Diagnostic Sleep Testing in the Evaluation of Snoring and Sleep Apnea
Dentists may not always know when they should test a patient who complains of snoring;
this article discusses how diagnostic sleep testing works.

By Jerald H. Simmons, MD

The dilemma frequently encountered by the dentist wishing to offer an appliance for treatment of snoring or sleep apnea is whether there is a need for extensive testing of patients who present with a complaint of snoring. This article describes diagnostic sleep testing in the evaluation of patients with snoring and sleep apnea.

Article copyright 1998 Journal of the California Dental Association. Photographs copyright of the authors.

Snoring and sleep apnea are extremely common, and patients with these conditions require proper evaluation by the health care system. The dilemma frequently encountered by the dentist wishing to offer an appliance for treatment of snoring or sleep apnea is whether there is a need for extensive testing of patients who present with a complaint of snoring. This article will describe diagnostic sleep testing in the evaluation of patients with snoring and sleep apnea. To understand the role of sleep testing, it is also important to recognize some of the physiology associated with the sleeping process.

Basics of Sleep Physiology
Sleep testing evaluates the state of the patient throughout the night. The standard procedure is to assign a sleep stage (defined below) for each consecutive 30-second period throughout the study.1 This results in a tabulation of the patient's sleep state throughout the night.

Sleep Stages

The sleep process can be divided into two main stages, rapid eye movement (REM) and non-rapid eye movement (Non-REM). Non-REM sleep normally precedes REM sleep and can be further divided into stages 1, 2, 3, and 4. Frequently stages 3 and 4 are combined and referred to as slow wave, or delta, sleep. Non-REM sleep occupies most of the night.1 There are many important aspects of non-REM sleep, but most of them are beyond the scope of this article. For the purposes of this discussion, two main stages of sleep, REM and non-REM, will be referred to.

REM sleep was first described in 1953.2 REM sleep is regulated by the brain stem.3 Features of REM sleep include the following:

  • It occurs about every 90 minutes during sleep.
  • Each episode becomes longer as the night progresses.
  • Vivid dreaming occurs during REM sleep
  • Muscle paralysis (hypotonia) occurs, including the muscles of the upper airway.
  • During REM sleep, the airway muscles are more vulnerable to collapse because of their state of hypotonia. During REM sleep, obstructive respirations are most pronounced, particularly in obese individuals such as those with obstructive sleep apnea.4,5 This is particularly true when a person is sleeping supine because gravity plays an additional role, which increases the vulnerability of airway collapse. Therefore, if a person is not evaluated while supine in REM sleep, a diagnosis of a sleep-related breathing disorder cannot be excluded.5

    The progression of sleep that occurs through the night is such that REM primarily occurs during the last half of the night. The first REM episode typically occurs 90 minutes after sleep onset. This REM episode is usually very brief, lasting only several minutes. This is usually followed by a return of Stage 1 and the process repeats. As the brain transitions through the various sleep stages, each REM episode becomes longer, and the slow wave sleep of non-REM becomes shorter. Normally, people have most of their REM in the early morning hours, i.e., 3 to 6 a.m.4,6

    Sleep Fragmentation

    A brief event called a micro-arousal is a disruption of sleep continuity that usually does not result in complete awakening and therefore occurs without the recollection of the patient. Nonetheless, repetitive arousals during the night usually result in daytime sleepiness and fatigue the next day.

    Obstructive Respirations

    Since sleep studies evaluate the respiratory process, it is important to understand the dynamics of the upper airway that are associated with obstructive respirations during sleep. As air passes through the back of the throat, it can create a negative pressure as a result of the Bernoulli effect. The narrower the airway passage, the greater the negative pressure. When the pressure becomes great enough, the soft tissue of the pharynx, such as the soft palate and uvula, are pulled and begin to vibrate. This vibration causes the snoring sound.4 When the negative pressure increases to a certain point, the airway may completely collapse. This is what is known as an apneic episode, during which breathing ceases. During this event, the oxygen level typically drops at least 2 percent. The apneic episode terminates in an arousal, which results in increased muscle tone of the airway, opening up the pharynx so breathing is re-established. To be tabulated as an apnea during a sleep study, the event must last a minimum of 10 seconds.7

