Neurostimulation in sleep medicine …

Sleep Disorders

Updated 02.27.2025
Released 06.10.2018
Expires For CME 02.27.2028

Neurostimulation and neuromodulation in sleep medicine

Authors: Thomas R Gossard MD, Erik K St. Louis MD MS

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Editor: Bradley V Vaughn MD

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Neurostimulation and neuromodulation in sleep medicine

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Introduction

Overview

Applications for neurostimulation, also known as neuromodulation of the central and peripheral nervous systems, are rapidly expanding across all fields of the clinical neurosciences and other related fields of medicine, including sleep medicine and sleep science. Advantages of neuromodulation include the possibility of excellent and specific efficacy when modulating well understood or relatively straightforward neural circuits, with an excellent safety profile and limited adverse effects. Applications in the field of sleep medicine specifically currently include neuromodulatory devices for obstructive and central sleep apnea and restless legs syndrome; research frontiers, including auricular vagus nerve stimulation for insomnia; as well as acoustic, electrical, and magnetic stimulation modalities aiming to promote slow-wave sleep.

The use of hypoglossal nerve stimulation for obstructive sleep apnea has become a standard therapeutic approach for patients with moderate to severe obstructive sleep apnea who are intolerant of first-line continuous positive airway pressure (CPAP) therapy. Additionally, phrenic nerve stimulation is now an approved treatment for central sleep apnea, a disorder that traditionally has had relatively limited treatment options due to its complex pathophysiology. The future of sleep medicine and neuromodulation appears to be quite promising, with additional developments, such as the recently FDA-approved neuromodulatory tonic muscle activation device “TOMAC” for medication-resistant restless legs syndrome, auricular vagus nerve stimulation for insomnia, transcranial magnetic stimulation for several sleep disorders, transcranial direct current for hypersomnia or insomnia, and ongoing expanding research in slow-wave sleep neuromodulation. As we continue to better understand the basic neuroscience and physiology of sleep, future potential therapeutic intracranial targets for sleep manipulation have been proposed and preliminarily explored in proof-of-concept studies.

Key points

	• Neuromodulation of the central and peripheral nervous systems is a rapidly expanding field being utilized or tested in a broad array of disciplines and applications.
	• Advantages of neuromodulation include the possibilities of excellent and highly specific efficacy, with an excellent safety profile and limited adverse effects.
	• Current sleep neuromodulation approaches include devices utilized for obstructive and central sleep apnea and restless legs syndrome; research applications for vagus nerve stimulation for insomnia; as well as neuromodulatory approaches toward slow-wave sleep promotion.

Historical note and terminology

Although lore has held that neurostimulation began in Mesopotamia with the use of an electric eel to treat foot pain and headache, the first documented use of neurostimulation was in ancient Greece whereby an electrically charged torpedo fish known as the Thunderer of the Nile was utilized for the treatment of prolonged headache (11).

Later in the 17th century, William Gilbert described electromagnetism for the treatment of pain, and Ewald Georg von Kleist and Pieter van Musschenbroek harnessed energy in an electrical current storage device known as the Leydeg jar. In 1746, Jean Jallabert used electricity to stimulate muscle fibers of paralyzed individuals. The father of modern neurostimulation is thought to be Luigi Galvani, who in 1780 used electrical sparks to stimulate frog leg muscle movement, becoming the first to apply electricity to produce a specific outcome in mammals.

Modern neurostimulation, hereafter neuromodulation, began in the 1960s. Norman Shealy was the first to adapt a cardiac pacemaker to modulate the nervous system for severe visceral pain in an individual with advanced thoracic cancer (36). The first device designed for neuromodulation by Medtronic was approved by the U.S. Food and Drug Administration (FDA) in 1968 and was used by Yoshio Hosobuchi in 1973 to treat facial pain in a pioneering approach to applied deep brain stimulation (18).

Currently, neuromodulation is applied toward an ever-expanding array of neurologic and medical diseases, including chronic pain, movement disorders, epilepsy, psychiatric disorders, stroke, brain injury, dementia and cognitive disorders, and cardiovascular, gastrointestinal, genitourinary, and colorectal disorders. This article discusses the current array of neuromodulation devices and the indications, results, adverse effects, special considerations, and scientific basis for each.

