Sleep Medicine for the Otolaryngologist

Sleep Medicine for the Otolaryngologist

Pell Ann Wardrop

Kathleen L. Yaremchuk

Otolaryngologists are frequently the portal for diagnosis and treatment of sleep disorders for patients with snoring or other airway complaints. Although sleep apnea is the most common sleep disorder encountered in an otolaryngology practice, most patients have a combination of several sleep disorders contributing to their symptomatology. Sleep affects every aspect of life from the feeling of general well-being to insulin metabolism, cardiovascular health, and cognitive functioning. Because of this gateway role, an awareness and expertise in the diagnosis and management of all sleep disorders are necessary for otolaryngologists.


The average adult needs 8.25 hours of sleep to feel rested. Normal sleep is divided into non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. NREM sleep accounts for 75% to 80% of sleep time in normal sleep. NREM sleep is further divided into progressively deeper stages of sleep: stage N1, stage N2, and stage N3 (deep or delta-wave sleep) (Table 135.1). Each of these four stages of sleep has identifying patterns on electroencepha-lography (EEG) tracings. Sleep is entered through NREM sleep, and the normal sleep cycle is generally approximately 90 minutes in length with a period of REM sleep. Delta- or slow-wave sleep, stage N3, usually dominates the first third of the night’s sleep, while REM sleep dominates the last third (Fig. 135.1). After age 55, stage N3 or slowwave sleep decreases, and wake after sleep onset (WASO), arousals, and awakenings increase (Fig. 135.2).


The International Classification of Sleep Disorders (ICSD-2) lists more than 80 specific sleep disorder diagnoses within eight major categories (Table 135.2) (1). The list demonstrates the complexity involved in making an accurate diagnosis. Review of the differential diagnosis and evaluation of the sleepy patient serve to highlight many of the common sleep disorders encountered in an otolaryngologic practice. Fatigue or excessive daytime sleepiness (EDS), defined as an Epworth Sleepiness Scale (ESS) ≥10, is one of the most common complaints among patients who present to an otolaryngologist with snoring. EDS affects approximately 12% of the general adult population. The number of affected patients climbs to 20% to 25% in the primary care physicians’ practice (2). The 2008 National Sleep Foundation (NSF) survey revealed that 36% of Americans drive drowsy or have fallen asleep while driving. Sleepiness and fatigue are usually caused by voluntary sleep deprivation or by an underlying sleep disorder. Anything that disturbs or disrupts sleep can lead to sleepiness or fatigue.

Sleepiness is a presenting complaint in a wide range of sleep disorders including obstructive sleep apnea (OSA), obesity-hypoventilation syndrome (OHS), central sleep apnea (CSA), voluntary sleep restriction, poor sleep hygiene, restless legs syndrome (RLS), periodic limb movement disorder, narcolepsy, circadian rhythm disorders, and insomnia (Table 135.3). The sleepy patient can even be dif- ficult to identify with the standard questionnaires, such as the ESS. Many patients with obstructive sleep apnea syndrome (OSAS) and other sleep disorders will complain of tiredness, fatigue, and lack of energy rather than sleepiness (3). Failure to ask about these additional symptoms may lead to a failure to diagnose a significant, treatable sleep disorder. Some sleep disorders, particularly OSAS and RLS, disrupt sleep and cause functional sleep deprivation. These patients have manifestations of sleep deprivation even if they spend adequate time in bed. Medical problems including fibromyalgia, genitourinary disorders, gastrointestinal disorders, and chronic pain may disrupt sleep. The sleep disruption may manifest in an increased arousal index in the polysomnogram (PSG). The arousal
index represents the number of EEG arousals or partial awakenings per hour of sleep.


Sleep Stage

Arousal Threshold

Identifying Characteristics in EEG/PSG Tracings

% of Total Sleep Time

Stage N1


Theta waves on EEG Slow rolling eye movement, vertex sharp waves


Stage N2


K complexes

Sleep spindles


Stage N3


Delta waves


REM or Stage R


Sawtooth waves or EEG activation, REMs and muscle atonia


Sleep-Disordered Breathing

Obstructive Sleep Apnea

Sleep-disordered breathing (SDB) describes a group of disorders characterized by abnormalities of respiratory pattern (pauses in breathing) or the rate of ventilation during sleep. The spectrum of SDB includes OSA, OHS, and CSA. OSA is a common medical condition with significant adverse consequences, but OSA remains undiagnosed in many individuals. The prevalence of OSA in the United States is currently estimated to be between 5% and 10% (4). Higher prevalence rates are found among specific population subsets, such as individuals who are older, over weight, or have concomitant medical comorbidities (5). It is estimated that only 10% of the population has been adequately screened for appropriate diagnosis (6). Risk factors for the diagnosis of OSA include male gender, obesity, age over 40, history of hypertension, smoking, alcohol use, anatomic characteristics that narrow the upper airway, and a family history of sleep apnea (7).

