In 1875, Richard Caton (4), an English neurophysiologist, first recorded electrical activities from rabbit and monkey brains. It was, however, Hans Berger (1), an Austrian psychiatrist, who in 1924 first obtained electrical activities from the scalp surface of a 17-year-old young man with a skull defect and published his findings in 1929. Although sleep was known since antiquity, brain activities in sleep could not have been recorded before the discovery of EEG. It was in 1937 that Loomis and his colleagues classified sleep into five stages (A-E) based on the EEG activities during the deepening stages of sleep (5). It is interesting to note that Kohlschutter (6,7), a 19th century German physiologist, thought that sleep was deepest in the first few hours and became lighter as time went on, and he also described the varying arousal thresholds throughout the night. The REMs of sleep were not known in those days. In 1953, Aserinsky and Kleitman (2) obtained characteristic REMs during sleep using surface electrodes over the eye lids. Over the 4-year period, Loomis and his colleagues (5) published 12 papers, describing the oscillating nature of EEG along with five distinct stages of sleep as well as arousals manifested by increased body movements and respiratory effort. In 1957, Dement and Kleitman (8) described sleep evolving through non-rapid eye movement (NREM) and REM sleep states in a cyclic manner throughout the night. All the components of REM sleep, however, have not been described by them until Jouvet and Michel (9) in 1959 observed markedly decreased muscle tone during REM sleep in cats. In 1961, Berger (10) recorded markedly decreased muscle tone from extrinsic laryngeal muscles during human REM sleep. In order to standardize the scoring of different stages of sleep, an ad hoc committee led by Rechtschaffen and Kales (R-K) (11) in 1968 produced the now-famous sleep scoring technical manual (The R-K Scoring Technique). This remained the “gold standard” until the AASM published the AASM Manual for the Scoring of Sleep and Associated Events (12), which modified the R and K technique and extended the scoring rules. The R and K sleep scoring manual (11) was devised only for normal sleeping adults, but later infant sleep scoring manual was developed. R and K sleep scoring technique is based on three physiologic characteristics: EEG, electro-oculography (EOG), and electromyography (EMG). PSG, however, includes more than just sleep staging, and other physiologic characteristics such as respiration, limb muscle activity, blood oxygen saturation, electrocardiogram (ECG), body position, snoring, and other special recordings have been incorporated, which are described later in this chapter. Since the discovery of REM sleep, dream was thought to be associated with REM sleep during 80% of the time. In 1868 Griesinger (13) suggested that dreaming was associated with eye movements and in 1895, Freud (14) indicated that dreaming was associated with relaxation of the major muscles of the body. Amazingly, centuries ago (ca. 1000 BC), Upanishads (15), the ancient Indian text of Hindu religion, sought to divide human existence into four states: the waking, the dreaming, the deep dreamless sleep, and the superconscious (“the very self”). This is reminiscent of modern classification of three states of existence.

The control of sleep is quite complex. Whereas for the most part during the whole sleep period we are in an unconscious state, changes occur that are physiologically quite distinct. During slow wave sleep, the cortical neurons fire in relative synchrony, producing what is described as slow wave sleep, so named after the polygraphic pattern of this brain activity. During REM sleep, the eyes show phasic, rapid conjugate movements, whereas at the same time skeletal muscle tone is at its lowest levels. Brain activity during REM sleep is rapid and desynchronous, almost like waking, which is why it is also referred to as “paradoxical sleep.”

There are two major branches to the ascending arousal or reticular activating system (ARAS) (16). One is an ascending pathway from pedunculopontine (PPT) and laterodorsal tegmental (LDT) nuclei to the reticular nucleus and thalamic relay nuclei in the thalamus. These thalamic relay neurons transmit signals to the cortex. Neurons in the PPT and LDT fire most rapidly during REM and wakefulness, and are at their most inactive state during NREM.

The second branch of the ARAS comes from locus coeruleus (LC), dorsal and median raphe nuclei, periaqueductal gray matter, and tuberomammillary neurons. Cortical input goes through lateral hypothalamic neurons and basal forebrain neurons. The neuron groups in the two branches of the ARAS are shown in Figure 41.1 along with their respective neurotransmitters (17).

The Hypocretin (Orexin) peptidergic system (18) located in the lateral hypothalamic and perifornical regions with its widespread ascending and descending projections is thought to play an important role in the control of arousal and wakefulness. A reduction of activities of the hypocretin projections to the LC, midline raphe, mesopontine, and posterior hypothalamic and tuberomedullary regions will cause sleepiness.

