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Sleep medicine constitutes a spectrum of disorders, which combines the specialties of neurology, pulmonary medicine, psychiatry, psychology, otolaryngology, and pediatrics.  Sleep disorders may be divided based on symptoms into four types: 1) insomnia, or difficulty initiating and maintaining continuous sleep, 2) excessive sleepiness, 3) circadian sleep-wake rhythm disorders, in which the sleep-wake cycle is out of sync with the day-night cycle, and 4) parasomnias, in which undesirable motor, behavioral and autonomic activity occur before, during, or after sleep.

The International Classification of Sleep Disorders, revised in 1997, lists 84 disorders which are divided into four categories: 1) dyssomnias which include causes of insomnia and excessive sleepiness, 2) parasomnias, 3) sleep disorders associated with medical or psychiatric disorders, and 4) proposed sleep disorders, for which there is suggestive, but not unambiguous data, for a sleep disorder.  This chapter will review the properties of normal sleep and sleep disorders based on the symptomatic classification.

            The neuropharmacology of sleep is related to the anatomic regulatory centers of sleep.  The fact that the raphe nuclei and locus coeruleus are crucial to REM sleep suggests that serotonin and norepinephrine, respectively, play a crucial role in sleep mechanisms.  In clinical practice, however, serotonin precursors have conflicting effects on sleep.  Drugs which alter the storage, release and re-uptake of serotonin have minimal effects.  Acetylcholine may play an important role in REM sleep because of the cholinergic neurons in the brainstem, which regulate REM sleep.  The effect of norepinephrine and dopamine on sleep has been extensively studied in patients with parkinsonism, but no significant changes have been found.  Pharmacologically, we know that stimulants, such as amphetamines, act by increasing brain norepinephrine and dopamine concentrations.  The stimulants reduce total sleep and REM sleep times.  Hypnotics, such as benzodiazepines, act by enhancing inhibitory GABAergic neurotransmission.  Clinically, they promote sleep onset and reduce slow wave and REM sleep.

            In normal day-night conditions, the sleep-wake cycle is 24 hours long. With external time cues removed, the sleep-wake cycle lengthens to about 25 hours.  The intrinsic cycling of bodily functions, such as the sleep-wake cycle and body temperature, is referred to as the circadian rhythm.  It is determined by an internal pacemaker, which for the sleep-wake cycle, is located in the suprachiasmatic nucleus (SCN) of the hypothalamus.  The SCN has connections to the retina, which regulate the light-dark synthesis and release of melatonin by the pineal gland.  Individuals blind from birth, who lack the SCN-retinal connection, do not have a 24-hour sleep-wake cycle.  In normal individuals, the internal 24-hour clock is stable.  However, it can be reset by external cues, particularly light, as in travel across time lines.  Body temperature is the most reliable marker of circadian rhythm in humans and the biological rhythm most closely linked with sleepiness.  Low body temperature correlates with sleep onset while rising body temperatures correlate with sleep offset.  Body temperature reaches a nadir twice a day: a relatively small drop in mid-afternoon and a more drastic fall in the early hours of the morning, coinciding with REM sleep.

            Normal sleep consists of several stages.  Each stage is associated with certain physical properties and EEG findings.  Drowsiness or light sleep is Stage 1.  The subject is relaxed.  Slow random eye movements and slow pupillary constriction and dilatation are noted.  On EEG, background activity is slow compared to wakefulness.  As sleep continues, Stage 2 is entered.  In this stage, bursts of EEG activity called sleep spindles, vertex sharp waves and K complexes appear.  With continued sleep, during which the subject is harder to awaken, stages 3 and 4 are entered.  During these stages, collectively referred to as slow wave sleep, the EEG shows high amplitude slow waves.  About 90 minutes after the onset of sleep, the subject enters rapid eye movement (REM) sleep.  This stage of sleep is associated with vivid dreams that follow a story line and are accompanied by realistic imagery.  Dream recall is more frequent in awakenings from REM sleep than from non-REM (NREM) sleep.  There is loss of skeletal muscle tone except for brief twitching and rapid eye movements.  Autonomic changes also occur, including elevated blood pressure, irregular heart rate, and irregular respirations.  Arrhythmias such ventricular tachycardia, atrial fibrillation, and heart block are more likely to occur during REM sleep.  It is suspected that myocardial infarction and strokes that occur during sleep happen during REM sleep because of the associated autonomic changes.  Penile erection also occurs during REM sleep.  Patients with psychological causes of impotence will have an erection during REM sleep, while patients with organic etiologies do not.

            NREM sleep, which consists of stages 1, 2, 3 and 4, usually occupies the first 60 to 90 minutes of sleep, followed by REM sleep.  A night of sleep usually consists of four to six NREM-REM cycles.  The duration of slow wave sleep is longest during the first half of the night, while REM sleep becomes more prolonged during the second half of the night.  Age-related changes in sleep architecture have been reported.  During the neonatal period, most of the day is spent asleep, with half of the sleep time in active sleep, the equivalent of REM sleep.  As one ages, the percentage of total sleep that constitutes REM sleep remains fairly constant at 20 to 25 %.  During adolescence, there is a peak in the percentage of slow wave sleep after which it declines with aging.  Conversely, stage 1 sleep increases with age.  Nocturnal sleep efficiency, or the percentage of time in bed spent asleep, is reduced to about 70 to 80% in the elderly, most likely as a result of increased nocturnal awakenings.  Total sleep time, which takes into account daytime napping in addition to nocturnal sleep, is fairly constant between young and old.  Thus, it is a myth that old people need less sleep.

            The functional importance of individual stages of sleep has been investigated with selective sleep deprivation studies.  These studies, which eliminate one or more stages of sleep, most commonly REM sleep and, less frequently, slow wave sleep, find that total sleep time, not selective sleep stage deprivation, is the most important predictor of cognitive performance.

            Insomnia can assume several patterns.  Transient insomnia usually lasts just a few nights.   The most common cause is anxiety related to stress, travel across time zones or shift work.  Chronic insomnia lasts longer than a month.  It is a common complaint of the elderly.  Daytime somnolence is usually not a major complaint, either by patient report or by objective test measures of sleepiness.

Four common etiologies may be identified: 1) medical illness, 2) psychiatric or psychological disease, 3) primary insomnia, and 4) organic sleep disorders.  Medical conditions involving chronic pain or discomfort, such as arthritis, peptic ulcers, and parkinsonism; frequent awakenings from nocturia; respiratory distress from asthma or sleep apnea; and metabolic diseases that alter sleep patterns, such as hyperthyroidism, can cause insomnia.  Major affective disorders, particularly depression, result in difficulty maintaining sleep and early morning arousals in about one-fourth of patients.  Seasonal affective disorder is associated with insomnia and transient depression during the winter season.

