The Recognition and Management of Sleep Disorders
The Recognition and Management of Sleep Disorders
Author: David N. Neubauer, MD, Associate Director, Johns Hopkins Sleep Disorders Center, Assistant Professor, Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD.
Peer Reviewer: Judith A. Owens, MD, MPH, Director, Pediatric Sleep Disorders Clinic, Rhode Island Hospital, Portsmouth, RI.
Editor’s Note—Sleep problems are widespread in our society, and primary care medicine is at the front lines of sleep disorder recognition and management. National Sleep Foundation surveys show that about one-half of U.S. adults have some problem with their sleep. It is clear that sleep disorders not only have major consequences for individuals, they also cause significant public health problems and a considerable societal economic burden. The challenge in primary care includes the identification of sleep-disordered patients, as well as the appropriate management of those patients presenting with sleep complaints.1 Identifying sleep problems is especially important since many patients either are not aware that they have a sleep disorder or they raise it as a problem to their physician. Sleep apnea, for example, is relatively common and may have significant consequences, but may not be evident to the affected individual.
The symptoms of sleep disorders are quite varied, ranging from the inability to sleep at desired times (insomnia) to the inability to stay awake at appropriate times (excessive daytime sleepiness), and even to assorted behaviors and physiological events that emanate from sleep (parasomnias). These symptom-based categories, while overlapping in some patients, nevertheless are useful in organizing the common sleep disorders and helpful in leading to appropriate evaluation and treatment.
Three major nosologies attempt to define and organize sleep disorders.2-4 Each has strengths and weaknesses. The DSM-IV and ICD-10 use rather broad categories, while the International Classification of Sleep Disorders (ICSD) lists scores of common and esoteric disturbances of sleep. Diagnostic coding requirements most commonly determine which nosology is used.
This sleep disorders review initially will consider the characteristics and regulation of normal sleep. Following this will be three sections reviewing the symptoms, causes, and treatment of disorders related to insomnia, excessive daytime sleepiness, and the parasomnias. These will emphasize the more common and important disturbances encountered in primary care practice. Finally, there will be a review of guidelines in the evaluation of sleep complaints and the potential value of sleep center consultation and testing.
Normal Sleep
An understanding of general sleep characteristics is necessary to appreciate the context of subjective patient complaints and the physiological processes that may undermine sleep and wakefulness. The regulation of the sleep-wake cycle involves two processes that usually operate in concert, but which can be dissociated under naturalistic (e.g., shift work) and experimental circumstances.5 The homeostatic process represents the overall balance of sleep and wakefulness with an approximate 1:2 ratio—eight hours of sleep and 16 hours of wakefulness. Sleep deprivation, acute or chronic, builds up homeostatic pressure resulting in sleepiness.6 Sleep discharges the pressure. Brain energy storage and metabolism may be important in this process.
A circadian process is responsible for the typical nighttime sleepiness and daytime alertness cycle driven by the suprachiasmatic nucleus (SCN), the brain’s timekeeper. This rhythm influences the typical nighttime pattern of melatonin production and secretion. Generally, circadian sleepiness peaks toward the end of the normal sleep period (about 4:00 a.m. - 5:00 a.m.), while circadian alertness peaks toward the end of the waking period (about 7:00 p.m. - 8:00 p.m.). In addition to the late night sleepiness peak, inherent in the normal daily rhythm is the familiar afternoon increase in sleepiness. Often sleep-wake problems occurring in the context of schedule changes (e.g., shift work and jet lag) can be understood in terms of the interaction of the homeostatic and circadian influences.
Under normal circumstances the homeostatic and circadian processes operate together to allow eight hours of sleep and 16 hours of wakefulness. The entire system is strongly influenced by the photoperiod, and for most people the timing of the clock is reset daily with dawn light. The circadian oscillator has a period of slightly more than 24 hours, producing a progressive phase delay tendency.7 The biological influence of light has significant therapeutic implications for selected patients.
Although many people sleep from about 11:00 p.m. until about 7:00 a.m., others have sleep-wake cycle phases with considerably earlier (early bird) or later (night owl) patterns. There is a general developmental tendency for adolescents to be phase delayed, with a later sleep onset and arising in the morning. With aging the phase advances, culminating in the common elderly pattern of early evening sleepiness and early morning awakening.