A vast number of physiologic changes take place during sleep in humans, affecting almost every system in the body (Table 41.1) (25). It is important to have a basic knowledge about these changes during sleep and how they affect various sleep disorders. These changes may be documented in the Polysomnography. A case in point is obstructive sleep apnea syndrome (OSAS) causing dramatic changes in the respiratory control of the upper airway muscles during sleep, directing our attention to a very important pathophysiologic mechanism and the therapeutic intervention for this disorder. These physiologic changes are most commonly noted in the respiratory, cardiovascular, gastrointestinal, and endocrine systems. Respiration is controlled by the automatic or metabolic and behavioral systems complemented by the third system known as the arousal system or the system for wakefulness stimulus. These respiratory systems receive inputs from various peripheral and central neural structures to maintain acid-base regulation and respiratory homeostasis. The location of the respiratory neurons makes them easily vulnerable to a variety of neurologic disorders, particularly those involving the brainstem. Some conditions may affect control of breathing only during sleep, causing undesirable, often catastrophic, results including cardiorespiratory failure or even sudden death. The two control systems (metabolic and voluntary) are active during wakefulness, but during NREM sleep, the voluntary system is inactive and respiration is entirely dependent upon the metabolic controller. The behavioral mechanism is probably responsible for controlling breathing, at least in part during REM sleep. Tidal volume and alveolar ventilation decrease during sleep. Arterial oxygen tension is slightly decreased and arterial carbon dioxide tension is increased during both NREM and REM sleep. Hypoxic ventilatory response is impaired in NREM sleep in adult men but not in women. Hypoxic ventilatory response during REM sleep is significantly decreased in both sexes. Hypercapnic ventilatory response is also decreased during NREM and further decreased during REM sleep. Thus, ventilation is unstable during sleep and few periods of apneas may occur particularly at sleep onset and during REM sleep in normal individuals. Respiratory homeostasis is thus relatively unprotected during sleep, making those individuals with intrinsic respiratory disease, such as chronic obstructive pulmonary disease (COPD) or bronchial asthma, highly vulnerable for respiratory failure during sleep.

As a result of increased parasympathetic and decreased sympathetic activity during sleep, heart rate, blood pressure, cardiac output, and peripheral vascular resistance decrease during NREM sleep and decrease still further during REM sleep. In REM sleep, however, there is an intermittent activation of the sympathetic nervous system accounting for rapid fluctuations in blood pressure and heart rate. Cardiac output falls progressively during sleep and the greatest decrement occurs during the last sleep cycle, particularly during the last REM sleep cycle early in the morning. This may explain why normal individuals and patients with cardiopulmonary disease are most likely to die during the early morning hours. Cerebral blood flow and cerebral metabolic rates for glucose and oxygen decrease during NREM sleep but increase to that of the waking values during REM sleep. Because of these hemodynamic and sympathetic changes during REM sleep during the last third of the sleep cycle in the early hours of the morning, there could be increased platelet aggregability, plaque rupture, and coronary arterial spasms possibly triggering thrombotic events causing myocardial infarction, ventricular arrhythmias, or even sudden cardiac death. These circadian variations in cardiovascular and cerebrovascular events with the highest rates of events occurring during the early morning hours have been documented by meta-analysis of epidemiologic studies.

There are profound changes in endocrine secretions during sleep. There is a pulsatile increase of growth hormone during NREM sleep in the first third of the normal sleep period. Prolactin secretion also rises 30 to 90 minutes after sleep onset. Cortisol secretion is inhibited by sleep, whereas thyroid-stimulating hormone reaches a peak in the evening and then decreases throughout the night. Testosterone levels in men increase during sleep, rising from low levels at 8 PM to peak levels at 8 AM, but there is no clear relationship noted between levels of gonadotrophic hormones and sleep-wake cycle in children or adults. Melatonin, the hormone of darkness released by the pineal gland, reaches its highest secretion level between 3 AM and 5 AM and then decreases to low levels during the day. Thermoregulation is maintained during NREM sleep, but it is nonexistent in REM sleep. Body temperature begins to fall at sleep onset and reaches its lowest point during the third sleep cycle.

