210220 Sleep Disorders

210220

Sleep Disorders

3 Contact Hours

Sleep Disorders

Notes

Care has been taken to confirm the accuracy of information presented in this course. The authors, editors, and the publisher, however, cannot accept any responsibility for errors or omissions or for the consequences from application of the information in this course and make no warranty, expressed or implied, with respect to its contents.

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Sleep Disorders

Instructions for This Continuing Education Module

Welcome to the Institute for Continuing Education.

The course, test and evaluation form are all conveniently located within this module to keep things easy-to-manage. To use the mail-in or Fax method of taking the test and receiving your credits follow the steps below: 1. Read and understand the material. 2. After reading and studying the lesson, proceed to the test. Notes 3. Take the test. Be sure to completely fill-in the answers. Use a pencil so if mistakes are made they can be neatly erased and corrected. 4. The final part is the lesson evaluation. Please fill out the evaluation as it helps us create a better learning experience for you. Feel free to add any comments you have about our service and any suggestions as to how we can improve. Completion of this form is essential to obtain continuing education credit. 5. Enclose the completed test and evaluation in an envelope and mail to: Institute for Continuing Education 8176 Center Street, Suite A La Mesa, CA 91942 6. Alternatively, you can Fax the registration, test and evaluation form to (503) 218-7415. If you decide to Fax the test and evaluation, make sure all your information is darkened. The date on the certificate is the day it is faxed or the date of the postmark. 7. We recommend you return the materials to us via certified or registered mail. This insures against possible loss and provides you with a dated receipt of mailing. 8. Upon successfully passing the test, you will receive your certification in the mail. Certificates are dated the day of the postmark. The test will be processed and the certificates will be mailed out within 24 hours of receipt. Please allow one week for delivery. 9. A passing score is 75%. If your score is below 75%, we will send or fax you another answer form, at no additional charge, so you can retake the exam. READ the material. COMPLETE the test and evaluation form. RETURN the answer sheet and the evaluation form. SEND by certified mail to insure against loss. SAVE your receipt of mailing.

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TABLE OF CONTENTS LEARNING OBJECTIVES...... 7

INTRODUCTION...... 7

PART I: WHAT IS CAUSING EXCESSIVE DAYTIME SLEEPINESS?...... 8 OVERVIEW ...... 8 Notes VOLITIONAL SLEEP DEPRIVATION...... 9 OBSTRUCTIVE SLEEP APNEA ...... 10

NARCOLEPSY...... 11

IDIOPATHIC CNS HYPERSOMNIA...... 14

MEDICATION-INDUCED HYPERSOMNIA...... 15

CONCLUSION ...... 15

FOR PATIENTS: WHAT TO EXPECT DURING SLEEP STUDIES ...... 15 THE POLYSOMNOGRAM...... 16 THE MULTIPLE SLEEP LATENCY TEST (MSLT) ...... 16 HOW IS THE MSLT PERFORMED?...... 16 WHAT HAPPENS AFTER THE MSLT? ...... 16 HOW SHOULD I PREPARE FOR THE MSLT?...... 17 REFERENCES ...... 17

PART II: HELPING PATIENTS WHO SAY THEY CANNOT SLEEP...... 19 OVERVIEW: PRACTICAL WAYS TO EVALUATE AND TREAT INSOMNIA...... 19 INSOMNIA...... 19 TYPES OF INSOMNIA AND UNDERLYING CAUSES ...... 19

DIAGNOSTIC TOOLS...... 23

PREVENTION AND TREATMENT ...... 25 PSYCHOPHYSIOLOGIC AND IDIOPATHIC INSOMNIA...... 25 RESTLESS LEGS SYNDROME ...... 27 MENOPAUSE-RELATED INSOMNIA ...... 27 SLEEP-STATE MISPERCEPTION INSOMNIA ...... 28 ILLUSTRATIVE CASE REPORTS ...... 28 CASE 1...... 28

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CASE 2 ...... 29 CONCLUSION ...... 29

REFERENCES ...... 29

ADDENDUM TO PART II:...... 33

BIOLOGIC BASIS OF PRIMARY INSOMNIA...... 33

REFERENCES ...... 33 Notes PART III: PARASOMNIAS ...... 34 TYPES OF PARASOMNIAS ...... 34 CLINICAL EVALUATION...... 34 PART IV: SLEEP DISORDERS IN CHILDREN AND TEENS 35 OVERVIEW...... 35 PREVALENCE...... 36 INFANCY THROUGH PRESCHOOL...... 37 ILLUSTRATIVE CASE REPORT:...... 37 ILLUSTRATIVE CASE REPORT...... 39 MIDDLE CHILDHOOD ...... 40 ILLUSTRATIVE CASE REPORT #1...... 40 ILLUSTRATIVE CASE REPORT #2...... 41 ILLUSTRATIVE CASE REPORT #3...... 42 ADOLESCENCE ...... 43 ILLUSTRATIVE CASE REPORT...... 43 SUMMARY...... 45

REFERENCES ...... 45

SOURCES OF INFORMATION ON SLEEP DISORDERS ...... 46

FACTOIDS ...... 46

SLEEP UPDATES ...... 48

GLOSSARY OF TERMS USED IN SLEEP DISORDERS...... 62

LIST OF ABBREVIATIONS...... 75

SLEEP DISORDERS EXAM...... 77

5 Sleep Disorders

Notes

Sleep Disorders

Sleep Disorders Course Number: 210220 3 CEUs

Learning Objectives

Upon successful completion of this course, you should be able to: • Define and recognize manifestations of major sleep disorders. • Identify the indications for formal sleep studies. Notes • Identify and explain current treatment options for obstructive sleep apnea and narcolepsy. • Identify the clues which lead to diagnosing the various types and causes of insomnia. • Explain how and when to use available diagnostic tools for evaluating insomnia. • Indicate which medication, behavioral therapy measure, or combination approach is effective for which type of insomnia. • Demonstrate and explain the tools needed for adequate history taking in children with sleep disorders. • Describe how common sleep disorders seen in various pediatric age-groups. • Explain how to help patients and their parents overcome sleep disorders.

Introduction

Over the past two decades, awareness and appreciation of sleep disorders and their effects have virtually exploded. Sleep is of the brain and for the brain. Although the functions of sleep remain unknown, it is clear that the organ responsible for generating sleep and the only organ served by sleep is the brain. Another indisputable fact is that sleep is vital for existence.

Much has been learned about the nature of sleep and wakefulness, and a wide variety of sleep disorders have been identified. When these disorders go unrecognized or untreated, the personal and societal consequences can be catastrophic. Therefore, it is important for practicing physicians to be aware of these disorders and to take sleep- wake complaints very seriously, particularly given the prevalence of sleep complaints among the general population.

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In the first part of this four-part course, we underscore the serious nature of excessive daytime sleepiness, with emphasis on practical differential diagnosis and treatment. In the second part, we discuss how the ubiquitous complaint of insomnia can usually be managed in the primary care setting with gratifying results. In the third part, we try to demystify the fascinating conditions known as parasomnias, focusing on the fact that, contrary to popular opinion; these phenomena are usually not caused by underlying psychiatric or psychological problems. In the fourth and final part of the course, we examine the fact that sleep-wake Notes complaints are far more prevalent in children than previously suspected and that proper diagnosis and treatment result in marked benefits for the patient and the entire family.

The take-home message from the combination of these sections of the course is that sleep-wake complaints are almost always caused by specific, identifiable, and--most important--treatable conditions. In most cases, patients do not have to suffer from hypersomnia, insomnia, or unusual behaviors arising from the sleep period, because help is at hand. Sleep disorder centers are a resource that can aid community physicians and patients. Many sleep-related complaints do not require formal sleep studies and can be managed quickly and economically with simple phone consultation between the primary care physician and the sleep medicine specialist.

Gratifyingly, most sleep-wake disorders are readily diagnosable and treatable. We hope that this course familiarizes healthcare professionals with the fundamentals of normal sleep and sleep disorders and provides guidance in recognizing and managing these common complaints.

Part I: What is Causing Excessive Daytime Sleepiness?

Overview Many people have a temporary spell, often in early afternoon, when they feel drowsy. This passing desire for a quick nap is completely different from excessive daytime sleepiness, which is a much more significant problem. Considering the potentially dire personal and economic consequences of falling asleep unintentionally or at inappropriate times, excessive daytime sleepiness must be taken very seriously. A thorough evaluation virtually always leads to a specific underlying cause, allowing effective treatment recommendations.

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Prevalence The prevalence of excessive daytime sleepiness, reported by up to 31% of the adult population, is extraordinary, and consequences of the complaint can be significant, including accidents, negative economic and public health outcomes, reduced work and school performance, and impaired psychosocial functioning. For instance, major industrial disasters, such as those at Chernobyl, Three Mile Island, and Bhopal, and serious accidents, such as those involving the Exxon Valdez and Challenger, have been officially attributed to errors in judgment caused by sleepiness in the workplace. Each year in the United States, car crashes Notes involving drivers falling asleep at the wheel exceed 100,000 in number and result in at least 1,500 deaths. This death rate may surpass that of alcohol-related crashes among young Americans. Given the number of people with excessive daytime sleepiness and the potential outcomes, it is important that physicians, educators, and public policy makers approach this complaint thoughtfully.