Psychophysiological insomnia occurs when the patient recurrently worries about his/her inability to sleep all night and thereby perpetuates insomnia.  About 10-25% of patients who complain of a life-long pattern of difficulty initiating or maintaining sleep have primary insomnia.  This condition is characterized by short sleep time, daytime fatigue, and irritability.  Most patients have symptoms dating back to childhood and may have a family history of insomnia.  Organic causes of insomnia are central sleep apnea and parasomnias.

            Drugs, caffeinated beverages and alcohol may cause insomnia.  Medications commonly causing insomnia include beta-blockers, alpha-methyldopa, phenytoin, monoamine oxidase A inhibitors, bronchodilators, CNS stimulants, weight loss medications, and nicotine.  Short-acting benzodiazepines, such as triazolam, when taken as a single oral nighttime dose, may cause rebound insomnia and anxiety early in the morning.  Withdrawal from short-acting benzodiazepines, taken chronically for periods longer than two weeks, may also cause severe rebound insomnia and anxiety.  Caffeinated beverages will increase sleep latency, which is defined as the time it takes to fall asleep, and nocturnal arousals.  Alcohol acutely disrupts normal sleep.  It shortens sleep latency, reduces slow wave sleep, shortens REM sleep in the second half of the night, and causes frequent arousals.  With chronic use, these symptoms become more severe and may persist for up to two years following abstinence.

            Fatal familial insomnia is a rare familial condition arising from a genetic mutation.  It is characterized by medically refractory insomnia, with progressive loss of slow wave and REM sleep, autonomic dysfunction, motor signs, and cognitive deficits.  Average age at onset is 49 with a mean duration of 13 months before death.  Pathologically, there is bilateral thalamic atrophy.

            The diagnosis of insomnia rarely requires a diagnostic sleep study, as these studies rarely yield useful information into the cause of symptoms.  Acute insomnia generally does not require a sleep study as the causes are related to psychiatric, situational or readily identifiable medical conditions.  In cases where insomnia is present for at least 6 months or there is no response to behavioral, medical, or psychiatric treatment or withdrawal of sedative or hypnotic medications, a sleep study should be considered.  For example, cryptic periodic leg movements of sleep, central sleep apnea or seizure-induced arousal presenting as insomnia may be diagnosed only by a sleep study.

            Treatment of insomnia is dependent on the cause, which can be difficult for both the patient and physician to discern.  Treatment options include behavioral and pharmacologic approaches, or a combination of the two.  Behavioral treatment assumes that chronic insomnia is due to a combination of predisposing, precipitating and maintaining factors.  Predisposing factors may originate from medical or psychiatric disease.  Examples of predisposing factors are biological factors, such as easy arousal, or psychological factors, such as inability to resolve stress.  Precipitating factors are an identifiable event that precedes insomnia, such as an illness or major life event.  Maintaining factors are behaviors used by the patient to compensate for insomnia, but which actually perpetuate it, such as use of hypnotic and sedative drugs.   Behavioral treatment targets predisposing and maintaining factors of chronic insomnia.  It is best applied to patients with psychophysiologic causes of insomnia and primary insomnia.

            The most common behavioral treatments are sleep hygiene, sleep restriction, stimulus control, and relaxation training.  Often, these therapies are combined for optimal success.  Sleep hygiene employs common sense advice on how to improve sleep onset and maintain continuous sleep.   The patient is advised to do the following: 1) avoid caffeinated beverages and nicotine for at least six hours before bedtime, 2) avoid alcohol, 3) exercise regularly but not for at least three hours prior to bedtime, 4) avoid naps if one has trouble falling asleep at night, 5) establish a regular routine for bedtime and morning awakening, even on weekends, sleeping only as necessary to feel refreshed, 6) use the bed only for sleep or sex, but avoid reading or watching television, 7) get out of bed and engage in some relaxing activity if one can not fall asleep after lying in bed for 30 minutes and return to bed only when one feels sleepy, 8) eat meals regularly and do not go to bed hungry, and 9) try not to take one’s problems to bed.  Sleep hygiene is most effective when combined with other behavioral therapies.

            Sleep restriction is a temporary treatment measure that is based on the notion that sleep deprivation leads to consolidation of sleep.  A sleep diary is maintained for two to three weeks, to determine sleep efficiency, which is expressed as a percentage and calculated by dividing the amount of time spent asleep by the amount of time spent in bed.  The amount of time spent in bed is reduced to the time spent asleep by delaying the bedtime and fixing the wake-up time.  The purpose of sleep restriction is to increase sleep efficiency to about 90%.  As sleep efficiency gradually improves, the bedtime is relaxed by 15-minute increments weekly.

            Stimulus control therapy is based on the assumption that the patient has conditioned himself to view the bedroom as a place where sleep cannot be obtained.  Therefore, the patient is instructed to change his behavior so that the bedroom and bed is associated strictly with sleep.  The patient is to get out of bed if he cannot fall asleep after 10-15 minutes.  However, the clock should not be watched as this behavior may condition sleeplessness.  Once up, the patient is to go to another room and engage in activity that is relaxing.  When sleepy, he should return to bed.  This sequence of behaviors is repeated as many times as necessary until the patient finally falls asleep.  Compliance is monitored through sleep diaries and weekly visits.  A trial of five to seven weeks is considered adequate.  Compliance with this therapy may initially be poor as patients want to sleep wherever they feel sleepy, even if not in their bedroom, and may feel that transferring to their bedroom when sleepy will result in loss of sleep momentum.

            Relaxation training may be helpful in patients who are anxious and tend to bring their problems to bed.  It employs biofeedback techniques or other maneuvers designed to reduce musculoskeletal tension.  These techniques are best performed before sleep.  However, in patients with obsessive-compulsive disorder or panic attacks, this therapy may produce paradoxical effects.

            The use of hypnotic and sedative drugs for the treatment of chronic insomnia is generally not recommended.  In certain circumstances, symptomatic relief may be obtained with benzodiazepines and antidepressants, the two most commonly prescribed classes of drugs for insomnia.  Benzodiazepines have hypnotic, muscle relaxing, antianxiety and anticonvulsant properties.  In general, benzodiazepines reduce sleep latency, increase stage 2 sleep, and mildly reduce REM sleep.  They minimally increase sleep time, but enhance patients’ perception of longer sleep duration.  Patients with coexisting sleep disorders may benefit or be adversely affected by benzodiazepines.  For example, benzodiazepines are effective in the treatment of periodic limb movements of sleep, which can cause cyclical nocturnal arousals.  Conversely, they can worsen sleep apnea by increasing its duration and frequency, and exacerbating oxygen desaturation.

