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  In this Article
 »  Abstract
 » Pathophysiology
 » Diagnosis
 » Management
 » Neuromodulation
 » Muscle Stimulation
 »  Hypoglossal Nerv...
 »  Procedure Detail...
 »  Procedure Detail...
 »  Submental Transc...
 » Conclusion
 »  References
 »  Article Figures

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Table of Contents    
Year : 2020  |  Volume : 68  |  Issue : 8  |  Page : 302-306

Neuromodulation in Obstructive Sleep Apnea

1 Department of Neurosurgery, Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India
2 Department of Medicine, Government Medical College, Nagpur, Maharashtra, India
3 Department of Functional Neurosurgery, West Virginia University Health Sciences, WV, USA

Date of Web Publication5-Dec-2020

Correspondence Address:
Dr. Vikas Naik
Department of Neurosurgery, Bangalore Medical College and Research Institute, K. R. Road, Bengaluru, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.302456

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 » Abstract 

Epidemiological studies show a steady rise in the prevalence of obstructive sleep apnea (OSA). Untreated OSA is responsible for numerous chronic health conditions, motor vehicle, and workplace-related accidents leading to substantial economic burden both to the individual and society. Multiple causes for OSA and a wide range of consequences has made its diagnosis and treatment difficult. Obstructive sleep apnea may be caused by anatomical variation, increased collapsibility of the upper airway, low sleep arousal threshold, and exaggerated response to desaturation. Lifestyle changes, anatomical corrective surgeries, and oral appliances have been used but patient compliance is poor as it interferes in the daily routine. Neuromodulation is a promising functional modifying option that addresses the cause of obstructive sleep apnea at multiple levels.

Keywords: Apnea hypopnea index, closed-loop stimulation, hypoglossal nerve stimulation, neuromodulation, obstructive sleep apnea
Key Message: Neuromodulation is safe and effective in treating obstructive sleep apnea and its consequences.

How to cite this article:
Naik V, Khandekar N, Deogaonkar M. Neuromodulation in Obstructive Sleep Apnea. Neurol India 2020;68, Suppl S2:302-6

How to cite this URL:
Naik V, Khandekar N, Deogaonkar M. Neuromodulation in Obstructive Sleep Apnea. Neurol India [serial online] 2020 [cited 2021 Dec 6];68, Suppl S2:302-6. Available from:

Obstructive sleep apnea (OSA) is a sleep-related breathing disorder (SRBD) characterized by periods of apnea (cessation of breathing) or hypopnea (partial cessation of breathing) due to complete/partial upper airway obstruction, hypoxia, and arousal from sleep.[1],[2],[3] OSA is a common sleep disorder with a prevalence of 14 to 49%[3],[4],[5] in various studies. Its incidence is increasing due to the epidemic of obesity and an increase in life expectancy.[1],[6]

The risk factors of OSA include obesity, age, gender, craniofacial anatomy, smoking, alcohol consumption, genetic, and familial history.[2],[7],[8] The main symptom of OSA is excessive daytime sleepiness with other associated symptoms such as snoring, fatigue, nocturnal choking, and the sequelae of these causing psychiatric, psychological, performance, and life-related problems.[2] OSA is commonly seen in heart failure, malignancies, maternal OSA affects newborns, and OSA leads to cognitive decline.[7],[9] Early identification of the problem is essential to prevent and treat the consequences of OSA.

 » Pathophysiology Top

There is neuromuscular dysregulation in OSA patients during wakefulness and sleep, with or without anatomical (structural) narrowing in the upper pharynx. During rapid eye movement (REM) sleep, there is a decrease in muscle tone that aggravates the inherent collapsibility of the pharyngeal lumen in OSA patients and has reduced airway dilation (phasic activity) and stability (tonic activity) leading to the collapse of the airway.[10],[11] Obstruction in the upper airways leads to a rise in transthoracic pressures leading to an increase in negative pleural pressure which is a hallmark of OSA. This leads to hypoxia and stimulates chemoreceptors in the carotid bodies which increase sympathetic discharge and central nervous system (CNS) arousal.[10],[11],[12],[13],[14] The reinitiation of breathing suppresses the sympathetic discharge. In a state of wakefulness, the sympathetic response to chemoreceptors persists leading to hypertension, cardiovascular, and metabolic dysfunction.[10],[11],[14]