True excessive daytime sleepiness is rarely, if ever (contrary to popular opinion), due to a psychological or psychiatric condition (e.g., depression), laziness, or boredom. In the absence of sleep deprivation, daytime sleepiness is almost inevitably caused by an identifiable and treatable sleep disorder. Those discussed in this article are sleep apnea, narcolepsy, and idiopathic central nervous system (CNS) hypersomnia. Less common causes of excessive daytime sleepiness are beyond the scope of this article but include Kleine-Levin syndrome, menstrual- related hypersomnia, idiopathic recurrent stupor, and circadian rhythm disturbances.

Volitional Sleep Deprivation

By far, the most common cause of excessive daytime sleepiness in modern society is chronic sleep deprivation. We sleep 25% less than our forebears did a century ago. There is no evidence that they required more sleep than we do or that we require less sleep than they did. Thus, our sleep deprivation is volitional, often driven by social or economic factors.

For instance, about 20% of employees in industrialized countries are employed in shift work. It has been shown that night-shift workers sleep an average of 8 hours less each week than do day workers--an amount equaling the loss of an entire night’s sleep every week. Nonstop availability of e-mail, shopping, and stock market information on the Internet as well as all-night television and 24-hour businesses are increasingly encouraging sleep deprivation.

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Sufficient sleep is not measured in absolute hours obtained but, rather, in terms of whether the patient awakens rested and restored. The amount needed appears to be genetically determined. Although the average total sleep time nightly is 7.5 to 8 hours, healthy adults can require anywhere from 4 to 10 hours of sleep. Therefore, people who need 10 hours of sleep a night but receive only 8 hours may become severely sleep deprived and notably hypersomnolent. Sleep deprivation is also cumulative. A person does not come to require less sleep or get used to being sleep-deprived. Notes

Obstructive Sleep Apnea

The prevalence of clinically significant obstructive sleep apnea in the general population is high. It is found in at least 2% of women and 4% of men, making it about as prevalent as asthma or diabetes. Although it is most common in adults, men, snorers, postmenopausal women, the elderly, and overweight people, obstructive sleep apnea is also seen often in children, young women, and asthenic people. The erroneous impression that sleep apnea is confined to middle-aged, overweight men has resulted in underdiagnosis in women and children. In addition, about one third of patients with sleep apnea are not obese. In fact, most obese men and the overwhelming majority of obese women do not have sleep apnea.

Consequences of obstructive sleep apnea fall into two major categories: excessive daytime sleepiness caused by sleep fragmentation, and physiologic aftereffects of sleep-related desaturation (e.g., systemic or pulmonary hypertension, right-sided heart failure, polycythemia). Morning headaches are a less reliable symptom of sleep apnea than previously thought.

Clinical diagnosis of sleep apnea may be difficult. Numerous studies have repeatedly shown marked discrepancies between the clinically suspected and the laboratory-documented presence or severity of the disorder. Commonly used subjective sleepiness questionnaires (e.g., the Epworth Sleepiness Scale) may have poor correlation with the presence or severity of obstructive sleep apnea and with the degree of objective sleepiness. For this reason, formal sleep studies (discussed later) are mandatory in suspected cases. Indications for formal sleep studies are well accepted, and numerous clinical-practice guidelines exist for both adults and children.

There is substantial evidence that in many patients with obstructive sleep apnea, the upper airway is smaller and more narrow laterally than in

Sleep Disorders people without the disorder. Techniques developed to evaluate the structure of the upper airway include cephalometric roentgenography, somnofluoroscopy, acoustic-reflection studies, flow-volume curves, and Müller’s and Valsalva’s maneuvers. Such studies have been proposed as selective and predictive for success of upper airway surgical procedures (particularly uvulopalatopharyngoplasty). Regrettably, the predictive value, with few anecdotal exceptions, has been disappointing. Efforts to develop ambulatory or screening studies are ongoing. Practice parameters for use of portable recordings in assessment of obstructive sleep apnea have recently been developed. However, before these Notes techniques are widely adopted, they must be thoroughly evaluated.

Currently, the treatment of choice for obstructive sleep apnea is nasal continuous positive airway pressure. Another option is one of the various surgical procedures, including permanent tracheostomy, uvulopalatopharyngoplasty, mandibular-advancement measures, and hyoid suspension. The variable and often disappointing results of upper airway surgery for apnea are likely related to the fact that craniofacial abnormalities in these patients may involve multiple levels of the upper airway. Mechanical devices designed to advance the mandible may be effective in certain (usually mild) cases.

Narcolepsy

Narcolepsy is a relatively common disorder (prevalence, 0.09%) that affects at least 250,000 people in the United States. The prevalence approximates that of Parkinson’s disease and multiple sclerosis. More than 90% of patients carry the HLA-DR2/DQ1 (under current nomenclature, HLA-DR15 and HLA-DQ6) gene, which is found in less than 30% of the general population. This association is present to varying degrees in different ethnic populations and represents the highest disease-HLA linkage known in medicine. Clearly, there is a genetic component in narcolepsy, and it is of intense scientific interest and research value. However, the variability in the presence of HLA associations in the general public and in patients with narcolepsy precludes the genetic component’s utility as a diagnostic test. The associated HLA type is neither necessary nor sufficient for the appearance of narcolepsy.

Age at onset of narcolepsy is usually adolescence or early adulthood, although it ranges from early childhood to senescence (3 to 72 years of age). Onset appears to peak about age 15, with a secondary peak about age 36. After a relatively brief period of progression as the disease

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declares itself, narcolepsy tends to stabilize. However, it rarely, if ever, completely disappears.

Manifestations Psychosocial and socioeconomic consequences of narcolepsy are significant. Excessive daytime sleepiness is the primary symptom. Unwanted or unanticipated sleep episodes last seconds to minutes and

occur at inappropriate times, particularly during periods of reduced Notes environmental stimulation (e.g., reading, watching television, riding in or driving a motor vehicle, during classes or meetings).

Ancillary symptoms may include cataplexy, sleep paralysis, and hypnagogic (at sleep onset) and hypnopompic (upon awakening) hallucinations. Notably, fewer than half (14% to 42%) of patients with narcolepsy report all three of these ancillary symptoms along with sleep attacks. In many patients, sleep attacks precede the appearance of ancillary symptoms, often by decades.

Cataplexy is sudden loss of muscle tone, typically triggered by emotion (e.g., laughter, anger, excitement, delight, surprise). About 65% to 70% of patients with narcolepsy have cataplexy, and about 30% never experience it. Although occasionally the muscle weakness is complete, resulting in falling down or being forced to sit, more commonly it is mild and more focal, taking the form of facial sagging, slurred speech, localized weakness of an extremity, or a feeling of the knees giving way. The absence of a history of cataplexy does not rule out the diagnosis of narcolepsy.

Sleep paralysis is experienced by up to 60% of patients with narcolepsy and is often very frightening. It consists of total-body paralysis, with sparing of respiration and eye movements, lasting from seconds to minutes. Hallucinations consisting of extremely vivid, often-frightening dreams that occur during the transition between wakefulness and sleep are reported by 12% to 50% of patients. Both sleep paralysis and hallucinatory phenomena are also found quite often among people who do not have narcolepsy.

Automatism occurs in as many as 80% of patients with narcolepsy and represents the simultaneous or rapidly oscillating occurrence of wakefulness and sleep. During such spells, the patient appears to be awake but does not have full awareness and may exhibit extremely inappropriate behavior. As a result, partial complex seizures or a psychogenic dissociative (fugue) state may be erroneously diagnosed.

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The underlying pathophysiology of narcolepsy results in impaired control of the boundaries that normally separate the state of wakefulness from rapid eye movement (REM) or non-REM sleep. Total sleep time per 24- hour period in people with narcolepsy is similar to that in people without the disorder. However, control of onset and offset of both REM and non-REM sleep is impaired. Moreover, there is a clear dissociation of various components of the individual wake and sleep states. Cataplexy and sleep paralysis simply represent the isolated and inappropriate intrusion or persistence of REM sleep-related atonia (paralysis) into wakefulness. The hypnagogic or hypnopompic hallucinations are REM Notes sleep-related dreams occurring during wakefulness.

Diagnostic Approach The diagnosis of narcolepsy may be suspected on the basis of the patient’s history. Some investigators believe that a report of cataplexy is pathognomonic of narcolepsy, but that is not necessarily the case. A history of “classic” narcolepsy with cataplexy may be the manifestation of a somatoform disorder. In view of the nature and duration of narcolepsy treatment with stimulant medications, objective sleep laboratory diagnosis is imperative.

In narcolepsy, formal sleep studies should consist of polysomnography and a multiple sleep latency test (MSLT). (See box below.) All-night polysomnography must be performed the night before the MSLT to determine the quality and quantity of the preceding night’s sleep. The MSLT is a well-validated measurement of the tendency to fall asleep during normal waking hours. It consists of four or five opportunities, at 2-hour intervals throughout the day, to take a 15- to 20-minute nap. Patients with narcolepsy typically fall asleep in 5 minutes or less and usually display REM sleep on at least two of the daytime naps, an occurrence rarely seen in people without the disorder. The MSLT is particularly valuable in differentiating between true sleepiness and fatigue or lack of energy.