The term “sleep architecture” refers to the pattern of sleep stages that cycle through the night in what is referred to as the REM-NREM cycle. During development, there are changes that occur in the general pattern of sleep stages, but the adult shows a pattern of stages N1, N2, and N3 followed by REM sleep, and the periodicity of this REM-NREM cycle throughout the night is generally 90 to 120 minutes in duration. The first REM period of the night is very often brief and may even be missed in young healthy sleepers.

During infancy, the sleep-wake cycle is approximately 50% dominated by REM sleep, and the sleep pattern involves frequent napping through the day. As the infant matures, there is a consolidation of sleep into the night period. During infancy, the mother’s melatonin rhythm is conveyed to the infant through breast milk, helping to consolidate the sleep period into the nocturnal dark phase. The last sleep to be given up during the day period is generally the afternoon nap.

In 2007, the AASM (12) published a new manual for the scoring of sleep and associated events, almost 40 years after the first consensus on the technical standards for the field was published by Rechtschaffen and Kales in 1968 (11). The AASM has a Web site (http://www.aasmnet.org/) with links to resources for sleep medicine clinicians, scientists, technical personnel, and laboratory managers, and to several position papers.

The hiring of technologists who are mature and competent and highly motivated is a critical step in the operations of a sleep laboratory. A feeling of trust between the patient and technologist is very important for sleeping in an unusual environment because electrodes and other devices attached to the body can put the patient in a somewhat uneasy state. Coupled with the fact that they are in the laboratory for reasons of disturbed sleep and/or wakefulness, and that continuous positive pressure may be tested, even on their first night in the laboratory, it is very important that they have a trusting professional interaction with the technologist.

In addition to professionalism, maturity, and excellent bedside manner, the technologist needs to be able to function well at night, and, as much as possible, maintain a consistent shift. Frequent rotations from night to day lead to stress and result in unnecessary sleep loss and misalignment of biologic rhythms. This can in turn lead to impaired performance and mood dysregulation.

Technologists chosen for performing diagnostic and treatment initiation sleep recordings frequently have full EEG technician training and/or training as a respiratory therapist. In addition, they require well-supervised training in specialized polygraphic recording methods and in visual sleep staging, including identification and classification of arousals, leg movements, and respiratory disturbance. Technologists are responsible for the maintenance of equipment and for the identification and fixing of technical problems at night during a recording if they should arise. Although most recordings are now performed with commercially available digital systems, the technologists still need to quickly and correctly identify problems and swap out parts as necessary. Therefore, they need to be able to make sure that adequate supplies and back up equipment are available. The “American Association of Sleep Technologists” has developed standards of training, practice, and certification for registration of technologists in North America (http://www.aastweb.org/).

A report for the technologist including the patient’s presenting symptoms and reason for the referral needs to be provided. The technologist should also have access to list of medications and other information pertinent to the care of the patient through the night in the laboratory. It is most common for patients to be studied outside of a hospital setting, but even within the hospital setting, it is important for the technologist to have explicit instructions for when and whom to call with respect to critical levels of oximetry, abnormal ECG, or other medical needs of the patient. As in any hospital ward setting, it is not desirable for a technologist to work alone, without any back up personnel immediately available, for safety reasons.

The equipment and technologist are usually housed in a room separate from that of the sleeping subject. Rather than an institutional-like bedroom, it is preferable for the patient to have an environment that is as home-like as possible, with a comfortable
mattress, a closet, and night stand. The sleeping room should be quiet and sound attenuated so that noises from outside the sleep laboratory and technologist’s area do not disturb the sleeping patient. An intercommunication system for contact with the patient is essential. Toilet facilities should preferably be attached to the bedroom and a shower should also be readily available.

Patients are generally asked to report to the laboratory facility 1 to 3 hours before their normal bedtimes. They are shown their room and the facility around to let them know they are appropriate. The technician asks them to change into their bed clothes and then they begin to attach the electrodes and recording devices. The technologist turns lights out after he/she conducts a test of the equipment and performs biologic calibrations. Biologic calibrations enable the technologist to demonstrate to the individual, who subsequently will review the recording, the normal waking eye movement pattern, and pattern of gritting teeth, breathing deeply, coughing, and pointing and flexing the toes and feet. All of these need to be documented by the technologist at the outset of the recording, and when lights are turned off for the night, the technologist must document the time, in the recording.