 » Diagnosis Top

The initial approach to the diagnosis of OSA involves a comprehensive history and examination of patients with symptoms of excessive daytime sleepiness, restlessness, fatigue, nocturnal choking, witnessed apneas, snoring, and signs of underlying medical conditions such as obesity, hypertension, coronary artery disease, diabetes, stroke, congestive cardiac failure, mood disorders, and cognitive dysfunction.[10],[15],[16] Increased risk of moderate to severe OSA is indicated by the presence of excessive daytime sleepiness and at least two of the following three criteria: habitual loud snoring; witnessed apnea or gasping or choking; or diagnosed hypertension.[15],[16] In moderate to severe OSA, polysomnography (PSG)/sleep study is ordered to know parameters related to sleep (electroencephalogram, electrooculogram, and submental electromyogram), to cardiac arrhythmias (electrocardiogram) and respiration (airflow, oximetry, and respiratory effort).[10],[15],[17] Nasal pressure monitors airflow PSG determines the apnea-hypopnea index (AHI) for the severity of OSA.[9],[16]

The American Association of sleep medicine (AASM) defines apnea as the cessation of breathing for 10 s or longer followed by arousal and hypopnea as drop-in nasal pressure by more than or equal to 30% for at least 10 s with a fall in oxygen saturation by at least 3% (recommended) or 4% (acceptable) followed by arousal.[16],[17] OSA is classified as mild 5–15 AHI, moderate 16–30 AHI, and severe if > 30 AHI. The respiratory disturbance index (RDI) is an inclusive index that measures respiratory effort-related arousals (RERA) along with apnea and hypopnea.[16] The AASM defines OSA as PSG determined RDI of more than or equal to 5 events per hour associated with typical OSA symptoms (excessive daytime sleepiness, fatigue or insomnia, awakening with a gasping or choking sensation, loud snoring, or witnessed apneas) or an obstructive RDI of more than or equal to 15 events per hour even in the absence of symptoms.[16]

 » Management Top

OSA needs individualized treatment as the cause and effect to vary significantly between individuals. The anatomical phenotype like a narrow collapsible airway and physiological ones such as pharyngeal dilator muscle dysfunction, low threshold for arousal, and abnormal response to blood gases (high loop gain) are potential targets for treatment.[11] Treatment options available are oral appliance therapy, positional therapy, weight loss, behavioral modifications, upper airway reconstructive surgery, pharmacotherapy, and neuromodulation.[1],[2],[10],[18]

Untreated OSA increases the cost of healthcare, daytime sleepiness reduces long-term productivity, affects cognitive ability, and interferes in social life. Obesity being a risk factor for OSA, weight loss should be recommended initially in mild-moderately obese patients, which induces a clinically significant reduction in AHI.[17],[19] Continuous positive airway pressure (CPAP) is the gold standard for OSA and reverses the acute pathophysiological mechanisms associated with OSA;[2],[12] however, low compliance to CPAP is a major disadvantage.[1],[7] Resective or ablation surgery to correct any upper airway blockage is also performed[20] but is irreversible with some complication rates and it is a one-time procedure for an evolving disease.

 » Neuromodulation Top

Neuromodulation is an important strategy to treat OSA with targets being nerve and muscle.

 » Muscle Stimulation Top

Anatomical factors, central tonic activity control of dilator muscles in the pharynx, arousal threshold gain play a key role in OSA.[18],[21],[22] Genioglossus plays an important role in preventing collapse caused by the negative pressure of the diaphragm and extraluminal pressure around the pharynx.[18] Genioglossal muscle shows denervation, reinnervation injury on? Electromyography (EMG) findings,[23] and delayed latency/low amplitude in hypoglossal nerve conduction in a few studies.[24] Many methods for stimulating genioglossus using submental, intraoral, or intramuscular electrodes showed improvement in obstruction and oxygen saturation but the major drawback was it induced arousal.[25],[26]

 » Hypoglossal Nerve Stimulation Top

Hypoglossal nerve stimulation (HNS) addresses both the anatomic and physiological factors involved in OSA.[18] In 2001, a pilot study of HNS for OSA was done (Inspire I, Inspire Medical system, Maple Grove, MN).[27] Upper neck incision for unilateral hypoglossal nerve stimulator placement, infraclavicular incision for implantation of battery and midline lower neck incision, drilling of superior part of manubrium to place bilateral subpleural respiratory censors. AHI reduced significantly but device malfunction and surgery were challenging.[18],[27] A decade later problems were overcome in 2011 HNS (Apnex Medical Inc., St Paul MN USA) where surgery was similar to the previous one but pressure sensors were subcutaneously tunneled to costal margin bilaterally.[25] Leads were verified fluoroscopy. In 2012, Inspire II UAS (upper airway stimulation), Inspire Medical system was similar to HNS (Apnex) but used a single respirator sensor tunneled to the ipsilateral coastal margin.[28] Tongue protrusion was demonstrated on stimulation. Imthera aura 600 uses continuous but different neuromuscular fibers stimulation at a given point of time to prevent fatigue without respiratory censor.[29] Stimulation therapy for apnea reduction (STAR) was a multicenter trial. Strollo et al. used an upper airway stimulation system (Inspire Medical Systems), which showed a reduction in the severity of obstruction and improvement in the quality of life after a follow-up of 1 year with median AHI falling 68% from 29.3 to 9 events per hour and oxygen desaturation index (ODI) decreased 70% from 25.4 to 7.4 events per hour.[30]