Sleep varies considerably during the night, with dramatic EEG pattern changes and periods of rapid eye movements and decreased muscle tone. Rapid eye movement (REM) sleep, typically accounting for 15-25% of total sleep, is quite distinct from the remainder of sleep, termed non-REM (NREM). By convention, NREM is divided into four stages of increasing depth defined by EEG characteristics, with the deeper stages associated with marked high-amplitude EEG slowing in the delta (0.5-3.0 Hz) range. A typical night’s sleep follows a general pattern of REM beginning about 90 minutes following sleep onset and repeating about every 90 minutes for a total of four to five episodes during the night. The REM episodes tend to increase in duration throughout the night, so the greater amount of REM sleep usually is during the latter part of the night. In contrast, most deep sleep (NREM, stages 3 and 4) occurs during the first few hours of a night’s sleep. These patterns are useful in diagnosing certain parasomnias.
With aging, the REM sleep duration and pattern are preserved; however, deep sleep diminishes considerably.8,9 There also are increased arousals and awakenings, as well as the above noted phase advance. Elderly individuals may have greater difficulty maintaining sustained nighttime sleep; however, it is not clear that the need for sleep decreases with aging.10
Insomnia
Insomnia, the most common sleep complaint, is the report of inadequate and unrefreshing sleep. The description may be difficulty initiating or maintaining sleep, and the presentation may include early morning awakening and inadequate total sleep time. Usually there is an integral daytime component, such as fatigue and exhaustion.11 The episode may be transient or chronic, single or recurrent, and of varying degrees of severity. The potential causes of insomnia are plentiful.12 (See Table 1.) It is important to consider long-term vulnerabilities and more acute precipitants in evaluating patients with insomnia complaints, as treatment may need to be multifaceted.
| Table 1. Causes of Insomnia |
| • Situational disturbances |
| • Psychiatric disorders |
| • Medical disorders |
| • Medication effects |
| • Stimulants (e.g., caffeine, nicotine) |
| • Primary sleep disorders |
| • Psychological conditioning |
| • Environmental factors (e.g., light, noise) |
| • Sleep-wake habits |
Everyone is vulnerable to situational disturbances that can interfere with sleep, at least transiently. Stressful episodes with insomnia mostly relate to life problems; however, excitement also can impair sleep. Psychiatric disorders account for a large percentage of insomnia.13 Major depression predictably promotes insomnia with sleep disturbance throughout the night, not just the classic early morning awakening. Most other psychiatric disorders, especially anxiety disorders, during acute phases readily can cause insomnia. A multitude of medical conditions associated with pain, discomfort, and fear can undermine the ability to sleep soundly. Examples include arthritis, chronic back pain, gastroesophageal reflux, hyperthyroidism, chronic lung disease, renal insufficiency, and fibromyalgia. Insomnia is a potential side effect of many medications, including some antidepressants and antihypertensives, corticosteroids, and decongestants.14 Nicotine is stimulating, and caffeine can continue to exert its alerting effects for eight hours or more. Bedtime alcohol, while initially sedating, after a few hours then promotes hyperarousal and increased awakenings during the night. Patients with primary sleep disorders, including circadian rhythm disorders, sleep-disordered breathing, restless leg syndrome, and periodic limb movement disorder, may present with insomnia as the chief complaint. Psychological conditioning of mental hyperarousal associated with attempts to sleep and the fear of not sleeping can perpetuate insomnia symptoms indefinitely. Finally, the fundamental processes promoting normal sleep can be undermined by assorted behaviors, routines, and habits. These may include irregular and changing schedules, inadequate evening relaxation, and strenuous exercise within a few hours of bedtime.
Surveys demonstrate that more than one-third of adult populations complain of at least occasional insomnia, and about 10-15% experience severe or persistent symptoms. Although insomnia occurs in all population subgroups, increased risk is recognized for the elderly and for women, especially with menopause and thereafter.10 Lower socioeconomic status, divorced and single status, and living alone additionally represent increased risk.
The consequences of insomnia include not only the immediate distress of sleeplessness, but also significant decrements in concentration, performance, mood, and other quality-of-life measures.15 Several studies have established the increased risk of new onset major depression in the context of persistent insomnia.13,16-18 The total direct costs of insomnia in the United States are estimated in the billions of dollars.19 Such values include office visits and medications (prescription and OTC), but not the huge indirect costs, such as those related to mistakes, accidents, and absenteeism.20 Sleep-wake cycle disruption may also contribute to the nursing home placement of individuals who otherwise might be managed by family members at home.