The measurement of respiration during sleep is critical to the diagnosis of sleep disorders and includes chest and abdominal excursion, most often using inductance plethysmography or sometimes strain gauges, and also a means of assessing nasal airflow. Syndrome definitions and measurement techniques are described for sleep-disordered breathing in an AASM task force report (33), and a more recent guidelines to the classification and scoring of respiratory events was published in the AASM Manual for the Scoring of Sleep and Associated Events in 2007 (12).

Careful monitoring of both upper airway airflow and thoracoabdominal movement in the respiratory tracings is used to categorize central, mixed, and obstructive sleep apnea (OSA), which is further discussed later. In addition, the monitoring and
quantification of blood oxygen levels are necessary and accomplished using pulse oximetry. Endoesophageal (intrathoracic) pressure recording is also sometimes used in the detection of partial obstructions or upper airway resistance that can exist without actual apneas or hypopneas. The nasal pressure transducer (NPT) is recommended for the measurement of subtle reductions in airflow and can also be used in the identification of absent airflow, characteristic of apnea.

Capnography refers to the monitoring of the concentration of carbon dioxide (CO₂) in the respiratory gases and is measured in the breath at the end of complete expiration (end tidal). A CO₂ analyzer is sometimes used to document CO₂ retention in sleep-related respiratory disorders, especially COPD and hypoventilation syndromes.

End tidal CO₂ refers to the measurement of the CO₂ in the air exhaled from the lungs, and the normal range is 4% to 6% (equivalent to 35 to 45 mm Hg).

This technique is rarely used in diagnostic testing because it involves the placement of an airtight mask on the face and uses a pressure transducer system to measure flow rate, tidal volume, and other respiratory variables. This method is adopted frequently in the sleep testing laboratory during CPAP pressure titration in order to monitor adequacy of pressure and flow (see Nasal Pressure heading above).

Long electrode leads are sometimes applied on the lower back intercostal muscles to aid in the detection of effort during breathing and the placement is sensitive to muscle activity during coughing.

In addition to the NPT method mentioned earlier in this chapter, both piezo sensors (encased in a rubber disk attached to the throat and plugged into the headbox) and microphones are used to monitor snoring. Snoring is associated with reduced upper airway diameter, and bursts of loud guttural inspiratory snorting are signs of OSA.

Body position is the useful information to have when interpreting a pattern of respiratory disturbance and can be obtained visually through infrared camera monitoring and/or with the aid of a position sensor. Such sensors are available and can be attached to respiratory bands with accurate output of information including prone, supine, right side, and left side.

Table 41.2 lists appropriate filter settings for recording various physiologic characteristics in the PSG.

In 1968, the publication of the sleep scoring atlas by Rechtschaffen and Kales (11) represented the consensus agreement between sleep researchers of the time to the scoring of sleep stages. Remarkably, this document remains the dominant force in sleep scoring and analysis. With the recent publication of the AASM Manual for the Scoring of Sleep and Associated Events, the standardization of sleep and event scoring has reached a new level of consensus (12). The scoring of sleep in this recent document varies only limitedly from that published in 1968 (11).

The nomenclature of sleep stages has changed with the recent AASM scoring manual with NREM stage 1 now called stage N1, and NREM stage 2 is now stage N2. What had previously been NREM stages 3 and 4 (or slow wave sleep) is now unified into a single stage N3. Stage REM is now labeled as stage R.

A sleep study is scored in 30-second epochs with each stage labeled as stage W (or wakefulness), stage N1, stage N2, stage N3, or stage R. If two or more stages coexist in an epoch, the epoch is labeled as the stage that represents the greatest portion of the epoch. Stage W represents the waking state ranging from full alertness through early drowsiness. Stage W is scored when more than 50% of the epoch demonstrates alpha frequency activity over the occipital region (Fig. 41.3). Stage W is scored in the absence of alpha activity (which occurs in 10% to 20% of individuals) if eye blinks, reading eye movements, or irregular conjugate REMs are identified with accompanying normal or elevated chin muscle tone. The chin EMG during stage W is variable but is usually higher than that seen during sleep stages.

Stage N1 represents late drowsiness and light sleep. It is scored when greater than 50% of an epoch shows alpha attenuation and is replaced by low amplitude, mixed frequency EEG activity (Fig. 41.4). K-complexes and sleep spindles are absent by definition. If an individual does not generate alpha activity, stage N1 is scored when over 50% of the epoch demonstrates theta range slowing (4 to 7 Hz), vertex sharp waves, or slow eye movements. In individuals who do generate alpha activity, slow eye movements are frequently seen before the disappearance of alpha activity, so individuals who do not generate alpha activity may have stage N1 scored slightly earlier than those who do generate alpha activity. During stage N1, chin EMG is variable but usually lower than that seen in stage W.

