Introduction

Sleep studies are commonly used to diagnose sleep disorders such as sleep apnea. Sleep studies can be divided into 4 types (See Image. Sleep Apnea Testing Modalities). A polysomnogram (PSG) is considered a type 1 sleep study and is usually performed in a laboratory under direct observation (attended) or as a type 2 study if performed at home (unattended). Therefore, PSG is an integral component of many sleep evaluations.[1][2][3][2] 

Attended (type 1) PSGs are the gold standard for diagnosing sleep-related breathing disorders, including obstructive sleep apnea (OSA). Many other sleep disorders are diagnosed and managed based on PSG results. The study consists of a simultaneous recording of several physiologic parameters during sleep and wakefulness, including the electroencephalogram (EEG) to identify wake versus sleep and its stages.[1][4] This article focuses on types of commercially available and approved sleep testing: sleep center–based attended PSG, where the patient must stay overnight in a specialized sleep laboratory, and home sleep apnea testing (HSAT).[1] This article will also provide an overview of the processes for obtaining and interpreting attended PSG as part of the diagnosis and management of a wide range of sleep concerns.

Specimen Collection

Several physiologic parameters are recorded during a diagnostic PSG, each with one or more channels displayed electronically during interpretation. These data inform the diagnosis of a range of sleep disorders. A PSG includes the following signals:[1]

• Bilateral frontal, central, and occipital EEG
• Surface chin and lower extremity electromyogram (EMG)
• Left and right eye electrooculogram (EOGs)
• Electrocardiogram (ECG) lead II
• Audio and video recording for snoring, body position, and other abnormalities
• Nasal pressure transducer
• Oronasal thermal flow sensor
• Thoracic and abdominal respiratory effort monitoring, most commonly with respiratory inductive plethysmography (RIP) belts.
• Pulse oximeter

The EEG electrodes are set up according to the international 10-20 system.[5] The recommended electrode placements for an EEG during a PSG are right frontal/left mastoid (F4/M1), right central scalp/left mastoid (C4/M1), and right occipital/left mastoid (O2/M1). Backup electrodes should also be placed to display the left frontal scalp/right mastoid (F3/M2), left central scalp/right mastoid (C3/M2), and left occipital/right mastoid (O1/M2) if there is a malfunction with the electrodes used for the recommended derivations. Chin EMG measures submental muscle activity, which is essential for identifying rapid eye movement (REM) sleep. Another set of EMG electrodes records activity in the anterior tibialis to evaluate for periodic limb movements of sleep.[6] Left and right EOGs measure the change in the electrical field potential between the cornea (positive) and retina. The recommended EOG derivations are E1-M2 and E2-M2.

Electrode Placement

• E1: Positioned 1 cm above and lateral to the outer canthus of the left eye
• E2: Positioned 1 cm below and lateral to the outer canthus of the right eye
• M2: Reference electrode (typically placed on the right mastoid)

Electrooculography is used to identify the waking eye movements, slow rolling eye movements of drowsiness transitioning into stage N1, and the rapid eye movements of stage R (also referred to as REM when scoring PSGs). All electrode impedances should be below 5 KΩ as per American Academy of Sleep Medicine (AASM) requirements. Snoring and body position are monitored using audio and video recordings. Changes in pressure measured by a nasal pressure transducer reflect nasal airflow. Oronasal thermal flow is defined as the difference in temperature between the nose and mouth during inhalation and exhalation. Respiratory inductive plethysmography belts measure respiratory effort.[7][8][9] A continuous pulse oximeter helps evaluate OSA. 

Home sleep apnea testing offers a cost-effective, less burdensome alternative for patients, serving as a limited-channel recording method for diagnosing OSA. Various technologies exist to record and monitor respiratory events using respiratory flow–based, ECG-based, or peripheral arterial tonometry signals. Currently, new technologies like wireless patches are being explored, and initial reports are encouraging. The effectiveness of the patch-based type 2 PSG in evaluating sleep stages and respiratory parameters was reported to be similar to that of traditional PSG.[10]

Procedures

A polysomnogram should be performed during the patient's habitual sleep period, usually beginning in the evening. They are given questionnaires to quantify their subjective sleepiness, such as the Epworth Sleepiness Scale (ESS) or the Stanford Sleepiness Scale (SSS). A careful medication review is also performed. After completing these forms, the patient should be allowed to use the restroom before attaching the monitoring sensors. The sleep technologist then instructs the patient to await further instructions for calibrations and leaves the room.