The multitude of potential insomnia causes demonstrate the need for a broad-based evaluation of patients complaining of sleep disturbance. Insomnia treatment first should address underlying disorders (medical, psychiatric, and other sleep disorders) and potential undesired stimulating or sedating medication effects. Specific questions for the patient and bed partner should address snoring and the breathing pattern, as well as body movements during sleep. Patient education about normal sleep will promote realistic expectations and create the foundation for any necessary schedule and behavior changes. Good sleep habits should be reviewed (see Table 2). The physician and patient may work in partnership in trying to isolate key factors that seem particularly influential on that person’s sleep. The use of a daily sleep log detailing times in and out of bed, estimated sleep onset and awakenings, daytime functioning, as well as behavior changes and medication trials can be quite useful for diagnostic and treatment efficacy purposes. For selected patients, more directive behavioral strategies can be therapeutic. One approach, termed stimulus control, is to have the patient with excessive mental arousal (e.g., "mind racing") while in bed spend more time out of bed when he or she is unable to sleep. The patient is instructed to go to bed only when sleepy, and to leave the bed if unable to fall asleep quickly or during extended nighttime awakenings. This can help decondition the association between being in bed and the experience of persistent frustration and agitation. A technique called sleep restriction involves limiting the time in bed available for sleep. A normal morning wakeup time remains constant and the bedtime, initially rather late, is gradually scheduled earlier as the percentage of sleep time increases. Psychotherapeutic techniques can address personal conflicts and distressing life situations, as well as help reframe cognitive distortions about sleep.21-23 These behavioral and psychotherapeutic strategies often are combined successfully with the use of short-acting hypnotics.
| Table 2. Sleep Habit Issues |
| • Wakeup time |
| • Bedtime |
| • Napping |
| • Evening routines |
| • Sleep environment |
| • Exercise |
| • Caffeine |
| • Alcohol |
Circadian rhythm influences are present in many insomnia cases. These are obvious in the context of jet lag and shift work, but also are important with the severe early birds (advanced sleep phase syndrome) suffering with chronic early morning awakening, and the severe night owls (delayed sleep phase syndrome) with chronic initial insomnia and a desire to sleep well into the daylight hours. In these situations treatment should include attention to the patient’s exposure to light and darkness. One approach to the advanced sleep phase problem is maximizing bright light exposure in the evening and minimizing light exposure around dawn. Therapeutic light boxes may be used in the evening. Dark curtains or an eye mask can help decrease the morning light. Generally, the individual with a delayed pattern may benefit from minimizing evening bright light and maximizing morning light.
Medications may play a valuable role in the treatment of acute and chronic insomnia for selected patients. Clearly, antidepressants are important when a depressive disorder is present. Antidepressant selection is complicated by potential side effects, including worsened insomnia due to stimulating action or daytime somnolence from the relatively long half-lives of many medications. The combination of an antidepressant and a hypnotic may be beneficial.
OTC antihistamines (diphenhydramine, hydroxyzine, doxylamine, and pyrilamine) are used widely because of the availability and perceived safety. Possible problems with these include morning grogginess after bedtime use because of the long duration of action, and also potential anticholinergic side effects. Theses may include dry mouth, constipation, urinary retention, and confusion. The anticholinergic effects may be especially detrimental for elderly individuals.
Most prescription hypnotics in current usage are positive allosteric modulators of the GABAA receptor complex and function as benzodiazepine receptor agonists.24 These include the traditional benzodiazepines and newer nonbenzodiazepine agonists, zolpidem and zaleplon. These newer agents are short half-life preparations, minimizing daytime sedation. Nightly use of long half-life agents increases the pharmacokinetic risk of accumulation and subsequent daytime sedation. The newer short-acting hypnotics generally are safe, efficacious, and well tolerated. These medications are appropriate for a variety of short-term uses (days to weeks). Selected patients appear to benefit from longer-term usage; however, further research regarding such extended hypnotic use is necessary to establish appropriate indications and guidelines.25 Intermittent dosing with general directions of the maximum number of pills per week or month can offer the patient a sense of control in dealing with the sleep disturbance. This strategy can be therapeutic even on those nights the medication is not taken since the fear of unending sleeplessness may be reduced. Dosing should follow the prescribing guidelines for each medication. Typically this involves a reduced dose for the elderly and those with hepatic impairment. Considering the current selection of available hypnotics (see Table 3), there is no reason to consider the barbiturates and rarely an indication for the long-acting benzodiazepines in the management of insomnia. Certainly, hypnotics should be used in the greater context of attention to the assortment of factors that may be stimulating and perpetuating the insomnia.