            The choice of drug for treatment of insomnia should depend on its hypnotic potency, elimination half-life, and rapidity of absorption, in combination with the patient's symptoms and comorbid conditions.  A short-acting medication with a half-life of less than eight hours, rapid absorption and no active metabolites, such as zolpidem (Ambien®), is preferable for patients with difficulty initiating sleep.  Zaleplon (Sonata®), which has rapid onset of action and a half-life of 1 hour, may be appropriate for middle of the night administration.  Some of the newer nonbenzodiazepine hypnotics, such as zolpidem, preserve sleep architecture and have been reported to have lower abuse potential than benzodiazepines.  In addition, zolpidem appears to result in no rebound insomnia at recommended dosages.  With some short-acting hypnotics, daytime rebound anxiety is a potential complication.  Long-acting benzodiazepines with active metabolites are more likely to lead to daytime somnolence, memory loss, and imbalance, particularly in the elderly.

            Benzodiazepines can be used short-term, preferably on an intermittent, as needed basis for periods of one month, after which tapering is recommended.  In general, short-acting agents are preferable because of the absence of residual daytime effects.  Chronic treatment with benzodiazepines is discouraged because of tolerance and dependence.  Rebound insomnia may occur in about 10% of patients in whom medication is abruptly discontinued.  Whenever, benzodiazepines are taken nightly for longer than two weeks, a gradual tapering by one-fourth the dose, weekly, is recommended.

            Antidepressants are prescribed for patients with coexisting mood or anxiety disorders.  It is not recommended for patients with primary insomnia due to lack of data supporting its efficacy.  Treatment for insomnia related to mood and anxiety disorders is indefinite, barring adverse side effects.  The sedating antidepressants, namely amitriptyline, doxepin, and imipramine, reduce nocturnal awakenings and promote sleep continuity.  Conversely, stimulating tricyclic antidepressants (TCAs), such as protriptyline and desipramine, will disrupt sleep continuity.  TCAs reduce REM sleep by varying degrees.  Selective serotonin reuptake inhibitors (SSRIs) affect sleep at higher dosages by disrupting sleep consolidation.  Their effect on sleep is unpredictable, whether taken in the morning or night.  As SSRIs are usually ineffective in treating insomnia associated with mood and anxiety disorders, a low dose of a sedating antidepressant or short-acting benzodiazepine is concomitantly prescribed at night.

            Trazadone is another sedating antidepressant.  It increases slow wave sleep and can minimally suppress or increase REM sleep.  Bupropion is a stimulant that disrupts sleep continuity but increases REM sleep.  Monoamine oxidase inhibitors (MAOIs) disrupt sleep continuity and strongly suppress REM sleep.

            In choosing an antidepressant, potential side effects should be considered.  The biggest concern about TCAs and MAOIs is potential lethal overdosage.  TCAs have anticholinergic side effects (i.e., dry eye, dry mouth, urinary retention, etc.) and cardiac side effects.  SSRIs can cause headaches, sexual dysfunction and GI side effects.  MAOIs can cause orthostatic hypotension, sexual dysfunction and tyramine reactions.  All antidepressants can intensify dreaming or nightmares, by consolidating REM sleep after increased wakefulness.  TCAs, SSRIs and MAOIs exacerbate restless legs syndrome and periodic limb movements of sleep.

            Primary insomnia, which is the result of chronic negative behavioral and conditioning factors, is best treated with a combination of sleep hygiene, stimulus control and sleep restriction.  In patients with suspected somatic tension, relaxation techniques may also be beneficial.  Alternatively, behavioral treatment combined with short term or chronic, intermittent benzodiazepine or nonbenzodiazepine therapy is also used to treat primary insomnia.

            For patients with insomnia due to a general medical condition, such as rheumatoid arthritis, the underlying medical condition should be treated with attention to pain, if relevant.  In some patients, low to moderate doses of a sedating antidepressant may alleviate chronic pain and promote sleep.  Patients who suffer from substance abuse, such as alcohol or cocaine, will also have disruptive sleep-wake schedules.  Both discontinuation and acute use will cause insomnia.  Medications such as benzodiazepines are contraindicated, but low dose TCAs or trazadone may be effective after substance abuse has been terminated.

            Obstructive sleep apnea (OSA) is due to complete or partial obstruction of the upper airway.   During sleep, the tone of pharyngeal muscles diminishes.  When pharyngeal muscles collapse, resistance to airflow increases and results in elevated negative intrathoracic pressures during inspiration.  Complete obstruction of the upper airway results in apnea or cessation of airflow across the nose and mouth, often, but not always, with associated hypoxemia.  Partial obstruction causes a hypopnea, which is defined as a 50 to 90% reduction in airflow.  At the end of an apnea or hypopnea, a person is often aroused.  An arousal or brief awakening stimulates pharyngeal muscle tone and normal inspiratory airflow resumes.  Severity of hypoxemia is dependent on baseline oxygenation, lung oxygen stores and apnea duration.  For example, a markedly obese patient is likely to have severe OSA-associated hypoxemia because elevated abdominal pressures are compressing the thoracic cavity and reducing lung oxygen stores.

            There are many causes of upper airway obstruction.  Tonsillar hypertrophy is a common cause of OSA in children and adolescents.  Craniofacial abnormalities such as retrognathia, micrognathia, and deviated nasal septum increase upper airway obstruction, as does fatty infiltration of pharyngeal soft tissues from weight gain.  Macroglossia, which may be associated with hypothyroidism, acromegaly, amyloidosis and Down’s syndrome, usually causes obstruction at the base of the tongue, lower down the pharynx.  Neuromuscular disorders, such as myotonic   dystrophy, often cause abnormal laxity of pharyngeal muscle tone during sleep.

            OSA is common in the general population.  The Wisconsin Sleep Cohort, a comprehensive epidemiologic study investigating the prevalence of obstructive sleep apnea in middle-aged adults, found that 4% of men and 2% of women had obstructive sleep apnea syndrome (OSAS), a diagnosis defined by both clinical criteria and a sleep study.  However, 24% of men and 9% of women had OSA as defined by sleep study results alone.  Among commercial truck drivers a high prevalence of OSA is suspected.