The calibrations include equipment and physiologic calibration. The initial calibration of the equipment is performed by sending a known signal through all recording channels. The signal is then sent through individual channels and frequency filters so the signals can be adjusted based on the center's standard operating procedures. Physiologic calibration occurs after the monitoring mechanisms are connected to the patient, which includes a series of eye, jaw, and foot movements and changes in breathing. The technologist observes the output to assess its correlation with the patient's actions. (See Image. Sleep Polygraph, 30-Second Window).

After the calibrations are complete, the patient should be left in a cool, dark, and quiet room to promote sleep. During the study, the sleep technician must remain vigilant while monitoring the patient's PSG recordings and video feed for any physiologic abnormalities. Emergency procedures should be implemented and practiced regularly. The procedure ends the following morning, and patients must be sufficiently rested to drive if driving themselves. The patient must sleep for at least 2 hours during the PSG to be considered a valid study.

Home sleep apnea testing is increasingly recognized as a viable alternative to PSG for diagnosing OSA, particularly in resource-limited settings. Electrocardiogram-based HSAT uses heart rate variability and advanced computational algorithms [Front. Sleep. Role of Auutomated Detection of Respiratory-Related Heart Rate Changes in the Diagnosis of Sleep Disordered Breathing. https://www.frontiersin.org/journals/sleep/articles/10.3389/frsle.2023.1162652/full] and has shown promise in detecting apneic events, differentiating sleep stages, and predicting cardiovascular comorbidities.[11] In results from a study of adults with a mean age of 50 years, HSAT showed a strong correlation with PSG in terms of apnea-hypopnea index (Pearson r = 0.93) and lowest oxygen saturation (Pearson r = 0.99).[12] 

Another modality of sleep testing at home is the WatchPAT technology. The new version of the WatchPAT ONE® device measures peripheral arterial tone and multiple other channels, including heart rate, oximetry, actigraphy, and body position. Studies comparing the apnea-hypopnea index between peripheral arterial tone and PSG found high sensitivity (94% and 92% at apnea-hypopnea index thresholds of 5 and 15 events/h, respectively). The WatchPAT® One disposable device provides a valid approach to detecting sleep-disordered breathing with reduced logistical burden and infection risk, and it instantly and securely transfers data. While it may have limitations compared to PSG, preliminary data indicate high accuracy in identifying moderate to severe sleep-disordered breathing with proper remote setup.

While peripheral arterial tone does not directly measure sleep and breathing, it provides validated data on the severity of sleep-disordered breathing and on the type of disease (central versus obstructive) in the general population and in individuals with obstructive lung disease.[13][14] However, its validity in special populations, such as those with neurological disorders, such as spinal cord injury, or in adolescents with obesity, remains to be determined.[15] Peripheral arterial studies may overestimate the severity of sleep-disordered breathing; nevertheless, in individuals with a high pretest probability of sleep-disordered breathing, a negative peripheral arterial tone study should be followed by in-laboratory PSG.[16] Future developments, including the integration of physiological signals, improvements in wearable technology, and multicenter clinical trials, will advance HSAT's role in OSA diagnosis and management.

Indications

Indications for PSG in adults include the following:[1]

• Suspected sleep-related breathing disorders (SDB)
• Patients with neuromuscular disorders and sleep concerns
• Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) titration
• Evaluation of response to positive airway pressure (PAP), oral appliance, or positional therapy
• Evaluation before upper airway surgery for snoring or OSA
• Assessing response after surgery for OSA or oral appliance treatment
• Follow-up PSG if the response to OSA treatment is inadequate or symptoms are not adequately controlled despite adherence to appropriate therapy
• Patients receiving CPAP with at least a 10% change in body weight to verify continued need and optimize therapy settings after gaining weight
• Patients with congestive heart failure and symptoms of SBD or persistent symptoms after optimal medical management
• Diagnosis of narcolepsy (PSG followed by a multiple sleep latency test the next day)
• Diagnosis of nocturnal epilepsy
• Diagnosis of REM sleep behavior disorder 
• Diagnosis of periodic limb movement disorder when the patient has significant daytime fatigue or a bed partner reports witnessing limb movement
• Insomnia, if a comorbid sleep disorder is suspected, or after failure of adequate treatment [17]