| Table 3. Hypnotic Medications | ||
| Generic Name | Brand Name | Dosage Range (mg) |
| Long-acting | ||
| Flurazepam | Dalmane | 15-30 |
| Quazepam | Doral | 7.5-15 |
| Intermediate-acting | ||
| Temazepam | Restoril | 7.5-15 |
| Estazolam | ProSom | 1-2 |
| Short-acting | ||
| Triazolam | Halcion | 0.125-0.25 |
| Zolpidem | Ambien | 5-10 |
| Zaleplon | Sonata | 5-10 |
Excessive Daytime Sleepiness
Excessive sleepiness during desired times of wakefulness is a major societal problem. The U.S. Department of Transportation estimates there are 100,000 fatigue-related driving accidents annually. Workplace accidents due to sleepiness are common, particularly in shift work situations. Chronic sleepiness and fatigue plague millions of people in our society, representing about 5% of the population. By far, the most common cause of excessive sleepiness is simply sleep deprivation resulting from inadequate time allotted for sleep; however, several sleep disorders may be primary causes. Due to the safety and health implications, complaints of excessive daytime sleepiness always warrant clinical evaluation.
Sleep-Disordered Breathing
Sleep-disordered breathing (SDB), which includes sleep apnea, involves repeated interruptions in airflow exclusively during sleep.26 Complete airflow cessation for at least 10 seconds is termed an apnea, while a partial (50% or greater) reduction is a hypopnea. The events typically are associated with a transient decrease in blood oxygen saturation. There also may be EEG-defined arousals, of which the sleeper generally is unaware. The frequency of the combined apneas and hypopneas is reported as the respiratory disturbance index (RDI) or apnea hypopnea index (AHI), which is the same value derived from polysomnographic studies. These may be listed separately for NREM and REM sleep. The former is more significant, since NREM sleep constitutes the majority of the night, although the rate during REM sleep may be greater due to the normal decrease in muscle tone associated with that sleep state. A minimum of five events per hour of sleep defines SDB, although a greater frequency is necessary for clinical significance. A general guideline is five to 29 events per hour being mild, 30-59 events being moderate, and 60 and above being severe. The degree of oxygen desaturation also will contribute to the assessment of severity. Apneic and hypopneic events may recur hundreds of times during a night’s sleep. The airflow reduction causes the oxygen decrease and an increase in carbon dioxide, which, in turn, triggers an arousal and normal breaths until the cycle repeats. Profound fragmentation of sleep can result. SDB has been reported to be present in a healthy community sample in 4% of women and 9% of men.27 The typical natural course is chronic and progressive.
Obstruction of the airway is by far the most common cause of SDB. Individuals may be anatomically predisposed for airway collapse during sleep, and severe cases may be seen in childhood. Enlarged tonsils and adenoids may contribute to the obstruction, especially in children. Obesity is a major risk factor, as is a large neck, particularly a collar size of 17 and greater. It is most common among males; however, the risk for women increases following menopause. Loud and interrupted snoring is common. Gasping and choking episodes may occur. The cessation of breathing may be evident and frightening for a bed partner, who feels the need to nudge him or her repeatedly throughout the night to maintain breathing. The patient may be completely unaware of the breathing disruption and arousals, and only report a sense of unrefreshing sleep and subsequent daytime sleepiness.
The daytime sleepiness resulting from SDB can be quite profound and dangerous, resulting in workplace and driving accidents. There are likely cumulative health detriments. There is a strong association with hypertension.28 Further, untreated sleep-disordered breathing increases the risk for other cardiovascular diseases (e.g., stroke, myocardial infarction, and arrhythmias).
The treatment of obstructive SDB depends upon the severity. For those who are overweight, weight reduction can be beneficial. In mild cases, weight loss alone may be sufficient to normalize breathing. Continuous positive airway pressure (CPAP), which supplies a prescribed amount of air pressure through a nasal mask, is the most common approach for clinically significant cases. CPAP can maintain airway patency and eliminate the repeated obstructive events. Selected patients may benefit from surgical approaches or oral appliances. Experimental methods are exploring alternate techniques to increase the upper airway muscle tone. In rare cases, hypothyroidism may be identified as an underlying cause. Treatment of the thyroid condition subsequently can improve the SDB.