Figure 135.1 Normal young adult sleep hypnogram.

Figure 135.2 Changes in sleep with age in normal humans. (Reprinted with permission from Ohayon MM, Carskadon MA, Guilleminault C, et al. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep 2004; 27:1255-1273.)

The typical patient with OSA complains of snoring, EDS, witnessed apneas, and disrupted sleep. However, up to 75% of patients with OSA present with fatigue, tiredness, or lack of energy as their primary complaint rather than sleepiness (8). Many patients with OSA do not have a history of witnessed apneas. Younger, leaner patients and women tend to experience sleep disruptions or arousals instead of apneas during sleep (9). Patients may also present with cognitive complaints such as memory deficits or mood disorders.

Women with OSA may have different presenting symptoms than those typically described in the male population (10). Women are more likely to complain of insomnia and are more likely to have a history of depression and hypothyroid disease. They drink fewer caffeinated and alcoholic beverages than their male counterparts with OSA. Awareness of the variety of presenting complaints of patients with sleep apnea assists in timely diagnosis and treatment.

The association of cardiovascular sequelae and OSA is well documented. There is an increased risk of hypertension,
myocardial infarction (MI), and cardiovascular accident in those with moderate to severe OSA (11). OSA syndrome significantly increases the risk of stroke or death from any cause, and the increase is independent of other risk factors, including hypertension (12). OSA is also associated with an increase in insulin resistance and metabolic syndrome (13). This association seems to be dose-related, more severe OSA, as defined by the apnea-hypopnea index (AHI), associated with more severe metabolic syndrome, and it is independent of the body mass index (BMI) (14). Physical characteristics including a BMI > 30, neck circumference greater than 17 inches in men and a BMI > 30,
neck circumference greater than 14½ inches in women, retrognathia, and tonsillar hypertrophy are associated with an increased risk of OSA.




Adjustment insomnia


Psychophysiologic insomnia


Paradoxical insomnia


Idiopathic insomnia


Insomnia due to mental disorder


Inadequate sleep hygiene


Insomnia due to drug or substance


For alcohol use


Insomnia due to medical condition


Insomnia not due to substance or known physiologic condition, unspecified (nonorganic insomnia, NOS)


Physiologic (organic) insomnia, unspecified



Sleep-related breathing disorders

Primary CSA


Cheyne-Stokes breathing pattern


High-altitude periodic breathing


CSA due to medical condition not Cheyne-Stokes


CSA due to drug or substance


OSA, adult


Sleep-related nonobstructive alveolar hypoventilation, idiopathic


Sleep-related hypoventilation/hypoxemia

Due to pulmonary parenchymal or vascular pathology


Sleep-related hypoventilation/hypoxemia

Due to lower airways obstruction


Sleep-related hypoventilation/hypoxemia due to neuromuscular and chest wall disorders


Other sleep-related breathing disorders



Hypersomnias of central origin not due to a circadian rhythm sleep disorder, sleep-related breathing disorder, or other cause of disturbed nocturnal sleep

Narcolepsy with cataplexy


Narcolepsy without cataplexy


Narcolepsy due to medical condition without cataplexy


With cataplexy


Narcolepsy, unspecified

Recurrent hypersomnia (including Kleine-Levin syndrome & menstrual-related hypersomnia)


Idiopathic hypersomnia with long sleep time


Idiopathic hypersomnia without long sleep time


Behaviorally induced insufficient sleep syndrome


Hypersomnia due to medical condition


Hypersomnia due to drug or substance (abuse)


For alcohol use


Hypersomnia due to drug or substance (medications)


Hypersomnia not due to substance or known physiologic condition


Physiologic (organic) hypersomnia, unspecified (organic hypersomnia, NOS)