False-negative MSLTs do occur. Therefore, MSLT results must be interpreted in light of the patient’s clinical symptoms and results of the preceding night’s polysomnogram. Telling a patient that he or she does not have narcolepsy on the basis of negative MSLT results is analogous to discharging a patient with chest pain from the emergency department on the basis of normal electrocardiography results.

The occurrence of symptomatic narcolepsy caused by identifiable CNS abnormalities is extremely rare. Further neurologic studies are indicated

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only in cases in which history taking or neurologic examination strongly suggests structural CNS abnormality.

Treatment Stimulant medications, such as mazindol (Mazanor, Sanorex), methylphenidate hydrochloride (Methylin, Ritalin), methamphetamine hydrochloride (Desoxyn), dextroamphetamine sulfate, and modafinil

(Provigil), are used to control hypersomnia. (Use of pemoline [Cylert] is Notes discouraged because it has been associated with fatal hepatic necrosis.) Only modafinil (200 mg once daily) has been studied and approved for use in narcolepsy, rendering recommended maximum doses for the other agents arbitrary and without scientific basis. Many practitioners gradually increase the dosage until symptoms are controlled. The abuse potential of such agents in patients for whom they are therapeutic has been greatly overrated, as have cardiovascular and psychiatric consequences.

Treatment of ancillary symptoms includes use of tricyclic antidepressants, selective serotonin reuptake inhibitors, and gamma-hydroxybutyrate (currently not available in the United States).

Idiopathic CNS Hypersomnia

Idiopathic CNS hypersomnia may represent one of several conditions that present as unexplained excessive daytime sleepiness in the absence of sleep deprivation or other identifiable abnormality. Chronic sleep deprivation must be aggressively ruled out. As with narcolepsy, the implications of indefinite treatment with stimulant medications require objective diagnosis with formal studies to confirm the subjective complaint of excessive daytime sleepiness and to rule out unsuspected sleep-related disorder.

In idiopathic CNS hypersomnia, results of the all-night polysomnogram are unremarkable, and the MSLT reveals objective hypersomnia without the occurrence of REM sleep during the naps. HLA studies are not indicated, nor are neuroimaging studies in the absence of clinical or neurologic examination findings suggestive of structural CNS abnormality.

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Medication-induced Hypersomnia

Certain agents may cause true hypersomnia. The best studied are the conventional sedative-hypnotic agents, such as barbiturates, benzodiazepines, and the newer nonbenzodiazepine sedative-hypnotic drugs (e.g., zolpidem tartrate [Ambien], zaleplon [Sonata], zopiclone [which is not available in the United States]). Many medications that are occasionally prescribed for insomnia, such as tricyclic antidepressants and antihistaminic agents, may cause drowsiness, but their ability to improve the quality or quantity of sleep has been poorly studied. Notes

Although it is common to attribute excessive daytime sleepiness to a wide variety of medications, few objective studies are available to document that non-sedative-hypnotic drugs truly cause hypersomnia. Obermeyer and Benca have published a review of this topic.

Conclusion

In the absence of obvious sleep deprivation, formal sleep studies are usually indicated in cases of hypersomnia that is severe enough to interfere with work, driving, or enjoyment of family activities or hobbies. An MSLT should be performed whenever any identified abnormality on the all-night polysomnogram is not clearly sufficient to explain the extent of daytime symptoms. Obstructive sleep apnea and periodic extremity movements during sleep are very common in asymptomatic patients, so their presence during polysomnography must be interpreted in the entire clinical context. Notably, although a given patient may have depression, depression is not an explanation for true excessive daytime sleepiness. Sleep disorders and depression certainly may coexist, however, and sleepiness may masquerade as or exacerbate depression. Use of sleep diaries and actigraphy (seen later in this course) may be invaluable in the setting of recurrent hypersomnia or circadian dysrhythmias.

For Patients: What to Expect During Sleep Studies

Sleep studies are used to evaluate excessive sleepiness during the day and the possibility of obstructive sleep apnea, narcolepsy, or other sleep disorder. The tests cause no pain or discomfort.

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The Polysomnogram A polysomnogram is a series of recordings of measurements taken while you sleep. The measurements help show your doctor what is happening during the various stages of sleep. You may be asked to remain in the sleep laboratory for the entire night to complete this study.

A technologist will glue electrodes to your scalp, face, chest, and legs. He or she will then attach a wire (called a lead) to each electrode, which is connected to equipment that will measure such functions as your eye and Notes leg movements and the electrical activity of your heart and brain. In addition, elastic bands may be put around your chest and abdomen to measure your breathing. You will be able to read or watch television until you are ready to fall asleep. The leads are long, so you can turn over and sleep in any position you wish.

The Multiple Sleep Latency Test (MSLT) This test is also a series of recordings that monitor your sleep patterns by measuring your eye movements, muscle-tone changes, and brain electrical activity. It takes 8 to 10 hours and is performed during the day.

How is the MSLT performed? • A technologist will glue recording electrodes to your scalp and face and then check with a meter to ensure that all electrodes are functioning properly. • You will be taken into a “sleeping” room, the lights will be turned off, and you will be asked to take a 15- to 20-minute nap. Recordings will be taken while you sleep. Even if you cannot sleep during the test, the information gained will still be useful. • After each testing (nap) period, the technologist will awaken you and disconnect all the wires. You may leave the area but will be asked to return in 2 hours for another testing period. There will be at least four testing periods, sometimes five depending on results, spaced 2 hours apart.

What happens after the MSLT? The electrodes will be removed with a liquid that dissolves the glue without hurting your hair or skin. Unless given other instructions, you will be ready to go home. You may wash your hair as you wish. Test results should be available from your doctor in about a week.

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How should I prepare for the MSLT? • If you are taking stimulant drugs for narcolepsy, you should discontinue them (under the direction of your doctor) about 2 to 3 weeks before the test. Continue taking any other prescribed medications unless your doctor gives you special instructions. • Wash any sprays, gels, or other products out of your hair before coming for the test. • Bring reading material or something else to keep you occupied during the 2-hour intervals between testing periods. You may want to bring a family member or friend along to help keep you Notes awake during these intervals.

References

American Electroencephalographic Society guidelines for the polygraphic assessment of sleep related disorders (polysomnography). J Clin Neurophysiol 1991;9:88-96 American Thoracic Society. Indications and standards for cardiopulmonary sleep studies. Medical Section of the American Lung Association. Am Rev Respir Dis 1989;139(2):559-68 American Thoracic Society. Standards and indications for cardiopulmonary sleep studies in children: Am J Respir Crit Care Med 1996;153(2):866-78 Billiard M. Idiopathic hypersomnia. Neurol Clin 1996;14(3):573-82 Broughton WA, Broughton RJ. Psychosocial impact of narcolepsy. Sleep 1994;17(8 Suppl):45-9S Chervin RD, Aldrich MS. The Epworth Sleepiness Scale may not reflect objective measures of sleepiness or sleep apnea. Neurology 1999;52(1):125-31 Ferber R, Millman R, Coppola M, et al. Portable recording in the assessment of obstructive sleep apnea: ASDA standards of practice. Sleep 1994;17(4):378-92 Goldman LS, Genel M, Bezman RJ, et al. Diagnosis and treatment of attention- deficit/hyperactivity disorder in children and adolescents: Council on Scientific Affairs, American Medical Association. JAMA 1998;279(14):1100-7 Guilleminault C, Stoohs R, Kim YD, et al. Upper airway sleep-disordered breathing in women. Ann Intern Med 1995;122(7):493-501 Guilleminault C. Narcolepsy syndrome. In: Kryger et al, eds (15), pp 549-61 Kripke DF, Simons RN, Garfinkel L, et al. Short and long sleep and sleeping pills: is increased mortality associated? Arch Gen Psychiatry 1979;36(1):103-16 Lowe AA. Dental appliances for the treatment of snoring and obstructive sleep apnea. In: Kryger et al, eds (15), pp 722-35 Mitler MM, Hajdukovic R, Erman M, et al. Narcolepsy. J Clin Neurophysiol 1990;7(1):93-118

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Mitler MM, Walsleben J, Sangal RB, et al. Sleep latency on the maintenance of wakefulness test (MWT) for 530 patients with narcolepsy while free of psychoactive drugs. Electroencephalogr Clin Neurophysiol 1998;107(1):33-8 Nishino S, Mignot E. Pharmacological aspects of human and canine narcolepsy. Prog Neurobiol 1997;52(1):27-78 Nobili L, Ferrillo F, Besset A, et al. Ultradian aspects of sleep in narcolepsy. Neurophysiol Clin 1996;26(1):51-9 Obermeyer WH, Benca RM. Effects of drugs on sleep. Neurol Clin 1996;14(4):827-40