Central apneas and hypopneas result from a decreased respiratory drive, which may be cardiovascular or neurological in origin. With congestive heart failure there may be an increased blood circulation time causing a cyclic pattern of increased and decreased respiration (Cheyne-Stokes). Cerebral, brainstem, and spinal cord lesions may impair the functioning of the respiratory center, thus affecting the breathing pattern. Treatment of the underlying disorder is necessary; however, the administration of oxygen and/or CPAP also may be helpful in some of these cases.
Suspected SDB is evaluated with a polysomnographic study to document the frequency of apneas and hypopneas, degree of oxygen desaturations, percentage of associated arousals, and the type of events: obstructive, central, or mixed. A sleep study also will be performed for proper titration of CPAP. A daytime multiple sleep latency test (MSLT) also may be performed to objectively document the degree of daytime sleepiness. This evidence can further direct treatment.
Restless Leg Syndrome/Periodic Limb Movement Disorder
Restless leg syndrome (RLS) is characterized by an uncomfortable and disconcerting motor restlessness and desire to move the limbs (especially the legs) in the evening when the person is at rest.29 With increasing severity, the restlessness is more intense and may begin earlier in the evening or afternoon. Sleep onset commonly is delayed, and once the person does sleep, usually it is interrupted. Most RLS patients experience episodes of repeated brief involuntary periodic limb movements (PLM) during sleep, and sometimes during waking. These most commonly are expressed as leg kicks and may be associated with arousals. The clinical course of RLS tends to be chronic, and often there is a positive family history. RLS is most prevalent among the elderly. It is exacerbated with caffeine use and may occur transiently during pregnancy. The risk is increased with anemia or simply low iron stores as indicated by a low ferritin level (< 50 mcg/L). Iron supplementation often is beneficial for these patients, so the ferritin level always should be checked in patients presenting with RLS symptoms. More generally, dopaminergic precursors (carbidopa/levodopa) and agonists (e.g., pergolide) have the greatest efficacy for the RLS and PLM symptoms. Secondary pharmacologic approaches include opioids and benzodiazepines. Caffeine elimination and either increases or decreases in evening exercise may benefit some RLS cases.
The PLMs noted above also may occur independent of RLS, and may be recorded in up to 10% of the adult population. These involuntary contractions range from 0.5 to 5 seconds in duration, and from 4 to 120 seconds in periodicity. The contractions involve one or both legs (hip and knee flexion, foot/great toe dorsiflexion), but may generalize to the arms to entire body. These "jerks" may awaken the individual, and may be quite evident to bed partners. The severity of the PLM disorder is represented by the frequency of the contractions and the percentage causing EEG-defined arousals. People with the vulnerability for PLM disorder often experience an increased severity while taking most antidepressants. While RLS is a clinical diagnosis based on the history, PLM disorder is documented with a sleep laboratory study.
Narcolepsy
Narcolepsy is a genetically influenced disorder with a prevalence in less than 0.1% of the population. Symptoms usually emerge by the late teens or early 20s; however, the onset often is insidious, and diagnosis and treatment may await many years. The primary symptom in narcolepsy is persistent excessive sleepiness with superimposed episodes of irresistible sleep. These symptoms may be debilitating, with effects in all aspects of one’s life: relationships, education, and occupation. Cataplexy, hypnogogic hallucinations, and sleep paralysis also may be seen as part of the narcolepsy symptom complex. Unlike hypnogogic hallucinations and sleep paralysis, cataplexy occurs almost exclusively with narcolepsy and its presence greatly strengthens the narcolepsy diagnosis. It is a sudden and transient (lasting several minutes) muscle weakness during wakefulness in response to an emotional stimulus (e.g., fear, laughter, competition, sexual excitement). It can be rather debilitating for those with frequent and severe episodes. The muscle weakness may be felt in the face and neck, trunk, and/or limbs, and may result in the individual being unable to speak or remain upright. Similarly, sleep paralysis, which may occur idiopathically, is a transient muscular paralysis; however, it occurs at sleep onset or with an awakening. Hypnogogic hallucinations are dreamlike sensory experiences associated with sleep onset. Narcolepsy is diagnosed by the history and polysomnographic and multiple sleep latency testing revealing rapid sleep onset during repeated daytime naps.