PSG is not indicated for the following:[1]

• Patients adequately treated with CPAP with a good clinical response
• Parasomnias (excluding nocturnal seizures and REM sleep behavior disorder)
• Seizure disorders occurring only during the day
• Restless legs syndrome
• Insomnia with a low concern for a secondary cause significant enough to cause periodic limb movement disorder (OSA or periodic limb movements of sleep) [17]
• Circadian rhythm disorders
• Other common conditions, such as bruxism, nightmares, and sleep talking

PSG should be avoided if the underlying clinical condition is unstable or there is a recent history of facial trauma or a surgical procedure. Special accommodation is likely needed for patients with certain disabilities or spinal cord injury.[18] For patients with a high probability of SDB and associated comorbidities, cardiopulmonary comorbidities, or suspected obesity hypoventilation syndrome, in-laboratory PSG is indicated rather than HSAT. Home sleep apnea testing is an alternative to PSG for diagnosing OSA in adults with symptoms of moderate to severe OSA. The American Academy of Sleep Medicine advises that the use of HSAT should be based on the patient's history and clinical assessment, whether conducted face-to-face or via telemedicine. HSAT is not recommended for screening asymptomatic patients.[19] 

Potential Diagnosis

In the absence of PSG or HSAT, questionnaires and prediction algorithms should not be used to diagnose SDB in adults.[20] The utility of HSAT is limited to identifying the presence and severity of SDB in high-probability cases. However, treatment decisions should not rely solely on automatically scored HSAT data, as this may compromise patient care. The raw data must be reviewed by a board-certified sleep medicine clinician or a healthcare professional under their supervision.[19]

The likelihood of detecting OSA before testing is higher among older individuals, men, and those with higher body mass index. Furthermore, combining clinical assessment with HSAT improves diagnostic precision.[21][22][23] (See Image. Sleep Apnea Clinical Assessment). The identification of OSA typically involves decreased airflow while sleeping. (See Image. Sleep Polygraph, 120-Second Window). The diagnosis of SDB normally depends on the number of respiratory events (apneas and hypopneas) during sleep, referred to as the apnea-hypopnea index. The scoring of respiratory events is based on the AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications, Version 2.3 (AASM Scoring Manual). An apena-hypopnea index of 5 events/h or fewer is considered normal for adults. Mild OSA is 5 to 14 events/h, moderate is 15 to 30 events/h, and over 30 events/h is severe.[24]. Furthermore, the AASM guidelines for diagnostic sleep studies recommend that the diagnostic PSG include at least 2 hours of recording time and that at least 3 hours be available for CPAP titration.[20] In addition, an ideal diagnostic PSG would incorporate supine sleep during the REM phase.

Obstructive apneas  are characterized by a reduction in airflow of at least 90% for 10 seconds or longer, typically measured using the oronasal thermal flow channel, with persistent respiratory effort. This effort is assessed using respiratory inductive plethysmography belts or by measuring esophageal pressure. Central apneas are identified by a similar reduction in airflow for the same duration, as measured with the oronasal thermal flow channel, without respiratory effort on respiratory inductive plethysmography (See Image. Polysomnography Showing Central and Obstructive Sleep Apneas). Mixed apneas occur when there is a 90% reduction in airflow for 10 seconds or longer, with respiratory effort on respiratory inductive plethysmography during the latter half of the apnea (See Image. Polysomnography Showing Mixed Apnea). (See Image. Polysomnography Showing Central and Obstructive Sleep Apneas).