Circadian rhythm sleep disorders

Circadian rhythm sleep disorder, delayed sleep phase type (delayed sleep phase disorder)


Circadian rhythm sleep disorder, advanced sleep phase type (advanced sleep phase disorder)


Circadian rhythm sleep disorder, irregular sleep-wake type (irregular sleep-wake rhythm)


Circadian rhythm sleep disorder, free-running type (nonentrained type)


Circadian rhythm sleep disorder, jet lag type (jet lag disorder)


Circadian rhythm sleep disorder, shift work type (shift work disorder)


Circadian rhythm sleep disorder due to medical condition


Other circadian rhythm sleep disorder (circadian rhythm disorder, NOS)


Other circadian rhythm sleep disorder due to drug or substance


For alcohol use




Confusional arousals




Sleep terrors


REM sleep behavior disorder (Including parasomnia overlap disorder and status dissociatus)


Recurrent isolated sleep paralysis


Nightmare disorder


Sleep-related dissociative disorders


Sleep-related groaning (catathrenia)


Exploding head syndrome


Sleep-related hallucinations


Sleep-related eating disorder



Sleep-related movement disorders



Periodic limb movement disorder


Sleep-related leg cramps


Sleep-related bruxism



Other sleep disorders

Other physiologic (organic) sleep disorder


Other sleep disorder not due to substance or known physiologic condition


Environmental sleep disorder


Index of the ICSD-2 reprinted with permission.


Inadequate Sleep

Poor-Quality Sleep

Central Etiology


Voluntary sleep restriction





RLS/periodic limb movement disorder

Idiopathic hypersomnia


Circadian rhythm disorder


Posttraumatic hypersomnia

Mood disorders

Poor sleep hygiene


The diagnosis of OSA is made with either in-lab polysomnography or a home sleep study.

The frequency of apneas and hypopneas per hour of sleep is expressed as the “apnea-hypopnea index” or the AHI (number of apneas plus hypopneas per hour of sleep).

The respiratory disturbance index (RDI) includes the total of apneas, hypopneas, and respiratory effort-related arousals (RERAs) per hour of sleep. When a portable monitor is used that does not record EEG or measure sleep, the RDI refers to the number of apneas plus hypopneas per hour of recording (15). OSA severity is defined by the AHI or the RDI as measured by a PSG or cardiorespiratory sleep study (Table 135.4).

Obesity-Hypoventilation Syndrome

OHS, historically known as the Pickwickian syndrome (16), consists of the triad of obesity, SDB, and chronic hypercapnia during wakefulness in the absence of other known causes of hypercapnia (17). Its exact prevalence is unknown, but it has been estimated that 10% to 20% of obese patients with OSA have hypercapnia (18). Of the patients with OHS, 90% have OSA, but 10% have nonobstructive hypoventilation with an AHI < 5 on polysomnography. This disorder is diagnosed in patients with an elevated body mass index (BMI > 30 kg/m2), arterial carbon dioxide level over 45 mm Hg, an increase in 10 mm Hg in the PaCO2 during sleep, and hypoxemia. Over the past 20 years, the epidemic of obesity has increased exponentially in the United States. The prevalence of BMI ≥ 40 kg/m2 has increased by fivefold, and the prevalence of BMI ≥ 50 has increased 10-fold. This marked increase in extreme obesity will likely result in the increase of OHS in OSA patients.










AHI, apnea-hypopnea index (mean number of apneas plus hypopneas/hour of sleep).

Patients with OHS have a blunted central response to hypercapnia and hypoxia and decreased lung compliance coupled with increased lung resistance, resulting in a threefold increase in the work of breathing. They have significantly increased morbidity and mortality when compared to eucapnic OSA patients; therefore, identification and prompt treatment are imperative (19).

Central Sleep Apnea/Complex Sleep Apnea

CSA is characterized by recurrent episodes of breathing cessation in sleep associated with the lack of respiratory effort. It is not a single disorder, but rather a manifestation of breathing instability that can be caused by many disorders. A form of CSA, Cheyne-Stokes breathing is a cyclical crescendo -decrescendo pattern of central apneas and hyperpneas that is seen in congestive heart failure, stroke, and renal failure. Other causes of CSA include opioid-associated central apnea, neuromuscular disorders, high-altitude periodic breathing, and brainstem lesions. Occasionally, treatment of OSA with positive airway pressure (PAP) can precipitate the emergence of central apneas or a Cheyne- Stokes pattern of breathing. This phenomenon has termed complex sleep apnea syndrome (CompSAS). Patients with CompSAS can have very disrupted breathing and fragmented sleep on continuous positive airway pressure (CPAP), with respiratory disturbances in the range typically found in patients with moderately severe sleep apnea (20).