Another study by Strollo et al. using the same STAR trial cohort showed significant improvement in the severity of OSA after 18 months of follow-up. The primary outcomes of AHI and 4% oxygen desaturation index (ODI) improved from baseline at 18 months with an excellent safety profile along with an improvement in the secondary outcomes i.e., the functional outcome of sleepiness questionnaire (FOSQ) and Epworth sleepiness scale.[31]

The prospective study by Kezirian et al.[32] used the HNS Apnex device and showed an improvement of 45.4 to 25.3 events per hour in the AHI and FOSQ score from 14.2 to 17 after 12 months. The only hypoglossal nerve stimulation device approved by the US Food and Drugs Administration (FDA) is made by Inspire Medical Systems.[31],[33] It is used in patients 22 years and above with moderate to severe OSA, who have failed positive airway pressure and do not have concentric collapse on sleep endoscopy.

 » Procedure Details of Unilateral Hypoglossal Nerve Stimulation Top

The procedure is done under general anesthesia (GA). The patient is placed supine, neck extended (to access hypoglossal nerve) and right arm abducted for implantation of respirator sensor. A horizontal 4 to 6 cm neck incision along skin crease placed 4 cm below the angle of right mandible, submandibular gland retracted away and digastric muscle was identified. The hypoglossal nerve was identified using a nerve stimulator in the digastric triangle observing contraction of the tongue. About 1–2 cm of nerve dissected to place the lead cuff. A long inner flap of lead is passed beneath the nerve and wrapped around the shortleaf to make optimum contact of electrodes with the nerve [Figure 1]a. Lead is tested by connecting to an impulse generator (IPG) and contraction of the tongue is noted. Lead is secured to the tissue surrounding and brought parallel to the nerve, the lead anchored to digastric muscle with no strain loop made and subcutaneously tunneled to the clavicular region to connect to the (IPG. A small subcutaneous pocket is made in the infraclavicular region to place the IPG. Similarly 5 to 6 cm incision made at 4th or 5th intercostal space, blunt and sharp dissection done to reach the space between external and internal intercostal muscle to place the sensor at the superior surface of rib at a shallow angle with sensing lead flat over pleura and lead anchored subcutaneously. The subcutaneous tunnel is made to pass the lead on to the infraclavicular pocket. Stimulating lead and sensor are connected to IPG and IPG placed into the pocket and anchored. IPG is programmed starting with 0.5 amp and gradual increments of 0.2 amp to see the adequate response. Programming is done after 6 weeks[18],[34] (Inspire Medical System, MN USA).
Figure 1: Schematic diagram of HNS and illustration of closed-loop stimulation with a sensor intercostal lead and a hypoglossal stimulating leads (A and B). (A) showing hypoglossal nerve (a) wrapped with the stimulator (b). (B) Showing pulse generator (c) and sensor (d)

Click here to view

The Inspire system (Inspire Medical System, MN USA) also uses a closed-loop stimulation with nerve stimulation happening on demand, based on feedback from the intercostal sensor lead [Figure 1]b.

More recently, bilateral hypoglossal nerve stimulated in moderate to severe OSA using a novel HNS device[33],[35] (Genio system®, Nyxoah S.A., Belgium). It requires a single incision to stimulate the bilateral hypoglossal nerve. No separate incision for stimulator device is required, as it is worn externally. The device has a submental implanted stimulation unit connected to both hypoglossal nerves and receives energy pulses from an external activation unit.[33] The mean AHI at the end of 6 months decreased from 23.7 to 12.9 events per hour whereas the mean ODI decreased from 19.1 to 9.8 events per hour in 22 participants.