Pawluk LK, Hurwitz TD, Schluter JL, et al. Psychiatric morbidity in narcoleptics on Notes chronic high dose methylphenidate therapy. J Nerv Ment Dis 1995;183(1):45-8 Powell NB, Guilleminault C, Riley RW. Surgical therapy for obstructive sleep apnea. In: Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. 2d ed. Philadelphia: Saunders, 1994:706-21 Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Assessment: techniques associated with the diagnosis and management of sleep disorders. Neurology 1992;42(2):269-75 Roth T, Roehrs TA. Etiologies and sequelae of excessive daytime sleepiness. Clin Ther 1996;18(4):562-76 Schenck CH, Mahowald MW. Somatoform conversion disorder mimicking narcolepsy in 8 patients with nocturnal and diurnal dissociative disorders. Sleep Res 1993;22:260 Schwab RJ, Gupta KB, Gefter WB, et al. Upper airway and soft tissue anatomy in normal subjects and patients with sleep-disordered breathing: significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152(5 Pt 1):1673-89 Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the use of laser-assisted uvulopalatoplasty. Sleep 1994;17(8):744-8 Standards of Practice Committee of the American Sleep Disorders Association. Practice parameters for the use of stimulants in the treatment of narcolepsy. Sleep 1994;17(4):348-51 [Erratum, Sleep 1994;17(8):748] Strollo PJ Jr, Sanders MH, Atwood CW. Positive pressure therapy. Clin Chest Med 1998;19(1):55-68 US Department of Health and Human Services. Health technology reports: polysomnography and sleep disorders centers. Bethesda: Dept of Health and Human Services, 1991; publication No. 92-0027 Wallin MT, Mahowald MW. Blood pressure effects of long-term stimulant use in disorders of hypersomnolence. J Sleep Res 1998;7(3):209-15 Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328(17):1230-5

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Part II: Helping Patients Who Say They Cannot Sleep

Overview: Practical ways to evaluate and treat insomnia Why do some people spend most of the night tossing and turning while others drop off as quickly as a cat in the sun? There are many possible explanations for problems with falling and staying asleep and, sometimes, patients actually get a lot more sleep than they think they do. Each type of insomnia has its own set of symptoms, which can be used, along with appropriate diagnostic tools, to help in identification. In this section of Notes the course, we describe differential diagnosis and summarize the best treatment approaches to the common causes of insomnia.

Insomnia Insomnia is the most common sleep-related complaint and the second most common overall complaint (after pain) reported in primary care settings. It affects 35% of the general population, according to the 1984 report of the National Institutes of Mental Health, and is a cause of significant morbidity and mortality. It costs the American public about $100 billion annually in medical expenses, ramifications of accidents, and reduced productivity due to absenteeism and decreased work efficiency.

Insomnia is not defined by total sleep time but by the inability to obtain sleep of sufficient length or quality to produce refreshment the following morning. For example, a person who needs only 4 hours of sleep does not have insomnia if he or she is refreshed in the morning after 4 hours of sleep, whereas someone who needs 10 hours of sleep may have insomnia if he or she does not feel refreshed after 8 hours of sleep. Contrary to popular lore, psychiatric or psychological factors are not often causes of insomnia. In fact, long-standing insomnia can be a significant risk factor for development of depression and anxiety disorders.

Insomnia is not a diagnosis in and of itself. It should be thought of as a constitutional symptom, not unlike pain, fever, or weight loss, requiring identification of an underlying cause before diagnosis and a treatment plan are established.

Types of Insomnia and Underlying Causes

Although the most common form of insomnia is psychophysiologic, insomnia may be the presenting symptom of any primary sleep disorder.

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In addition, it may be a part of another medical, psychiatric, or drug- induced condition.

Psychophysiologic, or Conditioned, Insomnia Psychophysiologic insomnia typically is acquired during a period when other factors (e.g., stress) are at work. After a few days of sleeping poorly, the patient becomes concerned and begins trying harder and harder to get to sleep. The result is arousal and aggravation of the insomnia. Notes Stimuli surrounding bedtime (e.g., the bedroom, the bed itself) may become triggers to arousal. Thus, such patients may have severe problems with sleep in their own bedroom but sleep remarkably well in other locations (e.g., on the living room couch, in a motel, in a sleep laboratory).

The essence of psychophysiologic insomnia is that attention is focused on the inability to sleep. Insomnia is perceived as the only source of distress, and other emotional or mental concerns are minimized. Typically, patients repress or deny awareness of stress factors and see the insomnia as occurring without any reason.

Idiopathic, or Childhood-onset, Insomnia This condition presents as a chronic, serious inability to initiate and maintain sleep, which can often be traced back to the first few weeks of life. Sleep latency (i.e., the time it takes to fall asleep after going to bed) may be very long, and sleep is riddled with awakenings. Daytime features typically include decreased attention and vigilance, low levels of energy and concentration, and deterioration of mood that is usually described as grim and subdued rather than obviously depressed or anxious.

The presumed underlying neurologic abnormality may vary from mild to severe, so the range of insomnia encountered also may vary from mild (essentially, the patient is a light sleeper) to severe and incapacitating. In mild or moderate idiopathic insomnia, psychological functioning is remarkably intact. In severe cases, daytime functioning may be severely disrupted, and affected patients may be unable to hold a job. During childhood and adolescence, idiopathic insomnia is often associated with such neurologic signs as dyslexia and hyperactivity. In many cases, diffuse, nonspecific abnormalities are seen on an electroencephalogram (EEG).

Although idiopathic insomnia appears in childhood, not all childhood insomnia is idiopathic.

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Sleep-state Misperception Insomnia In this fascinating disorder, complaints of insomnia occur without any objective evidence of sleep disturbance. Patients may report that they have not slept at all in weeks, months, or years. However, on objective sleep studies, they sleep several hours per night. When results of sleep evaluation are presented, patients with sleep-state misperception may vehemently insist that the studies are in error, because they are convinced that they sleep very little, if at all.

Notes Poor Sleep Hygiene In some patients, insomnia is the result of lifestyle. In others, poor sleep hygiene develops as a result of chronic insomnia. For example, in the latter case, patients may begin to drink more and more coffee to remain awake and more and more alcohol to fall sleep. They may stay in bed longer and longer in an attempt to get more sleep. However, such ploys only serve to perpetuate the insomnia.

Restless Legs Syndrome This common condition is found in varying degrees in up to 10% of the population. The four cardinal symptoms are a desire to move the legs, accompanying paresthesias that are characterized as uncomfortable or indescribable, motor restlessness, and worsening of symptoms at night and at rest. Symptoms of restless legs syndrome may worsen with administration of tricyclic antidepressants or selective serotonin reuptake inhibitors and during pregnancy.

Fatal Familial Insomnia This hereditary condition, with autosomal dominant transmission, is characterized clinically by progressive insomnia, dysautonomia, changes in circadian rhythm of hormone secretion, motor signs, and slight to moderate deterioration of cognition. The usual age of onset is between 35 and 60 years, and the course of the illness is between 7 and 32 months. In this condition, an abnormal prion protein (PrPsc) is present in the brain, and there is mutation of gene coding for this protein (12). The fatal nature of this illness is due to neurologic degenerative changes, not to the insomnia itself.

Sleep Disorders Occasionally, insomnia is the presenting complaint in obstructive sleep apnea. According to one study of a large group of patients with apnea,

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insomnia was the initial complaint in 16%. In a study of a large group of patients with insomnia, a respiratory disturbance index of at least 30 per hour was found in 2.3% of patients versus 1.3% of controls.

In circadian rhythm abnormalities, patients sleep well but not at socially acceptable times. Those with the advanced sleep phase syndrome have excessive sleepiness in the evening and undesired early morning awakening. Those with the delayed sleep phase syndrome have sleep- onset insomnia, excessive daytime sleepiness (particularly in the Notes morning), or both.

Occasionally, narcolepsy presents as insomnia, because 50% of patients with narcolepsy have disrupted sleep at night.

Neurologic and Medical Conditions Conditions that can cause insomnia, among other symptoms, include propriospinal myoclonus, Parkinson’s and other neurodegenerative diseases, sleep-onset central sleep apnea, pain, degenerative disorders, allergies, and asthma.

Menopause-related Insomnia There is a high level of sleep disturbance (occurring in about 42%, according to one study) in middle-aged women. Although cross-sectional analyses indicate that sleep disturbance may be independent of menopausal status, transition into postmenopausal status is associated with deleterious changes in sleep among women not receiving hormone replacement therapy. Given the extraordinary prevalence of insomnia in perimenopausal and postmenopausal women and the number of women who make up these groups, more studies on cause and treatment of the condition are urgently needed.

Insomnia in the Elderly (For more information, on Sleep Disorders in the Elderly, course #220422.) The elderly may experience dramatic changes in sleep quality and quantity caused by alterations in cerebral function. Changes include early onset and offset of sleep, increased awakenings, increased sleep-disordered breathing, frequent periodic leg movements, and frequent napping.

Medication-induced Insomnia Selective serotonin reuptake inhibitors, stimulants, theophylline,

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prednisone, and two of the newer anticonvulsants—felbamate (Felbatol) and lamotrigine (Lamictal)—may cause insomnia. Other medication- related causes of insomnia include withdrawal from sedative agents, idiosyncratic reactions to other medications, and toxin-related reactions (e.g., to alcohol, phenytoin [Dilantin], carbon monoxide).

Psychiatric Conditions In patients with insomnia, if anxiety permeates most aspects of

functioning, generalized anxiety disorder is the usual diagnosis. In contrast, if anxiety is focused almost exclusively on poor sleep and its Notes consequences on daytime functioning, psychophysiologic insomnia is the typical diagnosis.