Stage N2 represents the predominant sleep stage during an overnight recording and is scored when there is the appearance of a K complex or sleep spindle (Fig. 41.5). In sleep medicine, a K complex is defined as a biphasic negative sharp wave maximum at the vertex or frontal regions that lasts greater than 0.5 second. Sleep spindles are 11 to 16 Hz sinusoidal activity lasting at least 0.5 second seen maximally in the central head region. Less than 20% of an epoch of stage N2 can be delta activity (<2 Hz, >75 µV in amplitude). Stage N2 is scored from the first epoch of stage N2 until a clear epoch of stage W or another stage of sleep is identified. Although eye movements are usually absent in stage N2, slow eye movements can sometimes be seen. Chin or axial EMG is variable but usually lower than stage W.

Stage N3 (which encompasses both former stages 3 and 4 of R and K criteria (11)) is the deepest stage of sleep and is

associated with increasing delta activity. Stage N3 is scored when 20% or greater of an epoch is delta activity (Fig. 41.6). For the purposes of sleep scoring, delta activity is defined as activity of 0.5 to 2 Hz that is at least 75 µV in amplitude when measured over the frontal or central regions. Sleep spindles may persist into stage N3, but eye movements are usually absent. Axial EMG is usually lower than stage N2 and may approach that seen in stage R.

Stage R (formerly stage REM) requires three components for it to be scored: low-amplitude mixed frequency EEG, low chin EMG, and the presence of REMs (Fig. 41.7A,B). Phasic EMG activity may occur, but tonic EMG activity must be at a level that is as low as, or lower, than that occurring at any other time during the study. Sleep spindles and K-complexes are absent. Series of 2 to 5 Hz vertex negative “sawtooth” waves occur, particularly just before phasic REM activity.

Movement time (or stage M as described by Rechtschaffen and Kales (11)) is no longer scored. During major body movements that obscure greater than 50% of an epoch, the epoch is scored as stage W if alpha activity is present at any time in the epoch. If no alpha activity is identified, but an epoch of stage W precedes or follows the epoch with a major body movement, then the epoch is scored as stage W. If neither of these requirements can be met, the movement is scored the same as the epoch that follows it.

Normal sleep has a clearly defined architecture that occurs each night. Hypnograms are a graphic display of the ultradian cycle within a night’s sleep (34). Sleep stage is depicted in the vertical axis with the hours of sleep on the horizontal axis (Fig. 41.8). Sleep onset begins with a transition to stage N1 sleep followed quickly by stage N2. Stage N3 (formerly NREM stage 3 or slow-wave sleep) comes next and is particularly sustained in this first sleep cycle in children and young adults. Sleep then briefly lightens to stage N2 and transitions into stage R for the first time, usually about 90 minutes after sleep onset. This completes the first sleep cycle, a pattern that repeats itself three to five times during the typical night’s sleep. With each ensuing 90 minute sleep cycle, there is decreasing amounts of stage N3 sleep and an increasing amount of stage R sleep. Predictable changes are noted in sleep architecture with aging and are illustrated by the histograms in Figure 41.8. Beginning in middle age, stage 3 sleep lessens and more wakefulness after sleep onset (WASO) is noted. The number of arousals and awakening continues to increase with aging, becoming particularly notable in the elderly (35,36).

The original scoring guidelines of Rechtschaffen and Kales (11) focused primarily on the scoring of the stages of sleep (as discussed above). The R and K criteria defined that the appearance of 30 seconds or more of waking background (which resulted in the epoch being labeled as wake) would be labeled an awakening. The R and K manual made reference to movement arousals, but no other mention of brief EEG frequency changes was made. There was little standardization to the scoring of arousals before the publication of the position paper by the American Sleep Disorders Association (ASDA) task force in 1992 (37). This consensus paper carefully defined rules for scoring an arousal. In the recent AASM scoring manual (12), these rules were distilled to a single rule.

Score arousal during sleep stages N1, N2, N3, or R if there is an abrupt shift of EEG frequency to alpha, theta, or frequencies greater than 16 Hz (but not spindles) that lasts at least 3 seconds, with at least 10 seconds of stable sleep preceding the change in EEG frequency. Scoring arousals during REM requires a concurrent increase in submental EMG lasting at least 1 second (Figs. 41.9 and 41.10).