Hypoglossal nerve stimulation

	• There are currently three primary inclusion criteria for Inspire^® hypoglossal nerve stimulation specified by the U.S. Food and Drug Administration: (1) moderate to severe obstructive sleep apnea, (2) absence of complete concentric collapse at the soft palate level, and (3) absence of moderate levels of obesity at the threshold of BMI less than 40 kg/m² (37; U.S. Food & Drug Administration 2024).
	• Optimal hypoglossal nerve stimulation selection criteria include an AHI between 15 and 65 per hour without a substantial (< 25%) central/mixed apnea component.
	• Inspire^® hypoglossal nerve stimulation senses inspiration via a sensing lead over the intercostal muscles, providing closed-loop stimulation to the hypoglossal nerve.

Indication

Obstructive sleep apnea is characterized by repetitive disordered breathing events, either reduced (hypopneas) or stop breathing (apneas) events lasting at least 10 seconds, that are caused by the collapse or partial obstruction of the upper respiratory airway. Symptoms of loud disruptive snoring, witnessed apneas, snort or gasp arousals, nonrestorative sleep quality, and daytime sleepiness may be unrecognized for years, ultimately contributing to cardiovascular risk. Obstructive sleep apnea is usually treated by nasal continuous positive airway pressure (CPAP) therapy, although many patients are intolerant of CPAP. Patients with moderate obstructive sleep apnea, defined as an apnea-hypopnea index (AHI) of 15 or greater per hour, and severe obstructive sleep apnea, defined as an AHI of 30 or greater per hour, who are intolerant of CPAP may become candidates for alternative non-CPAP therapies, including surgical therapies. Surgical approaches, such as uvulopalatopharyngoplasty (UPPP), mandibular advancement surgery, or hyoid, are often effective, yet each have variable efficacy and substantial postoperative morbidities. Thus, suitable surgical treatment options for those with moderate or severe obstructive sleep apnea remained a therapeutic challenge until the recent advent of hypoglossal nerve stimulation.

Contraindications

Patients with mild obstructive sleep apnea (AHI < 15 per hour), patients with moderate to severe obstructive sleep apnea (AHI > /= 15 per hour) who are CPAP adherent, and patients with primary central sleep apnea or with a central/mixed apnea index constituting over 25% of overall AHI are contraindicated.

Results

Hypoglossal nerve stimulation is a safe and effective alternative surgical approach for moderate to severe obstructive sleep apnea. Initial hypoglossal nerve stimulation development in 1996 involved direct intramuscular stimulation of lingual musculature, which decreased obstructive sleep apnea severity (35). In 2001, hypoglossal nerve stimulation was demonstrated to relieve upper airway obstruction and decrease obstructive sleep apnea severity in eight patients (34). Three hypoglossal nerve stimulation devices were developed and progressed through phase II trials. The first device developed by Apnex showed promise for reducing AHI without significant adverse events (21), but the company dissolved prior to conducting definitive trials. In 2013, the ImThera aura6000™ also showed efficacy in AHI reduction without significant adverse effects in a small-scale phase II trial (31).

Currently, there is a single FDA-approved hypoglossal nerve stimulation device, which is produced by Inspire^®, Inc. In phase II trials, Inspire^® hypoglossal nerve stimulation was safe, tolerable, and efficacious in moderate to severe obstructive sleep apnea in CPAP-intolerant patients (43). The landmark phase III STAR trial (stimulation therapy for apnea reduction trial) fulfilled the primary outcome of AHI reduction (39); 126 participants had a median AHI decrease from 29.3 events per hour at baseline to 9.0 events per hour post-implantation at 12-month follow-up. Procedure-related adverse events were less than 2%. Sustained AHI reduction and adequate adherence were seen in roughly 85% of patients, with demonstrated improvements in quality of life, objective sleep parameters, and excellent tolerability with infrequent, mild adverse events demonstrated at 18 months (38), 3 years (44), and 5 years (45). Further long-term follow-up in the CARDIOSA-12 trial is focused on 24-hour ambulatory systolic blood pressure and various secondary cardiovascular outcomes (10). Subsequently, data from an ongoing observational study, ADHERE Registry, showed that individuals with higher AHI and BMI had results similar to the original trial. Thus, the U.S. Food and Drug Administration has included individuals with AHI under 100 events per hour and BMI less than 40 kg/m² (U.S. Food & Drug Administration 2024).