Affective disorder is sometimes difficult to differentiate from psychophysiologic insomnia, because a dysphoric mood, ascribed to the effects of poor sleep, often accompanies psychophysiologic insomnia. The two conditions can often be distinguished on the basis of other “vegetative” signs, such as loss of appetite or libido or the typical diurnal fluctuation (worse in the morning) of depression. In general, a diagnosis of psychophysiologic insomnia is inappropriate if the patient fulfills criteria for any other Axis I or II diagnosis in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (22). There is growing evidence that insomnia, initially unrelated to depression, is a major risk factor for development of depression or anxiety.

Diagnostic Tools

Insomnia is usually diagnosed by thorough clinical history taking. The complaint of daytime sleepiness is generally indicative of a primary sleep disorder, because patients with insomnia are hyposomnolent and often complain bitterly of the inability to take naps. Patients reporting daytime sleepiness should be evaluated with a polysomnogram and a multiple sleep latency test (MSLT) to rule out primary sleep disorders.

Polysomnogram and MSLT The polysomnogram is a polygraph of EEG findings, eye movements, electromyography readings, oxygen saturation, limb movements, airflow, and chest and abdominal movements taken during sleep, usually for the entire night. Polysomnography is not indicated in routine evaluation of insomnia, except when the diagnosis is uncertain and a primary sleep disorder is suspected and when insomnia does not respond to appropriate behavioral and pharmacologic treatments.

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An MSLT is a series of four or five opportunities, each separated by a 2- hour interval, to take a 15- to 20-minute nap. It is used to assess sleep latency and the possibility of such sleep disorders as obstructive sleep apnea and narcolepsy. In primary insomnia, results of the MSLT are usually normal.

Sleep Logs A sleep log is a graph on which, for 2 to 3 weeks, the patient records

bedtime, approximate sleep time, times and duration of awakenings Notes during the sleep period, final awakening time, and naps taken during the day. Although subjective, this record summarizes the patient’s perception of the amount and quality of sleep he or she is getting.

Actigraphy Actigraphy is a recently developed technique to record activity during waking and sleeping without application of any electrodes. An actigraph is worn on the wrist and is about the size of a watch. It consists of a movement detector and considerable memory, so it can record movement and nonmovement data plotted against time for a week or two. The patient can wear it continuously during sleep and as he or she goes about routine daily activities. Actigraphy is ideal for extended examination of the sleep-wake cycle because it is convenient and is readily accepted by patients. It can be used to supplement sleep logs and to evaluate unusual complaints, such as, “I have not slept for several nights”.

In general, patients have fewer limb movements during sleep than while awake. There is a very close correlation between the rest-activity findings recorded by the actigraph and the sleep-wake pattern as determined by a polysomnogram. Several investigators used actigraphy in groups of controls of different ages and found minute-by-minute agreement in sleep-wake scoring between polysomnography and actigraphy to exceed 90%.

In one study of 36 adults with insomnia who underwent both polysomnography and actigraphy for three nights, the mean discrepancy between the two tests was 49 minutes per night. In three fourths of the patients, the tests agreed to within 1 hour of total amount of sleep per night. In this study, minute-by-minute agreement for sleep-wake scoring between polysomnography and actigraphy was 82.1%, and in another study, minute-by-minute agreement was 78.2%.

Interestingly, in patients who have insomnia associated with mental illness, correlation between the two tests is lower. The actigraph tends to

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overestimate total sleep time in these patients because they are more likely to remain relatively motionless in bed without actually sleeping.

Actigraphy has two major advantages over polysomnography in evaluating insomnia: Sleep-wake patterns can easily be recorded over several days and nights rather than in the single night that is typical of a polysomnogram. In addition, patients can be evaluated in their home environment versus in idealized laboratory conditions. In many cases, the subjective complaint of severe insomnia cannot be determined without objective actigraphic confirmation of the true sleep-wake pattern. The Notes complaint “I only sleep an hour a night” may represent true, severe insomnia or may reflect sleep-state misperception insomnia. Clearly, management in the two situations differs greatly and cannot be undertaken without a correct diagnosis.

Laboratory Evaluation In patients with restless legs syndrome, a serum ferritin level of less than 50 micrograms/L is associated with increased severity of symptoms, which may exacerbate insomnia.

Prevention and Treatment

The consequences of ongoing insomnia can be serious and may include excessive use of prescribed medication, use of alcohol, and self-treatment of daytime somnolence with over-the-counter stimulants. A passive and defeatist attitude may be a psychological ramification. Tension-related disorders (e.g., head-aches, gastric upset, vasoconstriction of the extremities) are also seen. Increased motor vehicle accidents, decreased job performance, and decreased quality of life are common in patients who have chronic insomnia. Treatment of the underlying condition usually controls secondary insomnia. Specific therapy for primary insomnia depends on the cause of the problem.

Psychophysiologic and Idiopathic Insomnia Aggressive treatment of transient insomnia with use of hypnotic agents and instructions on good sleep hygiene (table 1), with attention to acute stressors, may prevent development of learned maladaptive associations that can lead to psychophysiologic insomnia. The best management of psychophysiologic insomnia is a combination of hypnotic medication and behavioral methods.

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Table 1. Rules for good sleep hygiene Decrease excessive time in bed Increase exercise and aerobic fitness Eliminate clocks in the bedroom Use distracting activities to induce sleep onset Curtail caffeine intake Notes Avoid nicotine Avoid alcohol Follow a regular sleep-wake schedule

Adapted from Hauri.

Although current US Food and Drug Administration recommendations for hypnotic agents are that they be prescribed for short-term use only, recent studies have shown that the risks of tolerance, addiction, dependence, and rebound insomnia are minimal in patients with true insomnia. Agents that have proven clinical effectiveness include low-dose trazodone hydrochloride (Desyrel), the benzodiazepines, and the newer nonbenzodiazepine sedative-hypnotics zolpidem tartrate (Ambien), zaleplon (Sonata), and zoplicone (not available in the United States).

Tricyclic antidepressants and antihistamines are rarely indicated because of the poor side effect profile and general lack of efficacy, according to available studies. Melatonin and other over-the-counter sleep aids and dietary supplements are of questionable value.

Behavioral methods include sleep restriction and consolidation with control of stimuli (table 2), relaxation therapy, and sleep-hygiene education. It is almost impossible to implement all of the sleep-hygiene rules at once; beginning with one or two of the most important ones usually works best. In addition, not all of the rules apply to all patients.

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Table 2. Program to achieve sleep restriction and consolidation and control stimuli* Restrict time in bed to achieve some degree of sleep deprivation. Do not spend more than 15 minutes awake in bed, either at the beginning of sleep or during awakenings. After 15 minutes, get up and leave the bedroom.

Avoid productive, accomplishment-achieving activities (e.g., balancing checkbook, doing housework) at bedtime, since they may Notes be subconsciously rewarding for being awake. Do not take naps. Get out of bed at a predetermined time, no matter how little sleep you have gotten. Once you are sleeping for 90% of the time in bed, you may add 15 minutes to either end of the sleep period. Use medications (e.g., benzodiazepines) as prescribed.

*Used at Washington University School of Medicine, St Louis.

Restless Legs Syndrome The most effective medications for treating symptoms of restless legs syndrome belong to three distinct classes: 1. the dopaminergics (e.g., pramipexole) [Mirapex], pergolide mesylate [Permax], bromocriptine mesylate [Parlodel], and levodopa [Dopar, Larodopa]), 2. the opiates and 3. the benzodiazepines, especially clonazepam (Klonopin). Recent studies have shown that an additional dopaminergic agent, ropinirole hydrochloride (Requip), and the newer anticonvulsant gabapentin (Neurontin) also are effective in controlling restless legs syndrome.

Menopause-related Insomnia Hormone replacement therapy or use of clonidine hydrochloride (Catapres) may control insomnia along with other menopause-related symptoms.

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Sleep-state Misperception Insomnia Patients with this type of insomnia usually improve dramatically after seeing results of actigraphy and realizing that they are getting normal sleep.

Illustrative Case Reports

The following two cases illustrate typical patient presentations and clues Notes to the cause of insomnia. In case 1, psychophysiologic insomnia is indicated by the patient’s report that insomnia started during a period when she was concerned about a health problem and by the significant improvement in sleep when she was in the laboratory versus when she was sleeping at home. In case 2, idiopathic insomnia is suggested by sleep latency and arousal problems that date back to infancy.

Case 1 Mrs. H, a 66-year-old woman, was referred to a sleep disorders clinic after 1 year of difficulties with sleep onset and maintenance. She reported that she had been an adequate but marginal sleeper, averaging 7 hours a night, until 1 year ago, when pituitary dysfunction was diagnosed and treated successfully. During that time, Mrs. H received corticosteroids for a short period and had secondary sleep-onset insomnia. Now, she reports that her health is fine and she no longer takes steroids, but insomnia continues. She has tried various nonbenzodiazepine hypnotics without gaining any benefit.

Mrs. H was asked to wear an actigraph continuously for 1 week while she went about normal daytime and nighttime activities at home. Actigraphy confirmed that she usually took 3 to 4 hours to fall asleep and slept for an average of 1 to 4 hours each night.