            A thorough history can provide clues to the diagnosis of OSAS.  Apneas or hypopneas during sleep are best confirmed by the patient’s family or bed partner.  The physiologic effects of apneas and hypopneas are equal.  The most prevalent complaint is fatigue or daytime somnolence, which results from fragmentation of nocturnal sleep by recurrent apnea-associated arousals.  Choking or gasping at the termination of an obstructive apnea is a common observation and can cause self-arousal.  The severity of daytime somnolence can be ascertained by the frequency and duration of naps and the likelihood of falling asleep during activities such as reading, watching television or driving.  Sleep deprivation from OSA often has a paradoxical effect on children, who are more likely to present with hyperactivity.  Hypoxemia and sleep fragmentation may result in impairment of memory, attention and concentration, changes in mood and personality, loss of libido, and morning headaches.  Snoring is a common, but not requisite, symptom in patients with OSA.  The intensity of snoring increases with weight gain and reflects increasing upper airway resistance.  Loud snoring in all positions of sleep is more likely to be associated with OSA than snoring in just the supine position.  Enuresis and nocturia may occur in patients with OSA as respirations against an obstructed upper airway lead to increased intra-abdominal pressure on the bladder.  Restless sleep, described as frequent movements of the limbs and trunk, is common in subjects with frequent apnea-associated arousals.  Lastly, a family history of OSA can identify individuals who are at risk for OSA as risk increases with the number of affected family members.

            Several factors increase upper airway resistance and thus exacerbate the frequency and duration of apneas.  Hypnotics, sedatives, and alcohol reduce pharyngeal muscle tone during sleep.  Inflammation of the nasopharynx and pharyngeal soft tissues from respiratory allergies increase upper airway resistance.  Smoking and high altitudes exacerbate apnea-associated hypoxemia.

            The physical examination can be used to identify conditions associated with OSA.  Obesity is reported in two-thirds of patients.  A neck circumference of greater than 17 inches in men and greater than 16 inches in women is associated with increased risk for OSA.  As previously mentioned, anatomical abnormalities of the head and neck, such as micrognathia, retrognathia, and macroglossia can cause upper airway narrowing.  OSA is more prevalent in men compared to women, at ratios reported between 2:1 to 10:1, most likely reflecting gender differences in head and neck anatomy.  Prevalence increases for both genders with increasing age.

            The diagnosis and treatment of OSAS is important in lieu of its potential hematologic and cardiovascular complications.  Polycythemia, from chronic hypoxemia, is relatively uncommon in patients with OSA.  Hypertension, ischemic heart disease and cerebrovascular disease occur with higher prevalence in subjects with OSA compared to the general US population.  However, the relationship between OSA and these diseases is poorly understood.  Pulmonary hypertension is a known complication of chronic, untreated OSA and is strongly associated with severe nocturnal hypoxemia and hypercapnea.  Cardiac arrhythmias are common in patients with severe hypoxemia.  The type of arrhythmias observed include premature ventricular contractions, sinus arrest, sinus bradycardia, second-degree atrioventricular block, atrial tachycardia, paroxysmal atrial fibrillation, atrial flutter, and unsustained ventricular tachycardia.  These cardiac arrhythmias are reversible with treatment for OSA.

            The differential diagnosis for OSAS includes disorders associated with loud snoring and daytime somnolence.  Primary snoring is characterized by loud snoring only and is not associated with daytime hypersomnolence.  Excessive daytime somnolence may be due to behavioral or psychophysiologic factors, psychiatric disorders, environmental factors, drug dependency from hypnotics or stimulants, central sleep apnea syndrome, parasomnias, disruption in the timing of the sleep-wake cycle such as shift work sleep disorder, narcolepsy, idiopathic central nervous system hypersomnia, degenerative central nervous system disorders, and hormone-related conditions such as pregnancy and menstruation.

            The evaluation of a patient with OSAS must include a sleep study.  There are two types of sleep studies: an overnight polysomnogram, performed in a laboratory under the guidance of a certified sleep technician, and an ambulatory sleep study performed in the patient’s own home.  Ambulatory studies tend to monitor a limited number of parameters, i.e. respiratory effort, airflow, heart rate and oxygen saturation.  Polysomnograms also record electroencephalography to stage sleep and determine total sleep time monitored, electrooculography and electromyography (EMG) of the chin to determine the onset of rapid eye movement (REM) sleep, airflow, chest and abdominal wall motion, EMG of the legs to detect periodic leg movements of sleep, oximetry, and body position (Figure 1).

            The major advantages of a laboratory study are the ability of the sleep technician to intervene when an electrode or monitor is displaced and the reliability and comprehensiveness of the sleep data obtained.  The major advantage of an ambulatory study is lower cost.  In patients suspected of severe OSAS, an ambulatory monitor can serve as a screening test, although a negative study should be followed up with a polysomnogram.  For most patients with OSAS, a polysomnogram is the preferred study.

            A sleep study is scored on several parameters, including sleep efficiency (total sleep time divided by total time in bed, expressed as a percentage), sleep latency (time it takes to fall asleep from the beginning of the study), percentage of each stage of sleep relative to total sleep time, number of apneas, range of apnea duration and oxygen desaturation, number of arousals, number of periodic leg movements with and without associated arousals, REM latency (time it takes to enter REM sleep from the time of sleep onset), and associated cardiac arrhythmias.  An apnea is defined as cessation of airflow for at least 10 seconds.  There are three types of apneas: obstructive, central and mixed.  Obstructive apneas imply the absence of airflow in the presence of continued thoracic and abdominal effort (Figure 1).  Central apneas are often due to dysfunction of regulatory respiratory centers in the central nervous system.  Airflow is absent and so, too, is thoracic and abdominal effort.  Insomnia, rather than daytime somnolence, is more likely to be the presenting symptom.  Mixed apneas have features of both obstructive and central apneas.  They are often due to upper airway obstruction.  The severity of OSA is determined by the apnea-hypopnea index (AHI), or the frequency of apneas and hypopneas per hour of sleep, the frequency of arousals and awakenings, body position during apneas, oxygen desaturation, and type of cardiac arrhythmias.  REM sleep and sleep in the supine position are of particular interest as obstructive apneas tend to be longer in duration and oxygen desaturation more severe.  In general, mild OSAS may be characterized by an AHI of less than 15, mild oxygen desaturation, no cardiac arrhythmias, and minimal or no daytime fatigue.  Moderate OSAS may be characterized by an AHI of 15-30, moderate oxygen desaturation (i.e., 70 to 85%), moderate daytime sleepiness, and sometimes premature ventricular contractions.  In severe OSAS, the AHI is usually greater than 40 and associated with oxygen desaturations below 70%, cardiac arrhythmias, and severe daytime sleepiness.  Polysomnogram results should be congruent with the clinical history.  If not, the diagnosis of OSAS must be reconsidered.  Occasionally, the polysomnogram may reveal frequent unexplained arousals or crescendo snoring just before an arousal, but no apneas.  In such cases, a repeat polysomnogram with esophageal balloon pressure monitoring of intrathoracic pressures may disclose upper airway resistance syndrome.  This condition is treated in the same manner as OSAS.