Both behavioral and pharmacologic measures may be useful in the treatment of patients with narcolepsy. Planned periods of activity and scheduled brief naps may reduce intrusive sleepiness. Maximizing nighttime sleep opportunities may be beneficial in reducing further daytime sleepiness. Strategic use of caffeinated beverages may temporarily promote alertness. Prescribed stimulants (pemoline, methylphenidate, modafinil, and dextroamphetamine) play a valuable role in combating sleepiness. Although pemoline (Cylert) has been used successfully for many years in the treatment of narcolepsy, the recent recognition of an increased risk of serious hepatic effects has resulted in the recommendation of biweekly liver function monitoring. Stimulants should be used relatively early in the day to avoid insomnia. The medications need not be used daily. Specific times to promote alertness may be scheduled on different days. REM-suppressant medications (most antidepressants) are useful in treating cataplexy. The newer generation antidepressants (e.g., SSRIs, venlafaxine) are desirable in not adding further sedation and minimizing anticholinergic and other side effects.
Parasomnias
An assortment of behaviors and other symptoms can emerge from and possibly interrupt sleep with subtle to dramatic results. While often benign, some of these events can be quite distressing for the patient and other household members, and there may even be dangerous consequences. Among the parasomnias are symptoms of medical and neurological disorders that for some individuals are more likely to be manifest in sleep. Examples of these include sleep-related seizures and asthmatic episodes. Discomfort from gastroesophageal reflux may occur with muscle relaxation and the recumbent position during sleep. As REM and NREM sleep are markedly different physiological states, certain parasomnias are more likely to be related to specific sleep stages.
Normal characteristics of REM sleep include the rapid eye movements, skeletal muscle atonia, intense mental activity experienced as dreaming, and, relative to NREM sleep, greater lability and irregularity of the heart rhythm, blood pressure, and breathing pattern. Especially intense and frightening dreaming can awaken the individual with a nightmare, which may be associated with considerable anxiety. Generally the person awakens fully with a recollection of the dream, usually a complex, emotion-laden narrative that may be bizarre and illogical. As greater REM occurs during the later part of the night, so do nightmares. Factors that lighten sleep and therefore decrease the arousal threshold, such as the stimulating effects of some medications, may temporarily increase the frequency of nightmares.
During REM sleep the brain is as active as when awake. With dreaming the motor areas are activated; however, in the brainstem a mechanism prevents the motor impulses from being transmitted, thus the normal atonia. REM behavior disorder results from faulty disinhibition of this mechanism with subsequent physical activity during dreaming. Examples include simple behaviors, such as repeatedly swinging an arm while dreaming about playing tennis, to physically aggressive behaviors during combat dreams. Thrashing during sleep may be observed. Injuries to patients and bed partners have been reported. This disorder is more common among the elderly, and in some cases may be associated with other neurological disorders.
The parasomnias specific to NREM sleep are more likely related to the difficulty in awakening fully from the deeper sleep with intense slow wave activity, and correspondingly these events are more likely to occur during the first few hours of the night. Most of the NREM parasomnias are more common in children, but may be seen in adults as well. Typically there is incomplete or delayed awakening, resulting in an apparent confusional state. Sleepwalking is one example. Confusional arousals are extended periods when one does not fully awaken. Sleep terrors occur suddenly with the individual sitting up or even bolting from bed, possibly screaming. The person appears intensely frightened, but usually unaware of his surroundings and is unresponsive to others who may be attempting to calm him. He may return to sleep with no memory of an event that might be quite memorable to others sleeping nearby. If the person does awaken fully during the event, generally he can describe a very concentrated fear, perhaps from being chased, but usually there is not the lengthy and complex narrative typical of a dream. Sleep-related eating occurs primarily in adults and may combine sleep walking with eating behavior. After initially sleeping, the individual arises, seeks food, and eats. It is more common among women. She may or may not have a clear memory of the event, and may be aware of the eating only because of crumbs, missing food, and empty wrappers. It tends to occur nightly for many years.