In the laboratory, a polysomnogram done with the full seizure montage revealed sleep latency of 161 minutes, sleep efficiency (amount of time spent sleeping divided by total time spent in bed) of 55.6%, and total sleep time of 6 hours. No other sleep abnormalities were found.

The next day, an MSLT revealed no objective hypersomnia, no rapid eye movement sleep on any of the naps, and a mean sleep latency of 17 minutes.

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After stimulus-control behavioral therapy and use of clonazepam (0.5 mg at bedtime as needed), Mrs. H’s sleep gradually improved to an acceptable level.

Case 2 A.S., an otherwise healthy 14-year-old girl, presented complaining of long-standing insomnia at bedtime and arousals during the night. Although she felt exhausted during the daytime, she was not able to take naps. Her mother stated that as a newborn, A.S. seemed to not sleep as Notes much as other infants and was more aroused overall. She remained a restless sleeper throughout infancy and childhood, with two or three arousals per night.

A.S. was taught the rules of proper sleep hygiene, started on a program to achieve sleep restriction and consolidation, and given a mild sedative- hypnotic agent. Satisfactory results were achieved.

Conclusion

Insomnia is a very common and easily treated condition. It may be the presenting symptom of many other medical conditions and usually is not a sign of psychological or psychiatric illness. Untreated, insomnia can cause significant economic hardship, morbidity, and mortality, and it may be a risk factor for development of depression or anxiety. Actigraphy and sleep logs are essential tools in evaluating insomnia. Their use usually results in a specific causal diagnosis, with effective therapeutic implications. Treatment includes both pharmacologic and behavioral interventions.

References

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington, DC: Am Psychiatric Assn, 1994 2. American Sleep Disorders Association, Diagnostic Classification Steering Committee. The international classification of sleep disorders, revised: diagnostic and coding manual. Rochester, Minn: American Sleep Disorders Assn, 1997 3. American Sleep Disorders Association, Standards of Practice Committee. Practice parameters for the use of polysomnography in the evaluation of insomnia. Sleep 1995;18(1):55-7 4. American Sleep Disorders Association. Practice parameters for the use of actigraphy in the clinical assessment of sleep disorders. Sleep 1995;18(4):285-7

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5. Arand DL, Bonnet MH. Activity, arousal, and the MSLT in patients with insomnia. Sleep 1999;22(Suppl 1):135 6. Becker PM, Ondo W, Sharon D. Encouraging initial response of restless legs syndrome to pramipexole. Neurology 1998;51(4):1221-3 7. Bonnet MH, Arand DL. Physiological activation in patients with sleep state misperception. Psychosom Med 1997;59(5):533-40 8. Brodeur C, Montplaisir J, Godbout R, et al. Treatment of restless legs syndrome and periodic movements during sleep with L-dopa: a double-blind, controlled study. Neurology 1988;38(12):1845-8 Notes 9. Chang PP, Ford DE, Mead LA, et al. Insomnia in young men and subsequent depression: the Johns Hopkins Precursors Study. Am J Epidemiol 1997;146(2):105- 14 10. Coope J. Hormonal and non-hormonal interventions for menopausal symptoms. Maturitas 1996;23(2):159-68 11. Dominguez RA, Goldstein BJ, Jacobson AF, et al. A double-blind placebo- controlled study of fluvoxamine and imipramine in depression. J Clin Psychiatry 1985;46(3):84-7 12. Eaton WW, Badawi M, Melton B. Prodromes and precursors: epidemiologic data for primary prevention of disorders with slow onset. Am J Psychiatry 1995;152(7):967-72 13. Erman MK, Poceta SJ. Obstructive sleep apnea presenting as insomnia. Sleep Res 1993;22:194 14. Estevill-Sancho EX, De La Fuente-Panell V. Ropinirol as a successful treatment of the restless legs syndrome: an open pilot study with polysomnographic data. Sleep 1999;22(Suppl 1):158S 15. Gillin JC. Are sleep disturbances risk factors for anxiety, depressive and addictive disorders? Acta Psychiatr Scand Suppl 1998;393:39-43 16. Hauri PJ, Wisbey J. Actigraphy and insomnia: a closer look. Part 2. Sleep 1994;17(5):408-10 17. Hauri PJ, Wisbey J. Wrist actigraphy in insomnia. Sleep 1992;15(4):293-301 18. Hauri PJ. Can we mix behavioral therapy with hypnotics when treating insomniacs? Sleep 1997;20(12):1111-8 19. Hauri PJ. Idiopathic insomnia. In: Gilman S, Goldstein GW, Waxman SG, eds. Neurobase. 1st ed. San Diego: Arbor Publishing, 1999 20. Hauri PJ. Insomnia. Clin Chest Med 1998;19(1):157-68 21. Hening W, Allen R, Walters AS, et al. Motor functions and dysfunctions of sleep. In: Chokroverty S, ed. Sleep disorders medicine. 2d ed. Boston: Butterworth- Heinemann, 1999:441-507 22. Hening WA, Walters A, Kavey N, et al. Dyskinesias while awake and periodic movements in sleep in restless legs syndrome: treatment with opioids. Neurology 1986;36(10):1363-6

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23. Hohagen F, Kappler C, Schramm E, et al. Sleep onset insomnia, sleep maintaining insomnia and insomnia with early morning awakening--temporal stability of subtypes in a longitudinal study on general practice attenders. Sleep 1994;17(6):551- 4 24. Johnson LC, Spinweber CL. Good and poor sleepers differ in Navy performance. Mil Med 1983;148(9):727-31 25. Kripke DF, Mullaney DJ, Messin S, et al. Wrist actigraphic measures of sleep and rhythms. Electroencephalogr Clin Neurophysiol 1978;44(5):674-6

26. Krystal AD, Edinger J, Wohlgemuth W, et al. Sleep in perimenopausal and postmenopausal women. Sleep Med Rev 1998;2:243-53 Notes 27. Leppik IE. Felbamate. Epilepsia 1995;36(Suppl 2):66-72S 28. Lichstein KL, Wilson NM, Noe SL, et al. Daytime sleepiness in insomnia: behavioral, biological and subjective indices. Sleep 1994;17(8):693-702 29. Lin SC, Kaplan J, Burger CD, et al. Effect of pramipexole in treatment of resistant restless legs syndrome. Mayo Clin Proc 1998;73(6):497-500 30. Mahowald MW, Kader G, Schenck CH. Clinical categories of sleep disorders I. Continuum 1997;3(4):35-65 31. Montagna P, Provini F, Plazzi G, et al. Propriospinal myoclonus upon relaxation and drowsiness: a cause of severe insomnia. Mov Disord 1997;12(1):66-72 32. Mullaney DJ, Kripke DF, Messin S. Wrist-actigraphic estimation of sleep time. Sleep 1980;3(1):83-92 33. NIH Consensus Development Conference Summary. Drugs and insomnia: the use of medication to promote sleep. JAMA 1984;251(18):2410-4 34. O’Hanlon JF, Freeman H. Categorising the behavioural toxicities of antidepressants: proposals and requirements. (Editorial) Br J Psychiatry 1995;166(4):421-3 35. Owens JF, Matthews KA. Sleep disturbance in healthy middle-aged women. Maturitas 1998;30(1):41-50 36. Peled R, Lavie P. Double-blind evaluation of clonazepam on periodic leg movements in sleep. J Neurol Neurosurg Psychiatry 1987;50(12):1679-81 37. Sadeh A, Alster J, Urbach D, et al. Actigraphically based automatic bedtime sleep- wake schedule: validity and clinical applications. In: Chase MH, Lydic R, O’Conner C, eds. Sleep research. Vol 18. Los Angeles: Brain Information Service/Brain Research Inst, 1989:399 38. Sadeh A, Hauri PJ, Kripke DF, et al. The role of actigraphy in the evaluation of sleep disorders. Sleep 1995;18(4):288-302 39. Sadeh A, Lavie P, Scher A, et al. Actigraphic home-monitoring sleep-disturbed and control infants and young children: a new method for pediatric assessment of sleep-wake patterns. Pediatrics 1991;87(4):494-9 40. Sadler M. Lamotrigine associated with insomnia. Epilepsia 1999;40(3):322-5 41. Salmi T, Punnonen R. Clonidine in the treatment of menopausal symptoms. Int J Gynaecol Obstet 1979;16(5):422-6

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42. Schenck CH, Mahowald MW. Long-term, nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med 1996;100(3):333-7 43. Seilhean D, Duyckaerts C, Hauw JJ. [Fatal familial insomnia and prion diseases.] Rev Neurol (Paris) 1995;151(4):225-30 (Fre, Eng abstr) 44. Soldatos CR. Insomnia in relation to depression and anxiety: epidemiologic considerations. J Psychosom Res 1994;38(Suppl 1):3-8 45. Spielman AJ, Nunes J, Glovinsky PB. Insomnia. Neurol Clin 1996;14(3):513-43