            The treatment of OSAS is dependent on its severity, the presumed cause, and the patient’s age.  In obese patients with OSA, weight loss or the correction of hormonal abnormalities can improve or eliminate OSA.  However, weight loss is an unrealistic goal for most patients.  Positional therapy, or conditioning the patient to sleep in the lateral recumbent position, is effective in patients with mild OSA in the supine position.  Younger patients and those with craniofacial abnormalities may prefer surgical over medical treatment.

            Mild to severe OSAS may be treated with appliances and/or surgical procedures, which maintain patency of the airway.  Oral appliances are used in patients with mild OSAS or primary snoring.  The basic working principle of oral appliances is that they advance the mandible or pull the base of the tongue forward to enlarge the upper airway.  Mandibular advancing devices, look like mouth guards and tongue retainers, hold the tongue in a bulb of negative pressure, which fits between the teeth and lips (Figure 2).  They can be bought over the counter as prefabricated devices or are designed from dental impressions made by a dentist.

            CPAP (continuous positive airway pressure) is the treatment of choice for moderate to severe OSAS.  It keeps the airway open during sleep by delivering positive air pressure via a nasal mask (Figure 3) or nasal pillows which fit snugly in the nostrils.  CPAP pressures are titrated to eliminate apneas and snoring in a follow-up polysomnogram to the diagnostic study.  In about 80 to 90% of patients, symptoms and cardiac arrhythmias are improved.  However, noncompliance with CPAP is a leading cause of persistent symptoms.  Skin breakdown over the bridge of the nose or, rarely, an allergic reaction to the silicone in the mask may prevent continued use of the mask.  Some patients find the mask uncomfortable or experience claustrophobia.  Several variations of CPAP may circumvent this problem: 1) nasal pillows, 2) a bilevel CPAP device (bi-PAP) which delivers lower positive pressure during expiration than inspiration, and 3) a ramp which gradually increases CPAP pressures over a period of time during which the patient is allowed to fall asleep.  A humidifier attachment prevents drying of mucosal membranes and nosebleeds.  CPAP will be ineffective if the patient is a mouth-breather, in which case a chin strap is used to prevent pressure loss.

            Surgery is considered when CPAP cannot be tolerated or fails to treat OSAS adequately.  Surgery is designed to reconstruct the upper airway at a particular site or bypass it altogether. Tracheostomy is the last option considered and rarely performed.  In most children with OSAS, tonsillectomy and adenoidectomy is effective treatment, but not so in adults.  Uvulopalatopharyngoplasty (UPPP) is the most common upper airway surgery performed in adults with primary snoring.  It enlarges the retropalatal airway through a tonsillectomy, excision of the uvula and posterior portion of the palate, and excision of tonsillar fossae mucosa if tonsillectomy has already been performed (Figure 4).

Complications from a UPPP are rare, but include nasal reflux of liquids, postoperative bleeding, nasopharyngeal stenosis, voice change, vague foreign body sensation and death secondary to airway obstruction.  While UPPP may initially improve mild OSAS, its success diminishes with time and is thus not considered a reliable treatment option for OSAS.  Laser-assisted uvulopalatopharyngoplasty (LAUP) is indicated for snoring only.  A LAUP involves laser-guided resection of the soft palate and uvula (Figure 5), which is less than the amount of tissue resected in a UPPP.

This procedure is highly successful for elimination of snoring, but postoperative pain in the area of surgery has caused it to lose favor as a treatment option.  Genioglossal advancement (GA) is designed to enlarge the retrolingual airway by pulling the base of the tongue anteriorly (Figure 6).

It is often performed after unsuccessful UPPP.  The success rate for GA, with or without previous UPPP, is high.  Maxillomandibular advancement (MMA) is typically performed after failed GA, except in patients with primary facial skeletal deformities in whom MMA is the treatment of choice.  It allows for maximal enlargement of the retrolingual airway, as well as enlargement of the retropalatal space.  Maxilla and mandible are advanced simultaneously, thereby advancing the base of the tongue more than GA (Figure 7). The response rate to MMA is close to 100%.   The major complication is transient anesthesia of the cheek and chin.  After all surgical procedures, a follow up polysomnogram is indicated to document the success of treatment.  Because of the diminishing efficacy of surgery in some patients, serial polysomnograms may be warranted, particularly if the patient complains of recurrent symptoms.

            Narcolepsy is a chronic disorder of unknown etiology.  It usually begins in the second to third decade of life, rarely before age 5 or after age 50.  It affects men and women equally.  Narcolepsy is characterized by a tetrad of symptoms: 1) excessive daytime somnolence, 2) sleep paralysis, 3) hypnagogic hallucinations, and 4) cataplexy.  Only 20 to 25% of patients experience the full tetrad of symptoms.  The symptoms of narcolepsy reflect the inappropriate intrusion of REM sleep and its properties of atonia and visual hallucinations into wakefulness and other stages of sleep.  For example, sleep paralysis occurs when REM-associated atonia intrudes on the transition between wakefulness and sleep.  The patient is consciousness, but unable to move his limbs.  Hypnagogic hallucinations are vivid, REM-associated dream-like visual hallucinations which occur at sleep onset, while hypnapompic hallucinations occur upon awakening.  Sleep paralysis, hypnagogic hallucinations and hypnapompic hallucinations can occur in normal people who have a disruption in their normal sleep pattern, as with sleep deprivation.

Cataplexy is unique to narcolepsy, although about 30% of patients with narcolepsy do not experience it.  REM-associated atonia intruding into wakefulness causes loss of axial and/or appendicular muscle tone for a few seconds, without loss of consciousness.  The longer the episode, the more likely it will lead directly into REM sleep.  This phenomenon is often precipitated by extremes of emotion, such as anger, fear, excitement, or, most commonly, laughter.  It can occur several times daily or rarely.  Cataplexy can endanger a person’s life if it occurs while driving, bathing or swimming.

Restless sleep is a common complaint among patients with narcolepsy, but not a major cause of daytime sleepiness.  Sleep apnea and periodic limb movements of sleep occur with higher frequency in patients with narcolepsy compared to the general population, but the treatment of these conditions does not improve daytime sleepiness.