Obstructive hypopneas are partial reductions in airflow with continued respiratory activity. Scoring hypopneas requires a drop in the signal of at least 30% for 10 or more seconds (typically scored from the nasal pressure transducer channel) associated with a decrease in peripheral oxygen saturation of at least 3% from baseline or an EEG arousal.[25] Although the 3% drop in oxygen saturation is the AASM's recommended criterion, Medicare requires a 4% drop to be considered an obstructive hypopnea, which the AASM also regards as an acceptable alternative for patients. These alternative criteria do not account for arousals when scoring obstructive hypopneas. The AASM also recommends scoring obstructive hypopneas when one or more of the following conditions are present: inspiratory flow limitation, snoring, or paradoxical effort on respiratory inductive plethysmography not present before the hypopnea (See Image. Polysomnography Showing Obstructive Hypopnea).

Recording signals such as EEG, EOG, and EMG from the chin and extremity muscles is essential for identifying supine stage R (REM) sleep. For most patients, obstructive apneas and obstructive hypopneas are most likely to occur during supine REM. Once identified, obstructive apneas and obstructive hypopneas are combined and averaged throughout sleep to give the apnea-hypopnea index. The acceptable duration of recording is debatable. The AASM task force for diagnostic sleep studies advised that diagnosing OSA requires obtaining at least 4 hours of high-quality data from HSAT recordings during the typical sleep period.

Normal and Critical Findings

Sleep stages are normal findings on a PSG and are crucial to interpretation. Sleep stage scoring is based on EEG, EOG, and submental EMG criteria. Sleep stage scoring was initially detailed by Rechtschaffen and Kales (R&K) but has since been replaced by the AASM scoring manual.[26] The AASM manual is mostly consistent with the original sleep-scoring manual by Rechtschaffen and Kales and is regularly updated.

The AASM scoring manual uses standardized nomenclature for wake and sleep: stage W for wake, stages N1, N2, and N3 for non–rapid eye movement (NREM) stages of sleep, and stage R for REM sleep. Stage N3 replaces stages 3 and 4 in the new classification. Sleep is staged in 30-second sections, known as epochs. Traditionally, PSGs were recorded on paper, and an epoch of sleep was a standardized length of paper given a standard recording time. Today, digital PSG has virtually replaced paper recording, and sleep is scored in sequential epochs that can be manipulated on a screen. If more than one sleep stage occurs in an epoch, the epoch is generally scored based on the sleep stage occupying the majority of time.[27]

To identify the sleep stage in an epoch, the EEG plays a central role. The EEG demonstrates several recognizable wave patterns from wake through the stages of sleep. These wave patterns are described in terms of frequency, amplitude, and morphology. Frequencies include:

• Alpha: 8 to 13 Hz
• Beta: > 13 Hz
• Theta: 4 to 7.99 Hz
• Delta: < 4 Hz

Amplitude is a measure of EEG wave voltage and varies across sleep stages. The overall morphology of the waves can also provide insight into the sleep stage. For example, K-complexes and sleep spindles occur in N2 sleep. K-complexes are waves with a sharp initial negative deflection, followed by a positive deflection, typically with maximal amplitude in the frontal derivations. Sleep spindles are sinusoidal 11- to 16-Hz waves lasting at least 0.5 seconds, with their maximal amplitude generally in the central derivations. Sawtooth waves, which are 2- to 6-Hz waves with a serrated appearance with maximal amplitude in the central leads, may be seen during or before stage R.

Stage W scoring on a PSG depends on whether the patient's eyes are open or closed. With eyes open, the EEG demonstrates low-amplitude, mixed-frequency waves, predominantly in the 4- to 7-Hz range. With eyes closed, the EEG demonstrates an alpha (posterior dominant) rhythm in most patients. The alpha rhythm is generally most prominent in the occipital leads. The EOG shows blinking, reading eye movements, or irregular, conjugate, sharply peaked, rapid eye movements. Chin EMG shows increased muscle tone. Stage W is scored when greater than 50% of an epoch contains the alpha frequencies.[27]

Stage N1 is the transition from wakefulness to sleep. Low-amplitude, mixed-frequency theta waves predominate on the EEG. The EOG shows slow, rolling eye movements. Chin EMG tone is lower than stage W but higher than stage R. An epoch with over 50% of these characteristics is scored as stage N1 in the absence of criteria for another sleep stage.[27]