Overall, hypoglossal nerve stimulation is an effective, safe, and tolerable therapy for patients with moderate and severe obstructive sleep apnea who cannot tolerate CPAP (29). Hypoglossal nerve stimulation is not currently a first-line obstructive sleep apnea treatment; the standard of care is initial CPAP therapy trial prior to consideration of hypoglossal nerve stimulation. CPAP-intolerant patients can become candidates for Inspire^® hypoglossal nerve stimulation treatment and must first undergo diagnostic polysomnography to ensure correct diagnosis of obstructive sleep apnea of moderate or greater severity (ie, AHI ≥ 15 per hour). Objective sleep parameters suggesting good hypoglossal nerve stimulation candidacy include an AHI between 15 and 65 per hour (moderate/severe obstructive sleep apnea) and less than 25% mixed/central apneas (03). In addition to polysomnography, patients must receive a formal otolaryngology evaluation of the upper airway, including drug-induced sleep endoscopy, to characterize the type of upper airway collapse and degree of obstruction. Those having complete concentric collapse at the level of the velum during drug-induced sleep endoscopy are poor candidates for Inspire^® hypoglossal nerve stimulation (03). Correspondingly, the three primary inclusion criteria for Inspire^® hypoglossal nerve stimulation specified by the FDA are moderate to severe obstructive sleep apnea, absence of complete concentric collapse at the soft palate level, and absence of moderate levels of obesity at the threshold of BMI under 32 kg/m² (37).

Adverse effects

Complications of surgery are quite rare but may include pain, tongue abrasion, local infection or hematoma in the neck, and tongue soreness or weakness.

Special considerations

Only adult patients with moderate to severe obstructive sleep apnea demonstrating antero-posterior oropharyngeal airway collapse during drug-induced sleep endoscopy and who have demonstrated intolerance to nasal CPAP therapy should be considered for Inspire^® hypoglossal nerve stimulation therapy. If the patient is deemed a suitable candidate for implantation, the device is implanted and then the incision is allowed to heal before the device is activated. Over a 3-month period, the intensity of the device is titrated and then the patient undergoes a polysomnogram during which the device is adjusted to optimize efficacy. Additional electrode settings may be tried for individuals who fail to achieve a satisfactory result, also involving a multi-month titration and repeat sleep study. An emerging application is use in highly selective adolescents with Down syndrome meeting similar criteria.

Phrenic nerve stimulation

	• Phrenic nerve stimulation is indicated for primary central sleep apnea syndrome.
	• Remede^® is a transvenous phrenic nerve stimulator system that simulates the diaphragm to improve central sleep apnea indices.
	• Remede^® has shown improvements in quality of life and objective sleep parameters in patients with central sleep apnea.

Indication

Central sleep apnea is caused by dysregulation of the brain networks that control ventilation and most commonly occurs secondary to cardiac disease or opioid medication (19). CPAP treatment is often ineffective for the treatment of central sleep apnea as CPAP targets upper airway patency, whereas the primary defect in central sleep apnea is lack of ventilatory drive rather than airway collapse. Bilevel PAP devices, such as adaptive servo-ventilation (ASV), are generally the treatment of choice for central sleep apnea (41). However, ASV has a black box safety advisory for patients with heart failure with compromised ejection fraction (< 45%) due to increased cardiovascular mortality with ASV in this setting (09). Other options include acetazolamide and nocturnal supplemental oxygen, but there is no high-grade evidence for efficacy supporting the widespread use of these therapies for central sleep apnea treatment. Similarly, some individuals carry genetic variations that impair their respiratory drive, such as congenital central hypoventilation, and therapies to support their ventilation are limited.

Contraindications

Contraindications include primary obstructive sleep apnea syndrome, phrenic nerve palsy, stage D heart failure, cardiovascular events in the past 12 months, central sleep apnea secondary to opioid use, and advanced renal disease.