            The cause of narcolepsy has yet to be determined.  An immunologic cause has been suggested by the high association of certain class II human leukocyte antigens (HLA) in patients with narcolepsy with cataplexy.  Greater than 85% of narcoleptic patients with cataplexy, of various ethnic backgrounds, share a specific HLA allele, DQB1*0602 (previously known as DQw1), often occurring concomitantly with HLA DR2, in comparison to 12 to 38% of the general population.  Other associated HLA antigens have been reported.  Nevertheless, class II HLA typing is not a routine diagnostic test as these antigens may be absent in some patients with narcolepsy with cataplexy and present in asymptomatic persons.

            The definitive diagnosis of narcolepsy is based on a polysomnogram that reveals no cause of hypersomnia and a multiple sleep latency test (MSLT).  The MSLT is a daytime study that consists of a series of four to five nap trials.  Severity of daytime sleepiness is based on sleep latency, or time it takes a subject to fall asleep, and presence of sleep-onset REM (SOREM), or REM sleep within 10 minutes of sleep onset.  A sleep latency of less than 5 minutes is indicative of a pathologically sleepy state, while a sleep latency of 5-10 minutes is only suggestive of it.  The laboratory diagnosis of narcolepsy requires an average sleep latency of less than 10 minutes and SOREM in at least two nap trials.  As SOREM can occur with REM-sleep deprivation from sleep apnea or drug and alcohol withdrawal, an overnight polysomnogram prior to the MSLT is done to screen out such causes.  A two-week period of alcohol or drug abstinence is required before an MSLT.  Compliance can be monitored with a drug screen prior to the study.

            The treatment of narcolepsy is often difficult.  Excessive daytime sleepiness and cataplexy are particularly difficult to treat.  The mainstay of treatment is a combination of several planned naps daily and CNS stimulants, such as pemoline, methylphenidate, amphetamine, and modafinil (Provigil®).  To avoid medication tolerance, weekly drug vacations for one to two days are recommended.  Cataplexy, sleep paralysis and hypnagogic hallucinations are treated with tricyclic antidepressants, namely clomipramine, imipramine, nortriptyline, and protriptyline, and other serotonin reuptake inhibitors such as fluoxetine.

            There are three major circadian rhythm sleep disorders: 1) delayed sleep phase syndrome, 2) advanced sleep phase syndrome and 3) non-24 hour sleep-wake syndrome.  In delayed sleep phase syndrome, patients usually go to sleep about 6-8 hours later than socially acceptable.  Once asleep, however, sleep architecture and duration are normal.  Patients complain of nocturnal insomnia and daytime sleepiness.  Psychopathology is common.  Delayed sleep phase syndrome occasionally coincides with the onset of bipolar disorder or schizophrenia.  Lifestyle, mood, personality, family problems and school problems may be contributing factors.  Sometimes, delayed sleep phase syndrome begins in childhood and persists throughout life.  It can be familial.  The success of treatment with hypnotics, melatonin, stimulants, and psychotherapy is highly dependent on patient motivation, but is usually disappointing.  Chronotherapy, which involves delaying bed time by one hour every day, until the desired bed time is achieved, is usually not successful.   Another way to advance the circadian rhythm is to expose the patient to a bright light of greater than 5000 lux in the early morning, between 5 and 8 a.m.  The results are highly dependent on patient motivation.

            Advanced sleep phase syndrome is very rare and is thus questioned as a true entity.  It is characterized by early evening sleep onset, i.e. 7 or 8 p.m., and early morning awakening.  Sleep duration and architecture are normal.  Attempts to delay the time of sleep onset are usually unsuccessful.  The sleep patterns of the elderly most closely match the advanced sleep phase syndrome.  The major difference is that the total duration of nocturnal sleep in the elderly is shorter and fragmented.  Chronotherapy may be beneficial, as with delayed sleep phase syndrome.  For patients with advanced sleep phase syndrome, exposure to bright light between 9 p.m. and 1 a.m. may induce a phase shift in bed time.

            The irregular sleep-wake pattern or non-24 hour sleep-wake syndrome reflects a complete loss of circadian rhythm.  There is disorganization and tremendous variability in the sleep-wake schedule.  Overall sleep in a 24-hour period is reduced and fragmented into short sleep periods.  The fragmentation of sleep parallels the random fluctuations in body temperature as well as the irregularity of other lifestyle habits such as meals.  Typically, patients complain of daytime sleepiness, fatigue, and insomnia.  Alzheimer’s dementia may be associated with the irregular sleep-wake pattern, although circadian rhythm of core body temperature is preserved.  Behavioral treatment is the mainstay of establishing a normal sleep-wake schedule.  A set bedtime is established.  The number of naps are restricted.  In some Alzheimer’s patients, bright lights have been used in the early evening with some success in reducing sleep fragmentation and sundowning.

            The diagnosis of circadian rhythm disorders is based on history and the examination of detailed sleep diaries.  A polysomnogram may be helpful in assessing time at sleep onset, total sleep time, and sleep architecture while the MSLT can be used to determine severity of daytime sleepiness in patients refractory to treatment for the assumed diagnosis.

            Hypnic jerks or sleep starts are brief jerks of one or more limbs during sleep onset.  They are normal.  Often, they may be accompanied by a sensation of falling.  Exercise, emotional stress or caffeine in the evening are precipitants.  No treatment is required.

            Sleep myoclonus refers to rhythmic leg jerking, usually involving the tibialis anterior.  It is commonly benign, often familial, and increases with age.  The diagnosis is based on history provided by the patient’s bed partner and the electomyographic appearance of rhythmic leg movements on polysomnogram.  Although the etiology is idiopathic, it has been associated with some medical conditions such as uremia and anemia, neurologic disorders such as sensory neuropathy, narcolepsy, and drug treatment with levodopa for Parkinson’s disease, clomipramine for depression, and amphetamines for narcolepsy.  Most patients with sleep myoclonus are asymptomatic.  Treatment with clonazepam is recommended only when patients complain of insomnia or daytime somnolence. 

            Periodic limb movements of sleep (PLS) are characterized by repetitive, stereotyped, and asymmetrical leg movements during sleep.  The leg movements are often, but not always, associated with cyclical arousals or awakenings.  The patient is usually unaware of the limb movements or fragmentation of sleep.  PLS may present as insomnia or, less commonly, as excessive daytime somnolence.  Men and women are equally affected.  Prevalence increases with age, but is rare before the age of 30.  The etiology is unknown.

