep in Obstructive Sleep Apnea

Hypoglossal Nerve Stimulation in Adolescents With Down Syndrome and Obstructive Sleep Apnea

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