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By Karl Doghramji, MD, Professor of Psychiatry, Neurology, and Medicine and Medical Director, Jefferson Sleep Disorders Center, Thomas Jefferson University

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Patient Education

Snoring is a raspy noise produced in the nasopharynx during sleep. It is quite common, occurring in about 57% of men and 40% of women; prevalence increases with age. However, because a bed partner's perception of and response to snoring is highly subjective and because snoring varies from night to night, prevalence estimates vary widely.

The sound ranges from barely audible to an extremely bothersome noise that may be loud enough to hear in another room. Snoring is distressing usually to others (typically a bed partner or roommate trying to sleep) rather than the snorer; uncommonly, snorers wake up to the sound of their own snoring.

Snoring can have significant social consequences. It can cause strife between bed partners or roommates; rarely, snorers have been assaulted and even murdered because of their snoring.

Other symptoms such as frequent awakening, gasping or choking during sleep, excessive daytime sleepiness, and morning headache may also be present, depending on the severity, cause, and consequences of the snoring.


Snoring results from airflow-induced flutter of soft tissues of the nasopharynx, particularly the soft palate. As in any fluttering physical structure (eg, a flag), flutter in the nasopharynx develops depending on interacting factors, including the mass, stiffness, and attachments of the fluttering element and the velocity and direction of airflow. The fact that people do not snore while awake suggests that sleep-induced muscular relaxation is at least part of the etiology because muscle tone is the only component of flutter that can change during sleep; tissue mass and attachments do not change. Furthermore, if pharyngeal dilators cannot keep the airway open in response to the negative intraluminal pressure induced by inspiration, the upper airway narrows, increasing local airflow velocity (for a given inspiratory volume). The increased flow velocity promotes flutter directly and decreases intraluminal pressure, further enhancing airway closure and thus promoting flutter and snoring.

Snoring is more likely to occur in airways that are already compromised by structural factors, including

  • Micrognathia or retrognathia

  • Nasal septal deviation

  • Rhinitis that causes tissue swelling

  • Obesity


Primary snoring

Primary snoring is snoring that is not accompanied by awakening or excessive arousals, limitation of airflow, oxygen desaturation, or arrhythmias during sleep and that occurs in people who do not have excessive daytime sleepiness (EDS). Arousals are brief transitions to lighter sleep or awakenings that last < 15 sec and are usually not noticed.

Sleep-disordered breathing

Snoring is sometimes a manifestation of sleep-disordered breathing, which covers a spectrum ranging from upper airway resistance syndrome to obstructive sleep apnea (OSA—see Obstructive Sleep Apnea). Each has similar upper airway obstructive pathophysiology but differs in degree and clinical consequences of the airway obstruction. The clinical consequences involve mainly disturbances of sleep and/or airflow.

Patients with OSA have ≥ 5 episodes of apnea or hypopnea per hour during sleep (apnea/hypopnea index [AHI]) plus ≥ 1 of the following:

  • Daytime sleepiness, unintentional sleep episodes, unrefreshing sleep, fatigue, or insomnia

  • Awakening with breath holding, gasping, or choking

  • Reports by a bed partner of loud snoring, breathing interruptions, or both during the patient's sleep

OSA can be categorized by severity: mild (5 to 15 episodes/hr), moderate (16 to 30 episodes/hr), or severe (> 30 episodes/hr).

Upper airway resistance syndrome causes EDS or other manifestations but does not meet full criteria for OSA.


Although snoring itself has no known adverse physiologic effects, OSA may have consequences (eg, hypertension, stroke, heart disorders, diabetes).

Risk factors

Risk factors for snoring include

  • Older age

  • Obesity

  • Use of alcohol or other sedatives

  • Chronic nasal congestion or blockage

  • A small or posteriorly displaced jaw

  • Male sex

  • Postmenopausal status

  • Black race

  • Pregnancy

  • Abnormal structures that can block airflow (eg, large tonsils, a deviated nasal septum, nasal polyps)

There may also be familial risk.