            PLS frequently occurs in association with restless legs syndrome (RLS).  RLS is characterized by an uncomfortable, ill-described sensation involving the calves, which results in an irresistible urge to move the legs.  Symptoms are most severe when the legs are at rest.  Most patients with RLS have PLS, but the reverse is not true.  In patients with RLS, the major identifiable cause is sensory peripheral neuropathy.

            The diagnosis of PLS is confirmed by a polysomnogram, which demonstrates a series of periodic bursts of muscle activity over the leg EMG leads.  These bursts of muscle activity are often followed by brief arousals or awakenings.  Occasionally, PLS is an incidental finding, often associated with no or infrequent arousals.  The polysomnogram can also exclude other causes of excessive daytime somnolence associated with frequent nocturnal limb movements, namely sleep apnea and fragmentary myoclonus. 

            Levodopa, benzodiazepines, and the opioids constitute first-line therapy for PLS and RLS.  Long-term treatment with these medications is hindered by tolerance.  Pergolide has been shown to be effective alternative therapy, although other antiparkinsonism medications and some antiepileptic medications are only anecdotally reported as promising to date.

            Head banging, otherwise called rhythmic movement disorder or jactatio capitis nocturna, often involves body rocking.  These movements, which are pleasurable to the patient, occur during sleep onset and stages 1 and 2 of sleep.  It is usually confined to infancy and early childhood.  Predisposing factors are low IQ, immaturity, and maternal neglect.  Most children are normal.  Trauma is unusual, although subdural hematoma and retinal hemorrhage may occur.  Treatment is recommended only if injuries occur.  Benzodiazepines reduce, but do not eliminate, this behavior.

            Sleep paralysis refers to paralysis of skeletal muscles during the transition from wakefulness to sleep or from sleep to wakefulness.  The severity of paralysis is variable from patient to patient.  Some patients have mild weakness of the limbs, while others cannot open their eyes or speak.  It is often described as a terrifying experience.  Respiration is unaffected.  Sleep paralysis may occur under four different circumstances: 1) an isolated, rare event, 2) familial, in which case it can occur several times nightly and may be associated with excessive daytime sleepiness, 3) as a symptom of narcolepsy, or 4) as result from sleep-onset REM secondary to sleep deprivation or sleep fragmentation.

            REM sleep behavior disorder is characterized by retention of muscle tone during REM, a finding confirmed by polysomnogram.  Under normal circumstances, REM sleep is characterized by loss of muscle tone and paralysis.   Patients with REM sleep behavior disorder are able to enact their dreams, which are usually frightening and combative.  Self-injury or injury to bed partners is usually the precipitating reason for medical attention.  This condition most commonly occurs in elderly men.  Most cases are idiopathic although it may occur in diseases that affect anatomical areas responsible for REM sleep, for example dementia, subarachnoid hemorrhage, stroke, brainstem lesions and multiple sclerosis.  Treatment is quite satisfactory in most cases with clonazepam 0.5-1.0 mg at bedtime.

            Sleepwalking, night terrors and nightmares are distinguished by the particular sleep stage in which these behaviors occur.  Sleepwalking and night terrors occur during slow wave sleep, usually within the first two hours of sleep.  They are more common in children and may be familial.  Most children are normal, contrary to popular belief, and outgrow these behaviors.  Sleep deprivation, anxiety or fever are predisposing factors.  Sleepwalking and night terrors are associated with variable degrees of responsiveness.  Night terrors are characterized by piercing, inconsolable crying and autonomic hyperactivity, i.e., tachycardia, piloerection, and sweating.  If awoken, children are disoriented and cannot recall what has happened.  The inability to recall a dream, as well as its occurrence during slow wave sleep, is what distinguishes night terrors from nightmares.  Most children with nightmares have some recall of content, as it is essentially a terrifying dream during REM sleep.

            A regular sleep schedule is usually effective treatment for sleepwalking.  When self-injury occurs as a result of sleep walking, diazepam 2-5 mg nightly may be beneficial because it reduces arousals.  Tricyclic antidepressants may also help reduce sleep walking although it can also exacerbate it in some patients.  Benzodiazepines can be prescribed to treat severe, frequent night terrors. 

            Bruxism or teeth grinding is relatively uncommon.  It may result in abnormal wear of teeth or jaw pain.  This behavior usually occurs during the early stages of sleep and is often associated with stress.  It is also observed in patients with mental retardation or in comatose states.  A tooth guard may prevent undue wear of teeth.

            Bed-wetting occurs in all stages of sleep, including REM sleep.  It is often familial and slightly more common in boys than girls.  The etiology is believed to be a combination of behavioral and psychiatric problems.  If bed-wetting occurs after a period of dryness at night, one should consider diseases of the urinary tract or spinal cord.  Behavioral therapy may be effective, with positive reinforcement for dry nights and negative reinforcement with a buzzer that goes off when a pad is soaked.  Tricyclic antidepressants, such as imipramine 10-25 mg nightly, may also be beneficial because urinary retention is one of the anticholinergic side effects.  Hypnotics, however, may worsen bed-wetting.

            Primary care physicians routinely see patients with chronic diseases or conditions that can interrupt, delay, or disrupt sleep.  Among them are chronic obstructive pulmonary disease, asthma, congestive heart failure, rheumatoid arthritis, back pain, sickle cell disease, osteoporosis, cancer, Parkinson’s disease, dementia, Alzheimer’s disease, incontinence, heartburn, gastroesophageal reflex, nocturnal cardiac ischemia, and peripheral vascular disease. 

            For patients with insomnia, male patients are more likely to be diagnosed with an organic illness than are female patients, and physicians tend to diagnose depression in women with insomnia more often than in men.   Office visits for insomnia are more likely for female patients between 45 and 64 years of age.  Menopausal symptoms may contribute to some patient encounters for insomnia.  For example, women who have hot flashes sleep less efficiently, wake more often, and stay awake longer.  Although estrogen replacement therapy reduces hot flashes and improves sleep, only about one-fourth of women use it. 

            Practitioners need to be aware of possible gender bias in treatment and recommendations for management of insomnia.  Early diagnosis and appropriate treatment for all patients is important because those with chronic insomnia are at higher risk of developing major depression than those with transient insomnia.  In addition, excessive sleepiness can lead to problems with attention, performing at work or school, or dangerous situations such as driving or working with machinery. 