Inadequate Sleep

The number one cause of sleepiness is self-imposed sleep restriction or inadequate time in bed. The 2008 NSF “Sleep in America” poll (21) reported that 16% of individuals obtained less than 6 hours of sleep per night on weekdays. Only 26% reported sleeping 8 hours or more per night despite the fact that this is the amount of sleep that the average individual needs to be adequately rested. This is a societal problem which, based upon the NSF annual sleep polls, appears to be increasing in prevalence.

Sleep deprivation has been shown to negatively impact cognitive functioning and performance and to increase the rate of automobile accidents and accidents in the workplace. On tests of reaction time, concentration, and memory, subjects who are experimentally sleep deprived or sleepy due to a sleep disorder perform poorly compared
to subjects who are not sleep deprived or have normal sleep. To put the degree of psychomotor impairment associated with sleep deprivation in perspective, studies that compared the effects of alcohol with sleep deprivation have been conducted. In one study, sleep-deprived subjects scored similarly to those subjects with a blood alcohol level of 0.08% (22).

The cardiovascular system also is adversely affected by sleep deprivation. There are increases in inflammatory markers including C-reactive protein and an increased risk of cardiovascular events and morbidity (23). Physiologic effects of sleep deprivation include changes in circulating levels of many hormones including growth hormone, thyroid-stimulating hormone, leptin, thyroxine, cortisol, prolactin, estradiol, luteinizing hormone, adrenaline, and noradrenaline (24). Short sleep time is associated with impaired glucose tolerance and obesity (25). Alterations in immune function occur with sleep deprivation including changes in natural killer cell activity, levels of interleukin-6, antibody titers, and increased rates of some cancers (26).

Sleep deprivation or voluntary sleep restriction has significance for physicians as well as patients. There is an extensive research relative to sleep deprivation and performance relevant to resident education (27, 28, 29). This literature demonstrates decrements in cognitive function, fine motor skills, learning, judgment, and reaction time. As a result of concern about the negative effects of sleep deprivation on residents and their patients, the Accreditation Council for Graduate Medical Education began limiting work hours for residents in 1990 and implemented mandatory standards to limit work hours for resident physicians in 2003. These standards are revised intermittently, most recently in 2011, as more research on the effects of sleep deprivation on performance becomes available (30).

This issue affects attending physicians as well. Although studies have shown that older and more experienced physicians have some resistance to the effects of sleep deprivation, all physicians are susceptible to the performance and judgment decrements caused by sleep deprivation. There is a growing movement to restrict all physician work hours given the prevalence of sleep disorders in our society overall and the increase in this incidence with age (31).


Chronic insomnia, defined as difficulty initiating or maintaining sleep or nonrestorative sleep lasting for over a month, affects 10% to 15% of the adult population. Chronic insomnia is associated with decreased quality of life and adverse health effects, particularly an increased risk of depression. Insomnia can be the result of another sleep disorder such as sleep apnea or RLS. It can also result from poor sleep hygiene such as caffeine or alcohol intake at night, irregular sleep/wake habits, exposure to light from a computer monitor before bed, medications, other medical comorbidities, or psychiatric disorders. Patients with insomnia may complain of excessive sleepiness, feeling tired or fatigued, or an uncomfortable feeling of hyperarousal. Treatment of insomnia is important for overall patient well-being. Cognitive behavioral therapy for insomnia (CBT-I) is a specific, highly practical therapeutic approach for chronic insomnia. This is usually performed by a medical psychologist or trained therapist. CBT-I is recognized as the most effective long-term therapy of chronic insomnia (32). If the insomnia is due to a medical or psychiatric condition, treatment of the underlying cause may be beneficial. The use of hypnotics has been found to be useful only as a short-term therapeutic measure.