46. Stoller MK. Economic effects of insomnia. Clin Ther 1994;16(5):873-97 Notes 47. Sun ER, Chen CA, Ho G, et al. Iron and the restless legs syndrome. Sleep 1998;21(4):371-7 48. Uhles ML, Duntley SP. Evaluation of the efficacy of neurontin in the treatment of restless legs syndrome. Sleep 1999;22(Suppl 1):157S 49. Vgontzas AN, Kales A, Bixler EO, et al. Usefulness of polysomnographic studies in the differential diagnosis of insomnia. Int J Neurosci 1995;82(1-2):47-60 50. Wagner ML, Walters AS, Coleman RG, et al. Randomized, double-blind, placebo- controlled study of clonidine in restless legs syndrome. Sleep 1996;19(1):52-8 51. Walsh JK, Schweitzer PK. Ten-year trends in the pharmacological treatment of insomnia. Sleep 1999;22(3):371-5 52. Walters AS, Hening WA, Chokroverty S. Review and videotape recognition of idiopathic restless legs syndrome. Mov Disord 1991;6(2):105-10 53. Walters AS, Hening WA, Kavey N, et al. A double-blind randomized crossover trial of bromocriptine and placebo in restless legs syndrome. Ann Neurol 1988;24(3):455-8 54. Walters AS, Wagner ML, Hening WA, et al. Successful treatment of the idiopathic restless legs syndrome in a randomized double-blind trial of oxycodone versus placebo. Sleep 1993;16(4):327-32 55. Webster JB, Messin S, Mullaney DJ, et al. Transducer design and placement for activity recording. Med Biol Eng Comput 1982;20(6):741-4 56. Wetter TC, Stiasny K, Winkelmann J, et al. A randomized controlled study of pergolide in patients with restless legs syndrome. Neurology 1999;52(5):944-50

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Addendum to Part II: Biologic Basis of Primary Insomnia

Insomnia is presumed to result from moderate hyperarousal or imbalance of the sleep-wake system toward alertness. Bonnet and Arand documented physiologic hyperarousal in many types of insomnia, and Broman and associates found excessive presleep arousal in psychophysiologic insomnia.

Patients with insomnia have faster heart rates, higher body temperatures, Notes and more electromyographic activity than people in control groups, and they are as alert as or more alert than controls during the day. According to electroencephalographic criteria, many of them have faster frequencies, both during waking and sleep. Lamarche and Ogilvie compared patients who had psychophysiologic insomnia with those who had psychiatric insomnia and with normal controls. Electroencephalographic activity showed higher cortical arousal in patients who had psychophysiologic insomnia than in the other two groups, which did not differ significantly from each other.

Recently, Vgontzas and colleagues discovered a positive correlation between objective sleep disturbance and activity on both limbs of the stress system (i.e., the hypothalamic-pituitary-adrenal axis and the sympathetic system) in a group of patients with chronic insomnia.

References

Bonnet MH, Arand DL. 24-hour metabolic rate in insomniacs and matched normal sleepers. Sleep 1995;18(7):581-8 Bonnet MH, Arand DL. Heart rate variability in insomniacs and matched normal sleepers. Psychosom 1998;60(5):610-5 Bonnet MH, Arand DL. Hyperarousal and insomnia. Sleep Med Rev 1997;1(2):97-108 Broman JE, Lundh LG, Hetta J. Insufficient sleep in the general population. Neurophysiol Clin 1996;26(1):30-9 Hauri PJ. Insomnia. Clin Chest Med 1998;19(1):157-68 Lamarche CH, Ogilvie RD. Electrophysiological changes during the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs, and normal sleepers. Sleep 1997;20(9):724-33 Merica H, Blois R, Gaillard JM. Spectral characteristics of sleep EEG in chronic insomnia. Eur J Neurosci 1998;10(5):1826-34 Vgontzas AN, Tsigos C, Bixler EO, et al. Chronic insomnia and the activity of the stress system: a preliminary study. J Psychosom Res 1998;45(1 Spec No):21-31

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Part III: Parasomnias (For more information, see course on Dealing with Parasomnias, course #220305)

Parasomnias are undesirable physical phenomena accompanying sleep that involve skeletal muscle activity or autonomic nervous system changes, or both. In persons with these disorders, sleep and wakefulness are not mutually exclusive, because dissociated elements of rapid eye movement (REM) sleep, non-REM sleep, and wakefulness can become

admixed or rapidly oscillate to produce abnormal nocturnal twilight states Notes with behavioral dyscontrol. Diagnosis is made on the basis of findings from the clinical interview and polysomnography (i.e., physiologic monitoring of sleep). Treatment is successful in the majority of cases.

Knowledge of parasomnias has expanded greatly in recent years. New disorders have been identified, and known disorders have been reported to occur more frequently, across a broader age-group, and with more serious consequences than previously thought. Parasomnias can cause sleep-related injuries and promote psychological distress from repeated loss of self-control during sleep. In adults, parasomnias are often misdiagnosed and inappropriately treated as psychiatric disorders because of their bizarre and dangerous manifestations. Diagnosis is further complicated by the fact that medical and psychiatric disorders and various medications can precipitate or aggravate parasomnias.

Types of Parasomnias Parasomnias can be classified according to whether the signs or symptoms are 1. primary phenomena of sleep itself or 2. secondary phenomena derived from various underlying disorders, with sleep facilitating such nocturnal manifestations as headaches, seizures, asthma, arrhythmias, and gastroesophageal reflux.

The focus of this section is sleepwalking, sleep terrors, REM sleep behavior disorder, nocturnal sleep-related eating disorders, nocturnal dissociative disorders, restless legs syndrome, and the interactions of parasomnias with obstructive sleep apnea and its therapy.

Clinical Evaluation Parasomnias can be detected with use of a screening questionnaire. The information from the patient alone may clarify the diagnosis and lead to appropriate management. Depending on their training, experience, and confidence level, primary care physicians may initiate pharmacotherapy in

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patients with restless legs syndrome or other non-injurious parasomnias and consider requesting a sleep medicine consultation. Other conditions may warrant referral to a sleep specialist for more complete evaluation.

At sleep disorders centers, evaluation of complex and violent nocturnal behaviors includes the following: 1. A clinical sleep-wake interview with the patient and his or her bed partner; a review of medical records; and a patient questionnaire to elicit information about sleep-wake patterns, medical history, psychiatric history, alcohol and drug use history, review of Notes systems, family history, and past or current physical, sexual, and emotional abuse 2. Psychiatric and neurologic interviews and examinations, including psychometric testing 3. Extensive overnight polysomnographic monitoring, with continuous audiovisual recording, at a hospital-based sleep laboratory. Polysomnographic paper speeds of 15 to 30 mm/sec are used to detect epileptiform activity. Such monitoring is generally reserved for patients with injurious or unusual parasomnias and those with persistent sleep-related eating. When indicated, urine toxicology screening also is performed. 4. Daytime multiple sleep latency testing, if excessive daytime sleepiness or fatigue is present or suspected

Part IV: Sleep Disorders in Children and Teens

In this the fourth and last part of our course on sleep disorders, we will discuss helping patients and their families get some rest.

Overview “Your parents are tired--go to bed!” Well-intentioned physicians trying to assist the fatigued family of a sleepless youngster may recognize this familiar refrain. Increased awareness of the problem, a firm grasp of the most common causes in each age-group, and an effective method of taking a history that is applicable to all age-groups are necessary to diagnose sleep disorders. In this section, we describe a practical approach to achieving results that are rewarding for caregivers, reassuring to young patients, and gratifying to bleary-eyed parents.

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Prevalence As many as 30% of children have a sleep disorder at some time in their childhood, and the impact on patients and families can be enormous. Thorough history taking is the single most important step in identifying the type and source of the problem.

A non-threatening, parent-cued way to uncover events that can affect sleep is to complete a 24-hour sleep-history questionnaire. Parents are asked to start with the evening meal and describe what happens during Notes the next 24 hours. The bedtime routine is brimming with important details. It is not unusual to hear accounts of struggles or tensions, vigorous sports practices, or viewing of energizing or scary TV shows or videos before bedtime.

A 24-hour history also chronicles the typical delay between going to bed and going to sleep, the total sleep time per night, the number and duration of nocturnal arousals, day-night reversal patterns, time of morning awakening, and whether morning awaking is spontaneous or aided by a parent. Continuing history taking throughout the course of the day uncovers napping patterns, unusual daytime sleepiness, impairment of school performance, and changes in behavior or mood. Asking families to complete a sleep log that documents sleep-wake patterns for at least 2 weeks before coming to the clinic is often extremely helpful in identifying the sleep problem.

The sleep-environment history is another important tool in sorting out sleep complaints. Sleep environment plays a role from cradle to college— from the infant who falls asleep nursing to the teen who slumbers in a dungeon-like basement. Reports of transitional objects (e.g., a special blanket or stuffed animal) that are necessary for sleep and of the amount of ambient light and noise (e.g., TV, computer) are often enlightening parts of the history.

A review of systems is critical to identifying sleep disorders in children and teens and primarily involves cardio-respiratory and neurologic features of sleep. Breathing disorders (e.g., obstructive sleep apnea) and primary snoring occur in as many as 11% of pediatric patients. Specific medical conditions (e.g., craniofacial disorders, tracheomalacia, bronchomalacia, prematurity, reactive airways disease) may predispose children to sleep-disordered breathing.