The primary goal is to identify snorers who are at high risk of having OSA. Many snorers do not have OSA, but most patients with OSA snore (the precise proportion is not known).

Because several important manifestations of OSA are noticed mainly by others, bed partners or roommates should also be interviewed when possible.


History of present illness should cover severity of snoring, including its frequency, duration, and loudness. Also, the degree that snoring affects the bed partner should be noted. A snoring severity scale may be used.

Review of systems should seek symptoms suggesting OSA, such as the presence of sleep disturbance as indicated by

  • Number of awakenings

  • Witnessed apneic or gasping/choking episodes

  • Presence of unrefreshing sleep or morning headaches

  • EDS

The Epworth Sleepiness Scale (see Table: Epworth Sleepiness Scale) can be used to quantify daytime sleepiness. The STOP-BANG score (see Table: STOP-BANG Risk Score for Obstructive Sleep Apnea) is a useful tool to predict risk of OSA for patients who snore.

STOP-BANG Risk Score for Obstructive Sleep Apnea

Item Evaluated



Loud snoring (louder than talking or loud enough to be heard through closed door)


Often fatigue or sleepiness during the daytime


Observed to stop breathing during sleep


High BP or current treatment for hypertension


> 35 kg/m2


> 50 yr

Neck circumference

> 40 cm (> 15 3/4 in)



≥ 3 findings = high risk of OSA.

< 3 findings = low risk of OSA.

BMI: body mass index; OSA = obstructive sleep apnea.

Past medical history should note presence of disorders that may be associated with OSA, particularly hypertension, coronary ischemia, heart failure, stroke, gastroesophageal reflux disease (GERD), atrial fibrillation, depression, obesity (especially morbid obesity), and diabetes. Patients are asked how much alcohol they consume and when it is consumed in relation to bedtime. Drug history may identify sedating or muscle-relaxing drugs.

Physical examination

Examination should begin by measuring height and weight, with calculation of body mass index (BMI).

The rest of the examination is of limited use and focuses on inspecting the nose and mouth for evidence of obstruction. Signs include

  • Nasal polyps and engorged turbinates

  • A high, arched palate

  • Enlargement of the tongue, tonsils or uvula

  • A small or posteriorly displaced mandible

A Mallampati score of 3 or 4 (only the base or none of the uvula is visible during oral inspection—see Figure: Mallampati scoring.) suggests increased risk of OSA.

Mallampati scoring.

Modified Mallampati scoring is as follows:

  • Class 1: Tonsils, uvula, and soft palate are fully visible.

  • Class 2: Hard and soft palate, upper portion of tonsils, and uvula are visible.

  • Class 3: Soft and hard palate and base of the uvula are visible.

  • Class 4: Only the hard palate is visible.

Red flags

The following findings are of particular concern:

  • Witnessed apnea or choking during sleep

  • Morning headaches

  • Epworth sleepiness score ≥ 10

  • BMI ≥ 35

  • Very loud, constant snoring

Interpretation of findings

The clinical evaluation is not completely reliable for diagnosis of OSA but can be suggestive. Red flag findings clearly correlate with OSA. However, all of these findings occur along a continuum, and there is no widespread agreement on cut-off points and relative weighting. Nonetheless, the more red flag findings a patient has and the more severe they are, the greater the likelihood of OSA.


Testing is done when a diagnosis of OSA is suspected; it consists of polysomnography (PSG—see Testing). However, because snoring is so common, PSG should be done only when clinical suspicion for OSA is significant. A reasonable approach is to test patients who have red flag findings (particularly witnessed apnea) as well as those who have several red flag elements that do not quite meet the listed scores.

People with no symptoms or signs of sleep disturbance other than snoring do not need to be tested but should be clinically monitored for development of such manifestations.


Treatment of snoring associated with other conditions, such as chronic nasal obstruction and OSA (see Obstructive Sleep Apnea : Treatment), are discussed elsewhere in The Manual.

Overall, treatment includes general measures to manage risk factors plus physical methods to open the airways and/or stiffen the involved structures.