Stage N2 is characteriized by K-complexes and sleep spindles occurring in a background of low-amplitude, mixed-frequency EEG activity. There are usually no eye movements on EOG. EMG tone is generally lower than during wakefulness. Stage N2 is scored when a K-complex (without an associated arousal) or sleep spindle occurs in the first half of the current epoch or the last half of the previous epoch, with less than 20% slow-wave activity. Stage N2 continues until a transition into stage N3, stage R, arousal, a significant body movement followed by slow eye movements, or an awakening occurs.[27]

Stage N3 is the deepest sleep stage, characterized by high-amplitude, slow waves. The delta frequency predominates between 0.5 and 2 Hz, with amplitudes exceeding 75 µV. There are generally no eye movements on EOG, and EMG is variable but often lower than N2. This stage is scored when greater than 20% of an epoch (6 seconds) meets these frequency and amplitude criteria.[27]

Stage R represents REM sleep. As the name implies, the EOG demonstrates rapid eye movements, similar to those seen during wakefulness. The EEG is low-amplitude, mixed frequency, without K-complexes or sleep spindles. The chin EMG tone falls below previous amplitude levels in the recording. Sawtooth waves, although often associated with stage R, are not always present. Stage R is scored when the combination of the 3 EOG, EMG, and EEG criteria is satisfied.[27]

Interfering Factors

Despite being the gold standard for diagnosing multiple sleep disorders, PSG has several limitations. For example, the first-night effect, attributed to sleeping in an unfamiliar environment, may lead to a missed OSA diagnosis because of decreased REM sleep.[28] Medication changes before a PSG may also interfere with the quality and quantity of sleep. Additionally, some sleep disorders, such as nocturnal seizures and REM sleep behavior disorder, may occur too infrequently to be captured during a single night study reliably. Equipment issues can contribute to PSG inaccuracies, given the many physiologic recordings and the potential for electrode and instrument cable malfunctions. 

In addition to diagnostic limitations, systemic interfering factors can limit access to PSG. Performing a PSG requires an adequate sleep period, highly trained technicians to administer the study, and sleep clinicians interpreting the survey, resulting in a high cost. As a result, payers usually require prior authorizations, creating barriers to obtaining a PSG even when indicated. The PSG data are also not portable in many cases, requiring unique software that is not readily exportable.

Complications

The most common complication is skin irritation surrounding electrode attachment sites. Other complications are rare in PSG. However, because of the length of the study and the potential to evaluate individuals with multiple other medical comorbidities, sleep technicians must remain watchful for physiologic derangements that require immediate medical assistance during a PSG.

Patient Safety and Education

When a PSG is necessary, the patient should be educated about the procedures and potential outcomes of the study. Electrodes, other monitoring devices, and their uses should be clearly explained to the patient, and the reasons for the monitoring in their specific case should be provided. The patient's usual sleep schedule should be identified to optimize the timing of the sleep study in relation to laboratory procedures and availability. Based on the study's findings, patients may need positive airway pressure if indicated. Positive airway pressure may be uncomfortable, and setting expectations can often lead to a more successful titration.

In general, patients should take medications as prescribed on the day and night of the PSG, including sleep aids. However, medication reconciliation must be performed and documented before a sleep study to avoid unintended effects on sleep, especially if benzodiazepines or opioids are among the medications, because these medications may exacerbate sleep-disordered breathing.[29][30] Alcohol use before a sleep study can have a similar effect.[30] Patients being evaluated for narcolepsy should also be carefully screened for medications before PSG and multiple sleep latency testing. Antidepressants can suppress REM sleep and should be documented to facilitate appropriate PSG interpretation.

Clinical Significance

Sleep dysfunction significantly impacts patients both physically and psychologically when untreated.[31] Polysomnography plays a crucial role in the evaluation and treatment of many sleep disorders, which can reduce morbidity and mortality.[32][33][34][35] However, polysomnography is technically complex and time-consuming because of its many monitoring systems, which also contribute to its high clinical utility in diagnosing and managing a wide range of sleep disorders. With proper training, execution, interpretation, and patient preparation, a PSG is a powerful tool for analyzing and managing sleep disorders. Furthermore, incorporating more physiological data is likely to enhance the sensitivity for diagnosing OSA.[36]

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Disclosure: Abdulghani Sankari declares no relevant financial relationships with ineligible companies.

Disclosure: Jennifer Slowik declares no relevant financial relationships with ineligible companies.