Decisions regarding the treatment of the parasomnias depend upon the frequency, severity, and dangerousness of the events. Of course, treatment of underlying medical, neurological, and psychiatric disorders should be optimized. Some REM and NREM parasomnias occur during stressful periods, so treatment efforts may be intensified at these times. Sleep deprivation with subsequent increased deep sleep may increase the frequency of the NREM events, so regular sleep schedule habits may be therapeutic. In significantly disruptive and/or dangerous situations, REM behavior disorder and sleep terrors in adults may be treated successfully with clonazepam 0.5-1.0 mg at bedtime. Safety precautions to minimize injury during partial arousals also should be considered.
Sleep Evaluation
The first and most important step in the recognition of potential sleep disorders is asking patients about their sleep and wakefulness. Questions regarding sleep should be included in the routine history and review of systems (ROS). A sleep category should be added to chart ROS forms and sleep questions should be incorporated into patient-completed history questionnaires. A few screening items about nighttime sleep and daytime alertness may be satisfactory to determine whether a significant clinical problem exists. At that point, more detailed questioning about specific symptoms may be pursued. With insomnia complaints, the duration and pattern will be important in developing a differential diagnosis. The sleep disturbance must be considered in the context of the 24-hour sleep-wake cycle. Daytime sleepiness should be reviewed in terms of actual situations during which inadvertent sleep would be likely. This may range from mild (reading) to severe (driving). A bed partner may be an invaluable informant, especially regarding snoring, breathing patterns, and physical movements during sleep. Having the patient maintain a sleep log can be helpful in identifying patterns, such as obviously inadequate time in bed and the advanced and delayed sleep phase syndromes. A routine physical examination also is an essential component of the evaluation of a sleep disturbance.
Consultation with a sleep specialist may be valuable in challenging clinical situations in patients with insomnia, excessive daytime sleepiness, and parasomnias. Excessive daytime sleepiness can be especially dangerous and cause marked impairment in daytime functioning; therefore, the threshold for sleep laboratory testing should be very low in theses cases. Accordingly, suspected SDB and narcolepsy should be referred for sleep testing. The sleep specialist may be helpful with further evaluation and treatment of patients with intractable insomnia symptoms.
Sleep and the Worldwide Web
A wide variety of sleep medicine resources are available for physicians, patients, and the general public on the Internet. Table 4 lists the Web addresses of several consumer information, professional society, governmental, and sleep disorder-oriented organizations.
| Table 4. Sleep Web Resources | ||
| Web Site | Web Address | |
| The Sleep Well | www.stanford.edu/~dement/ | |
| The Sleep Medicine Home Page | www.users.cloud9.net/~thorpy/ | |
| Sleep Home Pages | www.sleephomepages.org | |
| The American Academy of Sleep Medicine | www.aasmnet.org/ | |
| National Sleep Foundation | www.sleepfoundation.org | |
| The National Center on Sleep Disorders Research | rover.nhlbi.nih.gov/about/ncsdr/ | |
| The Restless Legs Syndrome Foundation | www.rls.org | |
| The Narcolepsy Network | www.websciences.org/narnet/ | |
| The American Sleep Apnea Association | www.sleepapnea.org | |
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Suggested Reading
1. Kryger MH, et al., eds. Principles and Practice of Sleep Medicine, 2nd ed. Philadelphia, Pa: W.B. Saunders, 1994.
2. World Health Organization. Insomnia: Report of an international consensus conference. Sleep 1999;(suppl 3):S415-S450.
3. Sateia MJ, et al. Evaluation of chronic insomnia. Sleep 2000; 23:243-308.
Physician CME Questions
33. In adults, the circadian sleepiness drive generally is at a maximum at about:
a. 4:00 p.m. - 5:00 p.m.
b. 8:00 p.m. - 9:00 p.m.
c. 12:00 a.m. - 1:00 a.m.
d. 4:00 a.m. - 5:00 a.m.
34. Normally, the homeostatic process promotes a sleep:wake ratio of:
a. 1:1.
b. 1:2.
c. 1:3.
d. 1:4.
35. The most common cause of excessive daytime sleepiness is:
a. narcolepsy.
b. medication effects.
c. insufficient sleep.
d. excessive slow wave sleep.
36. Survey data suggest that severe or persistent insomnia is reported by what percent of the general population?
a. 1-5%
b. 10-15%
c. 30-40%
d. 60-70%
37. Sleep-disordered breathing (SDB) would be considered clinically severe with a combined apnea and hypopnea rate of how many events per hour?
a. 5
b. 15
c. 30
d. 60
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