    The airway does not need to completely collapse for a significant event to occur. Even with only partial obstruction of the airway, a slight drop in the oxygen level and a brief arousal from sleep can still occur. This event is known as a hypopnea. Like apneas, hypopneas can fragment sleep and cause daytime sleepiness.4,7

    Recent studies have demonstrated that the spectrum of clinically significant obstructive respirations can include events that are more subtle than hypopneas.8 These subtle events consist of increases in upper airway resistance occurring from a partial blockage of the upper airway. This results in increased work of breathing, triggering an arousal (or micro-arousal) that fragments sleep. This can occur even without a measured decrease in airflow by the routine methods employed in most sleep laboratories.5,8,9 These events are usually associated with a crescendo increase in snoring, which culminates with the micro-arousal. When this occurs repetitively, it can also cause excessive daytime sleepiness. This is known as upper airway resistance syndrome.8-10 There is frequently no decrease in the blood oxygen level associated with the respiratory events of upper airway resistance syndrome.8-10 Measurements of the pressures within the airway can be performed by the addition of a pressure sensors within the airway below the point of obstruction, such as in the esophagus. The pressure sensor can identify a crescendo increase in respiratory effort with each breath, culminating with the micro-arousal. Most laboratories do not use the pressure catheter to establish a diagnosis of upper airway resistance syndrome but instead use the snoring pattern. The snoring increases in a crescendo pattern and leads to an arousal. These subtle events have only relatively recently been recognized as significant and are now known as respiratory arousals. The tabulation of respiratory arousals has only recently been adopted into the practice parameters established and promoted by the American Sleep Disorders Association.5 A person does not have to snore to have upper airway resistance syndrome. In the absence of snoring, the only way to establish the diagnosis is with the esophageal pressure catheter to detect the subtle respiratory-induced micro-arousals.

    The spectrum of obstructive breathing ranges from upper airway resistance syndrome to obstructive sleep apnea.8 Anywhere along this spectrum, the degree of obstructive respirations can be considered significant if sleep is disrupted. It is important to be aware of the cardiovascular consequences of severe obstructive respirations during sleep. Many studies have been done and more are currently under way that are characterizing the ill effects of repetitive obstruction of the upper airway during sleep. The main concerns are the increased risks of hypertension, stroke, and cardiac disease.11-16 Therefore, even if a patient is not sleepy during the day but suffers from severe obstructive sleep apnea, the apnea should be treated to prevent the development or worsening of these other medical conditions.

    Diagnostic Testing for Snoring and Obstructive Sleep Apnea

    Sleep testing is performed to identify and quantify the respiratory events described above. In addition, sleep quality is evaluated by measuring the presence of appropriate sleep stages and the absence or presence of frequent arousals.
    The most reliable method to identify obstructive sleep apnea is a nocturnal polysomnograph.5 This test measures a variety of parameters. The most common parameters used for nocturnal polysomnograph testing include the following:

  • Right and left eye movements or electro-oculograph;
  • Electroencephalograph, two to four separate channels;
  • Chin muscle activity, known as electromyography;
  • Electrocardiograph;
  • Leg electromyography, usually right to left anterior tibialis muscles;
  • Snoring or tracheal sounds, measured with a microphone taped to the throat;
  • Air flow through the nose and mouth;
  • Movement of the chest;
  • Movement of the abdomen;
  • Oxygen level, measured with a finger oximeter;
  • Body position; and
  • Esophageal manometry -- in some laboratories.
  • Table 1.
    The ASDA Standards of Practice Committee has adopted the following indications for sleep testing for the evaluation of sleep-related breathing disorders

    1. Nocturnal Polysomnography is routinely indicated to establish a diagnosis of sleep-related breathing disorders.

    1.1) For most patients a full NPSG is required.
    1.2) For patients with a high degree of clinical suspicion for Obstructive Sleep Apnea (OSA) a cardiopulmonary sleep study can be performed, but a negative study must be followed up with a full NPSG study.

    1. NPSG is indicated to establish the proper Continuous Positive Airway Pressure (CPAP) in patients with sleep-related breathing disorders.