            Elderly patients may not bring up sleep problems in an office visit because of misconceptions about sleep and aging.  For example, they may believe that poor sleep is a consequence of aging, that older people need less sleep, or that it is normal to feel sleepy in the afternoon and awaken early.  A study by the National Institute on Aging found that over half of persons aged 65 and older reported trouble in such areas as falling asleep or staying asleep, waking too early, needing to nap, and not feeling rested.  Complaints often were associated with respiratory disease, arthritis and other illnesses causing pain, nocturia, physical disabilities, prescription and nonprescription drugs, depression, changes in daily schedules (such as might happen after the death of a spouse), and self-perceived poor health.

            Identifying sleep disorders among children may be difficult because of differences in sleep patterns based on developmental stages.  Parents may have unrealistic expectations about when an infant should “sleep through the night.”  About 30% of children up to 4 years old still awaken at night and need some action or intervention from a parent to go back to sleep.  Social factors may disrupt a child’s sleep, and the child may then resume waking during the night.  Common sleep problems in children tend to be episodic and reflect CNS immaturity, and children generally outgrow them.  There may be a family history of parasomnias, including night terrors, somnambulism, somniloquy, nocturnal enuresis, narcolepsy (uncommon in children, but may occur in adolescence), obstructive sleep apnea syndrome (1-3% of children), or snoring associated with allergies. 

            Sleep problems need to be addressed in the context of the family and other caregivers in identifying sleep patterns and behaviors and in developing interventions that could or would be followed.  For example, persons in some cultures might be unwilling to let an infant cry itself to sleep.  Other families might not live in circumstances that allow an environment needed for ideal sleep hygiene.  Listen to family concerns, and offer (physician or staff member) support by phone or follow-up visit. Quality of life for patients of any age, as well as that of their families, is always a consideration in diagnosis, treatment, and management of sleep disorders.

References

1. Aldrich M, ed. Sleep disorders I. Neurol Clin 1996;14(3):493-670.
2. Aldrich M, ed. Sleep disorders II. Neurol Clin 1996;14(4):675-840.
3. Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. 3rd ed. Philadelphia: WB Saunders, 2000.
4. Lamberg L.  ‘Old and Gray and Full of Sleep’?  Not Always.  JAMA 19979;278(16):1302-1304.
5. Mahowald MW. Diagnostic testing. Sleep disorders. Neurol Clin 1996;14(1):183-200.
6. Namen AM.  Performance of sleep histories in an ambulatory medicine clinic.  Chest 1999;116:1558-1563.
7. National Center on Sleep Disorders Research Working Group.  Recognizing problem sleepiness in your patients.  American Family Physician 1999;(2) 59:937-944.
8. Radecki SE, Brunton SA.  Management of Insomnia in Office-Based Practice.  National Prevalence and Therapeutic Patterns.  Arch Fam Med;2:1129-1134.
9. Roth T, ed. Insomnia. Sleep 1999;22(Suppl 3):S413-S452.
10. Roth T, ed. Practical management of insomnia in primary care: An overview for the busy practitioner. Sleep 2000;23(Suppl 1):S1-S48.
11. Thiedke CC.  Sleep disorders and sleep problems in childhood.  American Family Physician 2001;63:277-84.  Article has tables of sleep disorders by age and suggested interventions and questions to ask parents about the child’s sleeping pattern (well child visit).

Internet Resources (Sources of patient education materials and support)

www.sleepfoundation.org - The National Sleep Foundation (NSF) is an independent nonprofit organization that supports public education about sleep disorders, sleep-related research, and advocacy.

www.sleepapnea.org - The American Sleep Apnea Association was founded in 1990 as a non-profit by persons with apnea, health care providers, and researchers.

www.narcolepsynetwork.org - Narcolepsy Network is a national, non-profit organization incorporated in 1986.

www.rls.org - Restless Leg Syndrome Foundation

www.aasmnet.org - American Academy of Sleep Medicine.  Web site includes MEDSleep Education materials, including a self-assessment instrument.

www.familydoctor.org/handouts, site for patient handouts developed for the AAFP.  A number of topics related to sleep disorders are available.

Self-Assessment

1.  Night terrors are characterized by:

A.  Occurrence during slow wave sleep
B.  Occurrence during REM sleep
C.  A child’s ability to recall the content of a terrifying dream
D.  Persistence into adulthood
E.  Psychopathology

2.  Obstructive sleep apnea is:

A.  More common in men than women
B.  Often associated with snoring
C.  Due to obesity
D.  All of the above
E.  A & B

3. The stage of sleep, which remains relatively constant throughout life, relative to total sleep time, is:

A.  Stage I
B.  Stage II
C.  Stage III
D.  Stage IV
E.  REM sleep

4.  Daytime somnolence and insomnia are most likely to be the presenting complaints of:

A.  Delayed sleep phase syndrome
B.  Non-24 hour sleep-wake syndrome
C.  Primary snoring
D.  Sleep walking
E.  Advanced sleep phase syndrome

5.  Narcolepsy is characterized by:

A.  Excessive daytime somnolence
B.  Sleep paralysis
C.  Periodic limb movements of sleep
D.  A & B
E.  A, B & C

6.  Sleep deprivation may cause or precipitate all of the following, except:

A.  Sleep paralysis
B.  Hypnagogic hallucinations
C.  Sleepwalking
D.  Periodic limb movements of sleep
E.  Sleep-onset REM

7.  Periodic limb movements of sleep most commonly coexists with:

A.  Narcolepsy
B.  Obstructive sleep apnea
C.  Central sleep apnea
D.  Restless leg syndrome
E.  Sensory peripheral neuropathy

Answers

1. A.   Night terrors occur during slow wave sleep while nightmares occur during REM sleep.
2. E.  Obstructive sleep apnea is more common in men than women and is often, but not always, associated with snoring.  Obesity, while commonly associated with obstructive sleep apnea, is not the sole cause.
3. E. The percentage of REM sleep, relative to total sleep time, remains fairly constant after the first year of life.
4. B.  In non-24 hour sleep-wake syndrome, sleep is reduced and fragmented. Patients complain of daytime sleepiness, fatigue, and insomnia.
5. D.  Narcolepsy is characterized by excessive daytime somnolence, hypnagogic hallucinations, sleep paralysis and cataplexy.  Periodic limb movements of sleep are not a symptom of narcolepsy although it occurs with higher frequency in patients with narcolepsy than the general population.
6. D.  Sleep paralysis, hypnagogic hallucinations, and sleep-onset REM can occur in normal individuals with a disruption in normal sleep pattern.  Sleep deprivation may predispose to sleepwalking.
7. D.  Restless leg syndrome and periodic limb movements of sleep often coexist and, together, constitute the fourth most common cause of insomnia.  Sensory peripheral neuropathy is the most common identifiable cause of restless leg syndrome.

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