The use of the 3-second duration of EEG change is not based on any judgment of physiologic impact, rather it is an arbitrary value chosen by the task force partly due to increased interobsever reproducibility of arousal scoring (as compared to shorter duration events). The requirement for an accompanying EMG change in stage R is due to the routine appearance of faster EEG frequencies during normal sustained stage R sleep.

The cyclic alternating pattern or CAP was first described by Terzano and colleagues in 1985 (46). CAP has been proposed as a tool for the comprehensive analysis of sleep microstructure in both normal and pathologic conditions. Traditional sleep scoring using the criteria of Rechtschaffen and Kales (11) has been the

gold standard for looking at sleep macrostructure. CAP presents another way of looking at NREM sleep within those sleep stages.

NREM sleep has been recognized to have high amplitude EEG bursts such as K-complexes or delta bursts. These are often seen as an arousal response to external stimuli but also occur when sleep disturbance was not evident. An alternative view to this arousal process is that these phenomena are associated with sleep instability (due to an internal or external challenge to the sleep process) and that this type of slow wave activity marks the brain’s attempt to preserve or sustain the sleep state. If sleep becomes too unstable, the preservation attempt fails and the high-amplitude activity is accompanied by a more complete EEG arousal. It is proposed that the addition of a periodicity dimension to the concept of sleep stability and arousal will provide a valuable perspective on sleep and its relationship to underlying physiologic and pathophysiologic mechanisms. CAP represents a slow oscillation of EEG activity that manifests in the appearance of EEG arousal patterns with a periodicity of 20 to 40 seconds.

CAP is represented by three characteristics:

A CAP sequence is composed of repetitive CAP cycles, with each cycle composed of a phase A and a phase B. Each phase of the CAP is 2 to 60 seconds in duration. If there is no phase A activity for >60 seconds, then that portion of NREM sleep is scored an non-CAP. Figure 41.14 illustrates an example of the CAP in stage 2 sleep. Figure 41.15 illustrates a brief period of CAP surrounded by non-CAP sleep on either side. Phase A can take on three patterns: A1 shows primarily slow (<1 Hz) delta activity with a small degree of autonomic activation; A3 demonstrates an increase in fast rhythms with strong autonomic activation (an EEG arousal as per ASDA rules) (37); A2 represents a middle ground between the A1 and A3 subtypes (Fig. 41.16). A summary paper outlining the rules for scoring CAP and including an atlas to illustrate those rules was published by Terzano and colleagues in 2001 (47).

In several studies, the CAP A-phase is identified as the “gate” or “amplifier” that allows the appearance of pathologic events such as PLMS, bruxism, sleepwalking, and sleep-disordered breathing to occur. The majority of nocturnal partial seizures presenting during NREM sleep also occur predominantly in CAP in association with phase A (in particular in association with K-complexes and delta bursts) (48). At this point, the clinical significance of CAP remains unclear but further research is warranted.

The indications for PSG have been summarized by the published practice parameters of the AASM (49,50). The dominant indication for PSG is for the evaluation of sleep-related breathing disorders. The increasing awareness of sleep apnea and its possible impact on long-term cardiovascular health has lead to a marked increase in evaluation of sleep-disordered breathing. While the obese individual who presents with snoring, witnessed apneas, and excessive daytime sleepiness (EDS) represents the obvious candidate for PSG evaluation, there are many others who likely need PSG evaluation. Symptoms of concern for possible sleep apnea include daytime sleepiness, loud snoring, witnessed apneas, and unrefreshing sleep. Additional medical conditions that warrant exploring a possible role of OSA include intractable hypertension, new-onset atrial fibrillation (particularly with onset in sleep), intractable congestive heart failure, and stroke. Once the diagnosis of sleep apnea has been documented, patients usually return for repeat study for CPAP titration. The goal is to document the minimum CPAP pressure that eliminates apnea, hypopneas, and arousals with particular attention to stage R sleep and supine sleep. It is recommended that patients undergoing upper airway surgery to treat snoring or apnea have a study to document apnea severity and ensure appropriate choice of therapy and perioperative management. Similarly, after upper airway surgery to treat apnea, a follow-up PSG is warranted to document the residual degree of sleep apnea and whether additional therapeutic efforts are warranted.