General measures

Several general measures can be used for primary snoring. Their efficacy has not been well-evaluated, primarily because perception of snoring is highly subjective; However, particular patients may benefit. Measures include

  • Avoiding alcohol and sedating drugs for several hours before bedtime

  • Sleeping with the head elevated (best accomplished by using bed- or body-positioning devices such as wedges)

  • Losing weight

  • Using earplugs

  • Implementing alternate sleeping arrangements (eg, separate rooms)

  • Treating any nasal congestion (eg, with decongestant and/or corticosteroid sprays or with elastic strips that hold the nares open)

Oral appliances

Oral appliances are worn only during sleep; they include mandibular advancement devices and tongue-retaining devices. These appliances must be fitted by specially trained dentists. They are helpful for patients with mild to moderate OSA and are generally regarded as highly effective for simple snoring, although studies into this area are scant.

Adverse effects include temporomandibular joint (TMJ) discomfort, dental misalignment, and excessive salivation, but most patients tolerate the devices well.

Mandibular advancement devices are most commonly used. These devices push the mandible and tongue forward relative to the maxilla and thus reduce airway collapse during sleep. These devices may be fixed or adjustable; with adjustable devices, how far the mandible is advanced can be adjusted incrementally after the initial fitting to optimize results. Adjustable devices are more effective than fixed devices.

Tongue-retaining devices (TRD) use suction to maintain the tongue in an anterior position. TRDs are more uncomfortable and probably less effective than mandibular advancement devices.

Continuous positive airway pressure (CPAP)

CPAP devices maintain a constant positive pressure in the upper airway via a small mask applied to the nose or nose and mouth (see Obstructive Sleep Apnea : CPAP). By eliminating the need for negative pressure during inspiration, CPAP prevents the narrowing or collapse of the airways at that time. It thus provides very effective relief of OSA and is effective for primary snoring. However, its use in primary snoring is limited because third-party reimbursement for this use is lacking and because patients are not sufficiently motivated. Although patients are often willing to use a CPAP device nightly to avoid the significant symptoms and long-term consequences of OSA, they are less willing to use the device to manage primary snoring, whose consequences are primarily social.


Because reduced nasal patency promotes snoring, surgically correcting specific causes of airway compromise (eg, nasal polyps, hypertrophied tonsils, deviated septum) would seem to be a reasonable way to decrease snoring. However, studies have not yet substantiated this theory.

Various pharyngeal surgical procedures that alter the structure of the palate and sometimes the uvula have been developed for OSA. Some are also useful for nonapneic snoring.

Uvulopalatopharyngoplasty can be highly effective for snoring, although effects may not last beyond a few years. It is an inpatient procedure requiring general anesthesia; thus, its usefulness for snoring alone is limited.

Therefore, a number of outpatient procedures that can be done using a local anesthetic have been developed:

  • Laser-assisted uvuloplasty is less invasive than uvulopalatopharyngoplasty. Although some patients report benefit, its usefulness in treating snoring has not been proved.

  • For injection snoreplasty, a sclerotherapeutic agent is injected into the submucosa of the soft palate to stiffen it and the uvula. Its usefulness for snoring alone requires further study.

  • For radiofrequency ablation, a probe is used to introduce thermal energy into the soft palate. Studies have shown its usefulness for snoring, but further study is needed.

  • Palatal implants, made of polyethylene, can be placed into the soft palate to stiffen it. Three small implants are used. Their usefulness for snoring alone has not been proved.

Key Points

  • Only some snorers have OSA, but most patients who have OSA snore.

  • Clinical risk factors such as nocturnal apneic or choking episodes, daytime sleepiness, and a high BMI help identify patients at risk of OSA and thus in need of testing with polysomnography.

  • Recommend general measures to reduce snoring (eg, avoiding alcohol and sedating drugs, sleeping with the head elevated, losing weight).

  • Consider specific measures such as mandibular advancement devices, uvulopalatopharyngoplasty, palate-altering procedures, and CPAP to treat snoring due to OSA.

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