Results

In a phase II study, efficacy and safety with the Remede^® device were demonstrated in patients with Cheynes-Stokes respirations with underlying congestive heart failure (01). The pivotal Remede^® phase III trial included patients with central sleep apnea and an AHI over 20 (08). This trial demonstrated significantly more Remede^®-treated patients than untreated controls meeting the primary outcome of a 50% or greater reduction in AHI at 6 months. The Remede^® treatment group trial also fulfilled secondary outcome measures of reduction in average AHI, ODI, and T90 (cumulative time of oxyhemoglobin saturation below 90%) (08). Subsequent secondary analysis of the trial data focused on patients with heart failure found that objective sleep metrics and quality of life improved at 6 and 12 months, with additional improvement noted on the Minnesota Living with Heart Failure Questionnaire (07).

Adverse effects

At 12 months, improvement in these measures was sustained, and 91% had no serious adverse events. There were two deaths in the Remede^® treatment group; both occurred in the daytime when Remede^® stimulation was off. No ventricular arrythmias were attributed to neurostimulation, and procedural complications were comparable with other implantable devices using transvenous lead technology (08).

Special considerations

This device is a novel therapeutic option for central sleep apnea; however, patient access is quite limited as only specialized centers offer Remede^®, and insurance coverage for this therapy remains limited (40). Device placement requires only moderate sedation, so many central sleep apnea patients with significant underlying cardiovascular disease could potentially receive Remede^® with limited risk of perioperative morbidity. The Remede^® device has two leads; a stimulation lead placed either in the left pericardiophrenic vein or the right brachiocephalic vein to stimulate the phrenic nerve, with an additional sensing lead placed in a thoracic vein, typically the azygos vein. The placement of the neurostimulator is based on patient venous anatomy, most often with placement in the right upper chest.

A potential advantage of Remede^® is that patient adherence is assured because it is a closed-loop device featuring programmable automated sensing and stimulation parameters. However, follow-up visits to assure optimal programming to achieve efficacy and tolerability are required. A typical course for Remede^® initiation involves implantation followed by a post-implant clinic visit 6 weeks postoperatively for a device activation visit with initial parameter programming, followed by stepwise titration over the next 6 weeks and subsequent clinic visits as needed. Approximately 6 weeks following activation, polysomnography is scheduled to determine outcome and monitor for stability of parameter settings. Clinical follow-up involves device interrogation every 3 to 6 months thereafter (40).

Frontiers of neurostimulation for sleep

	• Transcranial magnetic and direct current stimulation and vagus nerve stimulation are neuromodulation modalities that are thought to transiently modulate brain excitability and plasticity and are currently being used in sleep medicine and sleep science as research tools.
	• These research neuromodulation approaches hold potential, with some demonstrated proof-of-concept for the treatment of insomnia and various other sleep disorders and disturbances, as well as for slow-wave sleep modulation.

Results

Transcranial magnetic stimulation (TMS). Transcranial magnetic stimulation is an expanding research therapy in neurologic and psychiatric disease. Repetitive TMS (rTMS) transiently modulates brain excitability and plasticity. Clinically, effects of rTMS have been variable, including preliminary reported experience in the treatment of sleep disorders. A review examined 15 different publications in which rTMS was utilized for sleep disorders (32). Chronic primary insomnia is a common target for rTMS as it is thought to involve hyperexcitability of brain networks. In a study of 120 patients, rTMS was utilized to stimulate three regions of the brain and showed proof-of-concept efficacy for improving chronic primary insomnia symptoms by targeting the hypothalamic-pituitary axis (20). Another study found that rTMS helped reduce insomnia symptoms when administered in combination with acupuncture (48). Studies have also suggested that rTMS may be beneficial for restless legs syndrome by stimulating over the supplementary motor area (02; 25). rTMS may also improve upper airway mechanics without arousing patients from sleep and might also be used in combination with phrenic nerve magnetic stimulation for the treatment of sleep apnea (30). There is one case report of rTMS reducing symptoms of narcolepsy in an adolescent (23). rTMS was also used in sleep bruxism by targeting the masseter muscle control location in a group of 12 patients (49). A randomized controlled trial used rTMS to alter cognitive deficiencies following sleep deprivation (24) and found that administration of high-frequency rTMS during extended wakefulness following sleep deprivation exerted positive effects on the HPA axis and frontal regional brain activation and may improve cognitive impairments caused by sleep deprivation.