      2.1) Full NPSG with CPAP is recommended for patients with documented sleep-related breathing disorder in whom CPAP is warranted.
      2.2) NPSG with CPAP is appropriate for patients with any of the following NPSG results:

      a) An Apnea Index (AI, which is the number of apneas per hour of sleep) of at least 20 per hour or an Apnea Hypopnea Index (AHI, which is the number of apneas and hypopneas per hour of sleep) of at least 30 per hour, regardless of the patient's symptoms.
      b) AHI of at least 10 per hour in a patient with excessive daytime sleepiness.
      c) A respiratory arousal index of at least 10 per hour in a patient with daytime sleepiness.

      2.3) A cardiorespiratory sleep study without EEG channels is NOT recommended for CPAP titration (a study which is performed to determine the optimal CPAP pressure).
      2.4) For CPAP titration, a split-night study (first half for diagnosis and second half for CPAP titration) is an alternative to one full night of diagnostic NPSG followed by a second night of titration if the following four criteria are met:

      a) An AHI of at least 40 per hour documented during a minimum of 2 hours. A split-night may be considered with a AHI of between 20 to 40 based on clinical judgment.
      b) CPAP titration is carried out for more than 3 hours.
      c) The study documents that CPAP eliminates or nearly eliminates the respiratory events in both REM and Non-REM sleep, including REM sleep with the patient in the supine position.
      d) A second full night NPSG CPAP titration is performed if criteria b and c are not met..

    2. Preoperative NPSG or cardiopulmonary sleep studies are indicated to evaluate patients for the presence of obstructive sleep apnea before they undergo laser-assisted uvulopalatopharyngoplasty or other related surgical procedures.
    3. Follow-up NPSG or cardiopulmonary sleep studies are routinely indicated for the assessment of treatment in the following circumstances:

    4.1) After good clinical response to oral appliance treatment in patients with moderate to severe obstructive sleep apnea, to ensure therapeutic benefit.
    4.2) After surgical treatment of patients with moderate to severe obstructive sleep apnea, to ensure satisfactory response.
    4.3) After surgical treatment of patients with sleep apnea whose symptoms return despite a good initial response to treatment.

    1. Follow-up NPSG studies are routinely indicated in the following circumstances:

    5.1) After substantial weight loss has occurred in patients on CPAP for treatment of sleep-related breathing disorders to ascertain whether CPAP is still needed at the previously titrated pressure.
    5.2) After substantial weight gain has occurred in a patient on CPAP who again is symptomatic despite continued use of CPAP, and to adjust the CPAP pressure to a higher level in order to prevent obstructive respirations. 5.3) When clinical response is insufficient or when symptoms return despite a good initial response to treatment.

    1. Follow-up studies are not indicated in patients who continue to do well with treatment.

    Quantifying sleep into REM and non-REM sleep requires that eye movement, electroencephalograph, and muscle activity be measured.1 There are specific features in the signals from these channels that are used to categorize sleep into the different sleep stages. For example, REM sleep is characterized by a decrease in chin electromyography activity, rapid eye movements on the eye channels, and specific features in the electroencephalograph channels. Arousals, which are brief disruptions in the continuity of sleep, must last at least three seconds.17 Identification of arousals requires electromyograph and electroencephalograph signals for proper tabulation. It is possible to identify arousals using other parameters such as sudden fluctuations in heart rate, but these are less reliable. Therefore, sleep studies done without electro-oculograph, electroencephalograph, and electromyograph are not reliably able to quantify sleep, stage sleep, or identify arousals. These limited monitoring devices primarily record aspects of respiration. Studies performed with such devices are referred to as cardiorespiratory studies.5 The parameters included may range from oximetry with the addition of some measure of respiratory effort, to a six-channel unit that measures air flow, snoring, chest movement, oximetry, heart rate, and body position. The current position of the American Sleep Disorders Association is that obstructive sleep apnea is best diagnosed using nocturnal polysomnography.5 In some instances, cardiorespiratory sleep studies can be used to establish a diagnosis but never to exclude a diagnosis of a sleep-related breathing disorder.5 This is because sleep fragmentation cannot be identified, and therefore subtle breathing disturbances may go undetected.

    Diagnostic sleep testing in patients suspected of snoring or sleep apnea is primarily done to identify and quantify the occurrence of apnea, hypopnea, and subtle respiratory arousals that do not fall within the apnea or hypopnea definition but still disrupt sleep. Some patients may present only with a complaint of snoring and deny witnessed pauses in respirations or deny symptoms of daytime sleepiness. This is a common scenario that is handled differently by many in the field. Some practitioners may choose not to study these patients at all, but this approach is short-sighted.