Circadian Rhythm Disorders

Circadian rhythm sleep disorder is a persistent or recurring pattern of sleep disruption resulting either from an altered sleep-wake schedule or a misalignment between a person’s natural sleep-wake cycle and the sleep-related demands placed on him or her. These disorders, frequently overlooked by clinicians as a cause of sleep disorders, can result in excessive sleepiness, poor sleep quality, or insomnia. Frequently encountered types of circadian rhythm disorders include the following:

Shift work type—Shift work sleep disorder involves sleepiness or insomnia that occurs when the work schedule overlaps the usual wake time. There are over 6 million people in the United States working night or rotation shifts, so this is a common sleep disorder.

Delayed sleep phase type—Delayed sleep phase syndrome (DSPS) is a disorder in which the person’s sleep-wake cycle is delayed by two or more hours. Patients with DSPS generally fall asleep late at night, often in the predawn hours, and wake in the late morning or in the afternoon. Furthermore, there is a striking inability to fall asleep at an earlier, more typical bedtime. This disorder, which often develops during puberty, is estimated to affect 7% to 16% of adolescents.

Jet lag type—This is caused by a mismatch of the patient’s sleep-wake cycle and the time zone. The more time zones that are traveled, the greater the disruption. Eastbound travel, in which sleep-wake hours are advanced, typically causes more problems than westbound travel, in which sleep-wake hours are delayed. People who travel often and cross many time zones when they travel are most susceptible to this type.


Narcolepsy is a neurologic disorder affecting 0.05% of the US population that is characterized by EDS and abnormal manifestations of REM sleep such as cataplexy. The classic tetrad of narcolepsy, present in only 20% to 30% of patients
with narcolepsy, includes EDS, cataplexy, hypnagogic hallucinations, and sleep paralysis. Patients with narcolepsy experience EDS with ESS > 14 and intermittent, uncontrollable episodes of falling asleep during the daytime. Cataplexy, a loss of muscle tone without loss of consciousness elicited by an emotional stimulus, is present in 60% of patients with narcolepsy (33). These sudden sleep attacks may occur during any type of activity at any time of the day. Symptoms generally present in the second decade of life, but the diagnosis of narcolepsy is often delayed by more than 10 years after onset of symptoms (34).

While the presence of severe EDS and cataplexy strongly supports the diagnosis of narcolepsy, diagnosis is usually made with the multiple sleep latency test (MSLT) that demonstrates two or more episodes of sleep onset REM during the five-nap study.

REM Behavior Disorder

While patients with REM behavior disorder (RBD) do have disrupted sleep and daytime sleepiness, they will usually present with the complaint of dream-enacting behavior and violent dreams. These patients can harm themselves or their bed partners during these episodes. RBD is neurologic disorder with a lack of atonia during REM sleep. The majority of patients with RBD have Parkinson disease or a related synucleinopathy; however, RBD can precede the onset of Parkinson disease by over a decade.

Restless Legs Syndrome

Patients with RLS will often complain of difficulty initiating sleep and nonrestorative sleep with daytime sleepiness. RLS is defined as an urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs, worse at rest, and in the evenings and relieved by movement. Eighty percent of people who have RLS also have periodic limb movements of sleep (PLMS). These are jerks of the legs or arms that occur every 20 to 30 seconds on and off throughout the night. This can cause partial awakenings or arousals that disrupt sleep. RLS is diagnosed by history. The four basic criteria for diagnosis are listed in Table 135.5 (35).

Patients with a history of nocturnal limb movements, daytime somnolence, and a lack of daytime symptoms of RLS should be studied with a full PSG to identify any leg movements leading to arousals and sleep disruption. These patients may have periodic limb movement disorder leading to daytime sleepiness, sleep maintenance insomnia, and nonrestorative sleep.

The majority of patients with sleep apnea who kick at night do not have RLS or PLMS. Their kicking is a response to their airway obstruction and is relieved by resolution of the airway obstruction. A CPAP titration study in these patients will show that the leg movements resolve with adequate CPAP pressure.


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May 24, 2016 | Posted by in OTOLARYNGOLOGY | Comments Off on Sleep Medicine for the Otolaryngologist
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An urge to move the legs, usually accompanied or caused by uncomfortable and unpleasant sensations in the legs. (Sometimes the urge to move is present without the uncomfortable sensations, and sometimes the arms or other body parts are involved in addition to the legs).


The urge to move or unpleasant sensations begin or worsen during periods of rest or inactivity such as lying or sitting.


The urge to move or unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity continues.