Transcranial direct current stimulation (TDCS). Like TMS, TDCS noninvasively modulates neuronal excitability and plasticity. TDCS has been used as a cognitive neuroscience research tool. With TDCS, there are various wavelengths and stimulation paradigms. TDCS sleep applications include modulation of slow-wave sleep. The TDCS paradigm developed for sleep manipulation is a sinusoidally oscillating current (so-TDCS) to induce cortical slow oscillations (27). TDCS appears to enhance slow-wave and spindle sleep activity but decreases deep sleep stage time (28). TDCS may potentially benefit sleep in young healthy adults, but there has been difficulty replicating findings in an older adult population (12). In seven patients with multiple sclerosis, TDCS improved daytime sleepiness but had no effect on objective sleep measures (06). There is a randomized controlled trial underway analyzing whether bilateral prefrontal cortex anodal TDCS can improve sleep in athletes (13). Another system utilizing the transcranial application of alternating current to augment sleep spindles demonstrated enhancement of motor memory consolidation (26). These systems present an opportunity to understand the underlying effect of these electrical rhythms and offer potential implications for therapeutics.

Auricular vagus nerve stimulation. Vagus nerve stimulation (VNS) is most commonly used in drug-resistant epilepsy but has shown promise in migraine, heart failure, and inflammatory bowel disease. Vagus nerve stimulation can lead to adverse effects of de novo or worsened obstructive sleep apnea and central sleep apnea, which may be a function of vagus nerve stimulation parameter settings, such as output current intensity, signal frequency, or pulse width (15). There has been preliminary work with auricular vagus nerve stimulation for the treatment of insomnia. The neural underpinnings of insomnia remain unclear, so specific neuromodulation targets for sleep manipulation remain uncertain at present (05). Transcutaneous vagus nerve afferents provide somatosensory trafficking from the external ear to the brainstem nucleus tractus solitarius, so stimulation of this area can reduce sympathetic activity without substantial parasympathetically mediated adverse effects. A controlled trial examined 24 patients with chronic insomnia treated with 4 weeks of transcutaneous auricular vagus nerve stimulation (taVNS) by attaching stimulating electrodes to the bilateral cymba conchae on the skin surface (17). fMRI during taVNS demonstrated modulatory effects on the prefrontal cortex with accompanying improvement in Pittsburgh Sleep Quality Index (PSQI) and Flinders Fatigue Scale (FFS) scores. Another study had similar findings, with improvements of PSQI and decreased functional connectivity between the left medial prefrontal cortex and bilateral dorsal anterior cingulate gyrus (46).

Slow-wave sleep neuromodulation. Slow-wave sleep is important for basic physiological processes, such as brain plasticity, metabolic functioning, and immune system regulation. Growing evidence over the last decade suggests that slow-wave sleep is critical for sleep state–dependent glymphatic system functioning that enables clearance of wake-state dependent toxic metabolites and proteins that may underlie neurodegeneration, so enhancement of slow-wave sleep processes carries an exciting and novel potential for enhancement of sleep-related homoeostatic brain functions. Current therapeutic slow-wave sleep neuromodulation targets include enhancement of synaptic consolidation, improved glymphatic functioning, and promotion of deeper sleep. Approaches include auditory stimulation, transcranial electric current stimulation (both direct and alternate), and transcranial magnetic stimulation (14). Preliminary research has been provocative in demonstrating proof-of-concept for manipulating slow-wave sleep processes, yet much additional translational and applied clinical research is needed, particularly in patient populations with cognitive and sleep disorders. Whether slow-wave sleep modulation is capable of promoting brain functioning and improving symptoms of sleep disturbance remains a current research frontier. Prospective longitudinal studies will also be needed to demonstrate whether slow-wave sleep neuromodulation might hold promise as a neuroprotective intervention that could prevent neurodegenerative diseases.

Adverse effects

Adverse effects are generally reported as being very mild, including irritation at the site of stimulation, and have not yet been systematically characterized. TMS carries a low risk of precipitating epileptic seizures.

Scientific basis

The Inspire^® hypoglossal nerve stimulation system is a neuromodulatory device that senses inspiration from a sensing lead tunneled to the intercostal muscle, then provides closed-loop neuromodulation of the hypoglossal nerve. The patency of the upper airway is controlled by the upper airway dilator muscles, including the genioglossus (22). The genioglossus muscle, which is innervated by the hypoglossal nerve, is the primary muscle responsible for airway patency during inspiration.