 » Procedure Details of Bilateral Hypoglossal Nerve Stimulation Top

The patient is placed supine with a roll under the shoulder and neck in extension. The mouth is kept open to see tongue contraction by keeping the roll gauge laterally between the teeth on either side. Nerve monitoring is done by four electrodes inserted into the tongue to identify medial branches of the hypoglossal nerve and a set of electrodes each in genioglossus and styloglossus. Tongue contraction is observed by a video laryngoscope inserted nasally. A horizontal incision is given midway between mentum and hyoid bone, platysma elevated. A midline incision was given over the mylohyoid and separated in midline. Geniohyoid is divided in the midline. Hypoglossal nerve identified laterally entering genioglossus by dissecting in the fat pad and use of stimulator. Superior to the nerve, a pocket is made to fit the implanted stimulator on either side. The two sets of electrodes are on two flexible legs to accommodate the movement of the? GG (Genioglossus) muscles and have a receiving antenna in the center. The implant is placed and anchored to genioglossus after observing high activity in genioglossus and low activity in styloglossus with 0.1-amp current stimulation of lead. Skin closed with single suture and testing done with external stimulator to see a contraction of the base of tongue, epiglottis, and palate with an endoscope. Muscles are approximated and the skin closed. Reconfirmation is done with the external stimulator before extubation. Every night the patient wears an external stimulator or activation chip with an adhesive strip over the antenna to stimulate the electrodes [Figure 2]. The activation chip is removed and kept for charging and used with a separate adhesive the next night. The activation chip is programmed for specific stimulation parameters.[35]
Figure 2: Schematic diagram showing bilateral hypoglossal nerve stimulation [Figure 2] Stimulator (a) hypoglossal nerve (b) and external stimulator over adhesive strip Genio system®, Nyxoah S.A., Belgium. (Illustration by Dr. Mahendra Singh Chouhan)

Click here to view

 » Submental Transcutaneous Electrical Stimulation Top

This is a noninvasive method that has been tried in the past by Miki et al.[36],[37] in 1989 with promising results but other studies were unable to confirm these results as it caused arousal.

More recently, using a bipolar electrical stimulator Hu et al.[38] stimulated the branch of hypoglossal nerve innervating the genioglossus percutaneously below the mandible. The study showed a decreased RDI from 30.87 to 12.45 events per hour, improved upper airway patency, and minimal changes in the microarousal index.[36],[38] The study by Steier et al.[39] used two 40 × 40 mm patches in the submental area for transcutaneous stimulation of the genioglossus. It reduced the RDI from 28.1 to 10.2 events per hour without awakenings. To test the effectiveness and safety of these findings, a randomized cross-over double-blind trial was conducted using the same two patches and continuous overnight stimulation.[34] The study showed an improvement in the ODI with a mean of 4.1/h in the experiment group as compared to the sham group but no significant improvements in AHI. The acceptance of the device was good and there was no difference in the quality of sleep. In the responder group of 17 out of 36 patients, ODI improved by 10/h and the AHI by 9.1/h.[34] Currently, a sham randomized trial is underway for the domiciliary use of transcutaneous stimulation called transcutaneous electrical stimulation in OSA (TESLA) home method.[40]

Invasive neuromodulation therapy to be used in moderate to severe OSA, which is CPAP resistant, or the patient is CPAP noncompliant. It is used as an alternative to CPAP with no known obvious anatomical cause for upper airway obstruction, body mass index less than 32, and absence of concentric collapse on sleep endoscopy.[9] A detailed device activation and titration of parameters are beyond the scope of this article. After 6 weeks of surgery, the device is programmed with different lowest settings of pulse amplitude, width, and rate causing minimal discomfort to the patient. Gradually titrated with PSG to achieve favorable outcomes in AHI, ODI, and reduced daytime sleepiness with a subjective feeling of well-being. The stimulation parameters are company-specific with Inspire II having a closed-loop system with respiration sensor having amplitude (0 to 5 V), rate (20 to 40 Hz), pulse width (60 to 210 μs) with respiration sensor inhalation and exhalation threshold, sensitivity set at different levels, and stimulation time of 2–4 s.[33] Imthera uses continuous stimulation without a respiratory sensor.[29] Nyxoah (Genio system®, Nyxoah S.A., Belgium) system uses bilateral hypoglossal nerve pseudo-continuous stimulation without a sensor to prevent fatigue with the total amount of stimulation and percentage on time. The cycle repeats till the device is switched off.[33],[35] Neuromodulation invasive therapies appear promising but some limitations of hardware malfunction, need for battery replacement/charging, need for a surgical procedure, inherent risks of surgery, and inability to have MRI. Noninvasive therapies require daily compliance, should not cause arousal, and be effective.

 » Conclusion Top

Neuromodulation therapy is effective in treating OSA. Hypoglossal nerve stimulation appears promising in alleviating OSA. Large studies are required to identify OSA causes and personalized medicine to achieve greater patient objective and subjective satisfaction by identifying specific targets in individual cases. Refinement in hardware miniaturization and programming will help in treating OSA better. Long-term effects and benefits need to be seen for this chronic disease.


Medical illustration [Figure 2] Dr. Mahender Singh Chouhan Gertrude's Garden Children Hospital Muthaiga Nairobi, Kenya 0619. Email id: [email protected]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

 » References Top

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