    Even though the patient has not been witnessed to have pauses or abnormal breathing during sleep, most likely these observations are made at the beginning of the sleeping period, when a bed partner is still awake. Most patients with obstructive respirations have their worst respirations during REM, and most of the REM sleep occurs during the last portion of the night, as stated earlier.4 As explained earlier, REM episodes become longer with each sleep cycle as the night progresses. The hypotonia of REM results in vulnerability of the airway to collapse. It is during these early morning hours that the bed partner may also be asleep and therefore unable to witness any apneic events. Therefore, it is not adequate to rely on a bed partner's observation to exclude a diagnosis of sleep apnea. Even if the patient only complains of snoring, a sleep study is important to evaluate the degree of obstructive respiration before embarking on treatment methods.

    Many sleep laboratories have a backlog of patients, and the American Sleep Disorders Association advocates the use of cardiopulmonary sleep studies to shorten the waiting period for testing of patients with a high probability of sleep apnea.5

    The American Sleep Disorders Association published its most recent practice parameters in 1997 for the indications of sleep testing. A summary of these recommendations is outlined in Table 1.5

    The American Sleep Disorders Association has proposed an algorithm for the evaluation of snoring. The recommendations state that full nocturnal polysomnography be performed to exclude a diagnosis of a sleep-related breathing disturbance. The cardiorespiratory testing devices are only recommended when there is a high clinical suspicion of obstructive sleep apnea. The algorithm matrix does not recommend a cardiorespiratory sleep study be performed to exclude a diagnosis of a sleep-related breathing disorder, but rather only to establish the diagnosis. Therefore, the recommendation is for negative cardiorespiratory sleep studies to be followed up with full nocturnal polysomnography testing. The algorithm, however, is not designed to accommodate the typical situation encountered by dentists who may embark on treating patients with snoring. In fact, the algorithm states that if there is "simple snoring," then a nocturnal polysomnograph is recommended only if a laser-assisted uvulopalatopharyngoplasty surgery is being considered as a treatment option. No mention is made of appliance therapy. It is stated that the algorithm is a guideline, and in clinical practice it may be necessary to modify the approach to accommodate specific situations.

    Evidence is beginning to demonstrate that snoring alone is not a benign process. A recent study evaluated the histological changes within the upper airway muscles in habitual snorers and nonsnoring control subjects.18 The study demonstrated changes within the upper airway muscle tissue of the snoring subjects in a fashion compatible with a neuropathy, such as that caused by trauma. This suggests that the trauma on the tissues of the airway from snoring alone may cause changes that increase the dysfunction of the upper airway muscles, leading to further airway collapse. Therefore, the presence of snoring is an indication for some degree of objective testing.

    Future Directions
    No clear guideline has been presented for dentists to follow when making decisions on ordering sleep testing. No one would question the need for full nocturnal polysomnography on patients with severe daytime sleepiness, or possible sleep apnea if the patient has a condition that has been shown to be worsened by sleep-related breathing disorders, i.e., heart disease or hypertension. The confounding situation is the patient with a complaint of only snoring and otherwise good health, with no daytime sleepiness. The decision of whether to test this group and the type of testing for this group has not been elaborated on within current practice parameters, other than stating that a sleep study is indicated in this group prior to laser-assisted surgery of the upper airway. Because apnea may be occurring in REM sleep and may go unrecognized by a sleeping bed partner, a sleep study may be indicated to exclude a sleep-related breathing disorder prior to embarking on any treatment of the upper airway. One approach to be considered is to use cardiorespiratory testing devices for a screening study in the seemingly healthy, snoring, patient prior to fitting a dental appliance. This would allow the identification of moderate to severe apneas, which if present would need proper follow-up attention with a repeat study with the appliance in place. It may be argued that as long as the patient does not have any other conditions that could be worsened by mild sleep apnea, there seems little justification for dentists to perform full nocturnal polysomnograph sleep studies on mild, seemingly healthy, snoring patients. This approach relies on the dentist to take an extensive history from the patient to determine symptoms of daytime sleepiness, or the presence of cardiovascular or cerebral vascular disease. Using specific questionnaires designed to quantify symptoms of daytime sleepiness19,20 may assist the dentist.