The hypoglossal nerve stimulation device contains a generator with batteries and two ports, including respiratory sensing and stimulation leads. The respiratory lead senses respiratory effort and provides input to the hypoglossal nerve stimulation device, which provides closed-loop stimulation to the hypoglossal nerve (29). Surgical placement of the Inspire^® hypoglossal nerve stimulation device is typically an outpatient procedure lasting between 90 and 180 minutes. Implantation requires three small incisions with cuff placement around the hypoglossal nerve, a pulse generator, and the pleural respiratory sensing lead, each on the same side of the chest as the neck cuff placement. There is an accompanying mobile remote device that can be activated by the patient for turning the device on/off, pausing therapy, and decreasing or increasing stimulation strength within preset programmable parameters.

The novel Respircardia Remede^® device uses transvenous phrenic nerve stimulation to stimulate the diaphragm, driving ventilation in the absence of central neural ventilatory drive in central sleep apnea. The Remede^® device is comprised of a single stimulation lead placed at the junction of the superior vena cava and brachiocephalic vein, leading to improved central sleep apnea disorder breathing indices (47).

The presumed mechanism of action for tonic muscle activation (TOMAC) of the fibular (peroneal) nerve leverages the recognized key clinical diagnostic feature of restless legs syndrome, namely reliable relief of disturbing leg symptoms by leg movement. The TOMAC approach involves a pair of stimulating devices that may be self-applied nightly before bedtime, or on demand during the daytime as needed. The TOMAC devices are applied to each leg just below the level of the knees, corresponding to the position of the fibular head where the course of the fibular (peroneal) nerve travels to provide innervation of the anterior tibialis muscles. TOMAC provides high-frequency stimulation below the threshold for motor activation of the anterior tibialis muscles of both legs (ie, generally imperceptible to the patient and without generating noticeable movement of the feet or ankles), thereby providing relief of restless legs syndrome symptoms and comfortable sleep onset.

The research neuromodulation modalities of transcranial magnetic stimulation, transcranial direct current stimulation, and auricular vagus nerve stimulation are thought to modulate brain excitability and plasticity. A detailed discussion of the presumed mechanism of action of these neuromodulation methods is beyond the scope of this article.

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50: References especially recommended by the author or editor for general reading.

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

Thomas R Gossard MD

Dr. Gossard of Mayo Clinic Rochester has no relevant financial relationships to disclose.
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Erik K St. Louis MD MS

Dr. St. Louis of Mayo Clinic has no relevant financial relationships to disclose.
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Editor

Bradley V Vaughn MD

Dr. Vaughn of UNC Hospital Chapel Hill and University of North Carolina School of Medicine has no relevant financial relationships to disclose.
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Former Authors

Richard P Knudsen MD FAASM CNP FAAP
Antonio Culebras MD FAAN FAHA FAASM

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Neurostimulation and neuromodulation in sleep medicine

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Clinical Categories

Sleep Disorders

Neurostimulation in sleep medicine …

Neurostimulation and neuromodulation in sleep medicine

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Hypoglossal nerve stimulation

Indication

Contraindications

Results

Adverse effects

Special considerations

Phrenic nerve stimulation

Indication

Contraindications

Results

Adverse effects

Special considerations

Frontiers of neurostimulation for sleep

Results

Adverse effects

Scientific basis

Conclusions

References

Contributors

Authors

Editor

Former Authors

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Non-24-hour sleep-wake disorder

Sleep and parkinsonism

Sleep and alcohol use and abuse

Idiopathic hypersomnia

Jet lag disorder

Sleep and multiple sclerosis

Sleep and aging

Sleep and chronic pulmonary disorders

Neurostimulation and neuromodulation in sleep medicine

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Hypoglossal nerve stimulation

Indication

Contraindications

Results

Adverse effects

Special considerations

Phrenic nerve stimulation

Indication

Contraindications

Results

Adverse effects

Special considerations

Frontiers of neurostimulation for sleep

Results

Adverse effects

Scientific basis

Conclusions

References

Contributors

Authors

Editor

Former Authors

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Non-24-hour sleep-wake disorder

Sleep and parkinsonism

Sleep and alcohol use and abuse

Idiopathic hypersomnia

Jet lag disorder

Sleep and multiple sclerosis

Sleep and aging

Sleep and chronic pulmonary disorders

This is an article preview.
Start a Free Account
to access the full version.