    Another suggested approach eliminates pretreatment sleep testing completely in patients with asymptomatic snoring, i.e., snoring without witnessed pauses in breathing, daytime sleepiness, or other cardiovascular disease.21 Neither this approach nor the approach utilizing the cardiorespiratory screening test have been adopted by a consensus panel as of this time, and it is still the standpoint of the American Sleep Disorders Association to perform full nocturnal polysomnograph studies when evaluating to exclude a diagnosis of a sleep-related breathing disorder.

    Author Jerald H. Simmons, MD. is the director of Sadler Clinic Sleep Disorders Center and Director of Comprehensive Sleep Medicine Associates, PA. (CSMA)


    1. Rechtschaffen A and Kales A, eds, Manual of Standardized Terminology: Techniques and Scoring System for Sleep Stages of Human Subjects. UCLA Brain Information Service/Brain Research Institute, Los Angeles, 1968.
    2. Aserinsky E and Kleitman N, Regularly occurring periods of eye motility and concomitant phenomena during sleep. Science 118:273-4, 1953.
    3. Hobson JA, McCarley RW, and Wyzinski PW, Sleep cycle oscillation: reciprocal discharge by two brain stem neuronal groups. Science 189:55-8, 1975.
    4. Kryger MH, Roth T, and Dement W, Principles and Practice of Sleep Medicine, 2nd ed. WB Saunders Co, Philadelphia, 1994.
    5. Indications for Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee, Practice parameters for the indications for polysomnography and related procedures. Sleep 20(6):406-422, 1997.
    6. Zulley J, Distribution of REM sleep in entrained 24-hour and free-running sleep-wake cycles. Sleep 2:377-89, 1980.
    7. The International Classification of Sleep Disorders, Diagnostic and coding manual. 1990 American Sleep Disorders Association. Allen Press.
    8. Guilleminault C, Stoohs R, et al, From obstructive sleep apnea syndrome to upper airway resistance syndrome: consistency of daytime sleepiness. Sleep 15:s13-6, 1992.
    9. Srollo P and Saunders M, Significance and treatment of nonapneic snoring. Sleep 16(5):403-8, 1993.
    10. Guilleminault C, Stoohs R, and Duncan S, Snoring: daytime sleepiness in regular heavy snores. Chest 99(1):40-8, 1991.
    11. Palomaki H, Partinen M, et al, Snoring, sleep apnea syndrome, and stroke. Neurology 42(supp 6):75-82, 1992.
    12. Koskenvuo M, Kaprio J, et al, Snoring as a risk factor for hypertension and angina pectoris. Lancet 1:893-5, 1985.
    13. Koskenvuo M, Kaprio J, et al, Snoring as a risk factor for ischaemic heart disease and stroke in men. Br Med J 294:16-9, 1987.
    14. Podzus T, Greenberg H, and Scharf SM, Influence of sleep state and sleep-disordered breathing on cardiovascular function. In, Saunders NA and Sullivan CE, eds, Sleep and Breathing, 2nd ed. Marcel Dekker, New York, 1994, pp 257-310.
    15. Hla KM, Young TB, et al, Sleep apnea and hypertension: a population-based study. Ann Intern Med 120:382-8, 1994.
    16. Fletcher EC, The relationship between systemic hypertension and obstructive sleep apnea: facts and theory. Am J Med 98:118-28, 1995.
    17. Sleep Disorders Atlas Task Force of the American Sleep Disorders Association, EEG arousals: scoring rules and examples. A preliminary report from the Sleep Disorders Atlas Task Force of the American Sleep Disorders Association. Sleep 15:174-84, 1992.
    18. Friberg D, Ansved T, et al, Histological indications of a progressive snorers disease in an upper airway muscle. Am J Repir Crit Care Med 157(2):586-93, 1998.
    19. Johns MW, A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale. Sleep 14:540-5, 1991.
    20. Johns MW, Reliability and factor analysis of the Epworth Sleepiness Scale. 15:376-81, 1992.
    21. Perez-Guerra F, How to shorten the sleep laboratory waiting list. ASDA News 5(1):15-6, 1998.