Sleep quality is often disrupted in children with neurologic impairment and, in many cases, interferes with the family’s ability to continue caring for the child at home. Thorough developmental and behavioral history taking may uncover a range of issues affecting sleep, including separation

Sleep Disorders anxiety and attention-deficit disorder. These diagnoses are discussed in further detail in the following text, according to age-group.

Infancy Through Preschool

Common sleep problems found in infants, toddlers, and preschoolers are sleep-onset association disorder (sometimes accompanied by issues of parent and child sleeping together) and night terrors (a parasomnia that should be differentiated from nocturnal seizures). Notes

Sleep-onset Association Disorder A common presentation of sleep-onset association disorder is an infant or toddler who, parents report, just doesn’t sleep. Parents often describe a child who insists on being nursed to sleep or on having a parent lie alongside until he or she falls asleep. Parents are often unaware that their well-meaning habits have created the difficulty.

The problem occurs when, during normal nocturnal arousals, the child awakens fully if the parent (or other condition he or she has learned to associate with falling asleep) is not present. The child has learned to rely on the parent to fall asleep and may lack the self-soothing skills necessary to settle back into sleep independently.

Sleep-onset association disorder can lead to frequent nightly arousals for both child and parent. Waldo is an example of a child who has learned such behavior.

Illustrative Case Report: Waldo is a healthy, robust 18-month-old, but his parents report that ever since early infancy, “he falls asleep just fine but is quite restless and wakes up 3 to 10 times per night, fussing or screaming.” He calms fairly quickly when his parents attend to him and usually ends up spending part or most of the night between his parents in their bed. In the case of Waldo’s parents, this is not their preference. Waldo was nursed to sleep at bedtime until he was weaned at 11 months. He now falls asleep, most often in his father’s arms, while being rocked, at which point his father transfers him to his crib. Waldo’s parents report feeling exhausted and “at their wits’ end.”

Management of sleep-onset association disorder involves two critical elements:

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1. an understanding of the individual child’s “brain clock,” or typical time of sleep onset and morning awakening (based on sleep charts compiled by the parents), and 2. a period of training the child to shift from wake to sleep independently.

Making this transition requires that parents put the child to bed when he or she is drowsy but still awake—in other words, at a time that coincides with natural sleep onset rather than at an arbitrary hour they have chosen Notes as bedtime.

Even when timing is optimal, most children protest when their bedtime routine is changed. Parents vary in their ability or willingness to allow their child to cry for brief intervals during this period of training. Simply allowing infants to cry themselves to sleep is unnecessary and potentially harmful, particularly in babies with daytime symptoms of separation anxiety.

The delayed-intervention method, popularized by Richard Ferber, MD, in the book Solve Your Child’s Sleep Problems, is appropriate only in children older than about 10 months of age. It consists of gradually increasing the time parents remain away from a crying child at bedtime—from several seconds to 2 minutes on the first night (depending on the child and parent comfort level) and up to 5 minutes on subsequent nights. When they return to the room after each interval away, parents are advised to reassure the child over the crib rail, without picking him or her up, and without turning on the light.

Talking in a slow, quiet voice to a preverbal child who is distressed or angry can help calm both the parent and the child. After comforting the baby for a minute or two with endearments (e.g., “I am right here with you, you are okay, sleepy baby, slow down”), the parent may need to again step out of the room while the child is still crying. Many parents find looking at a watch with a second hand during these intervals helpful, because listening to their baby cry for just 1 minute feels like an eternity to many parents.

The goals are to offer nurturance, comfort, and safety; to enhance the baby’s self-soothing skills; and to set a clear, consistent limit regarding sleep location, assuming the parents choose not to have the child sleep with them. For many cultures around the globe and for many families in the United States, parents sharing their bed with their infants and children is the norm and a strongly felt personal preference. This is a sound option when both parents are agreeable to it and commonsense safety precautions are observed (e.g., avoidance of smoking in bed and of

Sleep Disorders consumption of intoxicating substances before bedtime). Whatever the sleep location, supine sleep positioning is recommended in babies.

Nighttime snacks and drinks, with the exception of water, should be avoided, because these can exacerbate nocturnal arousals from a physiologic standpoint and negatively affect dental health.

Night Terrors Night terrors, or sleep terrors, represent a sudden partial arousal Notes (parasomnia) associated with disorientation, emotional outburst, and often the appearance of fear, motor activity (e.g., walking, running in sleep), and profound autonomic discharge (e.g., flushing, sweating, tachycardia). Night terrors classically occur in the first half of the night during deep non-rapid eye movement (non-REM) sleep. This characteristic separates night terrors from nightmares, which usually, but not exclusively, occur in the second half of the night during REM or light non-REM sleep. Children usually have no memory of night terrors, whereas they often can recall the content of dreams and nightmares.

Therefore, night terrors may be more worrisome to the parents than the children and can be inadvertently prolonged when an understandably anxious parent attempts to awaken the frightened-appearing youngster. Carmen is an example of a child with neurodevelopmental disability who experiences night terrors.

Illustrative Case Report Carmen is a happy, affectionate 4-year-old with microcephaly and mild to moderate developmental disability of unclear etiology. Her parents report that she becomes aroused from sleep “shrieking and thrashing” three or four times per week and is hard to console, appearing to not recognize her parents. These episodes usually occur within 90 minutes after falling asleep at bedtime and rarely occur during daytime naps. Carmen has no history of seizures, and neither 24-hour video electroencephalography nor formal overnight polysomnography shows any electrical or clinical seizure activity.

The most effective first step in management of night terrors is to reassure the parents and recommend that any intervention be done as gently as possible. For example, parents might be advised to quietly guide the child back to bed and help him or her settle down without awakening. Safety precautions might include securing upper-story windows, doors leading outside, and stair landings and, when possible,

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opting for first-floor sleeping quarters. A noisemaker at the child’s bedroom doorway can alert parents to sleepwalking.

Parents should be questioned regarding a history of daytime seizures or staring spells, unusual posturing, limb jerking, and changes in skin color during episodes. If there is doubt, formal testing for nocturnal seizures, particularly in a child with underlying neurodevelopmental disability, should be considered. When nocturnal seizures have been ruled out, frequent or dramatic night terrors may, on rare occasions, warrant Notes medication, such as low-dose clonazepam (Klonopin), at bedtime. Typically, youngsters outgrow these parasomnias.

Middle Childhood

During the middle-childhood years, short sleep requirement, sleep-onset anxiety, and obstructive sleep apnea are commonly encountered problems.

Short Sleep Requirement and Sleep-onset Anxiety Taking a 24-hour sleep history helps differentiate the constitutional delays in sleep onset and relatively short sleep requirement (exemplified by Tamika in the case report that follows) from anxiety-related sleep- onset insomnia (seen in Patrick in the case report below). Children’s behaviors at sleep onset are rarely exclusive to bedtime. Therefore, it is not surprising to learn that Tamika is a spirited, high-energy youngster and that Patrick expresses other worries during the day. Although both children have bedtime struggles, the treatment approach is very different for the two.

Illustrative Case Report #1 Tamika is a bright, energetic 7-year-old who, her mother reports, “has always been a night owl.” Tamika’s bedtime is 8 PM on school nights, but she “seems wired” until 10 PM or often later. Some nights, she giggles and fools around with her sister (age 9), saying that she simply is not tired, and uses stalling tactics (e.g., getting up out of bed, asking to use the bathroom, asking for a drink). Other nights, she has tantrums when her parents are stricter about enforcing bedtime. Once asleep, she sleeps well through the night and wakes up easily at 7 AM for school.

Sleep charting may document that Tamika requires 9 hours of sleep per night (10 PM to 7 AM), whereas her parents have expected her to be in

Sleep Disorders bed for 11 hours (8 PM to 7 AM). Moving morning wake up to an earlier time may help Tamika feel drowsy earlier in the evening so that her eventual sleep phase might become closer to 9 PM to 6 AM. Changing or extending a child’s constitutional sleep requirement is rarely successful. However, it is reasonable to work on improving his or her ability to play or read quietly and independently while siblings are falling asleep. In truly hyperkinetic children, a dinnertime or late-evening dose of clonidine hydrochloride (Catapres) may help the settling-down process as bedtime approaches. Notes

Illustrative Case Report #2 Patrick is a bright, soft-spoken 10-year-old who, his mother says, “is a bundle of nerves at bedtime” and refuses to go to bed unless a parent stays upstairs with him. If his parents go downstairs, Patrick may fall asleep curled up on his 8-year-old brother’s bedroom floor. It often takes Patrick 2 to 3 hours to fall asleep at bedtime, and he frequently appears tired and “emotional” the next morning. He often awakens during the night, complaining that he cannot fall asleep or is afraid of monsters or the dark.

When dealing with sleep-onset insomnia caused by anxiety, physicians should ask about daytime complaints, fears, or worries, which may suggest a more pervasive anxiety problem warranting referral to a children’s mental health professional. Exposure to frightening media events and a history of stressful events (e.g., a death in the family, arrival of a new sibling) should be explored. More severe stressors, such as enduring sexual abuse or witnessing family violence, are considerations in some cases. A simple but common cause of sleep-onset insomnia in children is rumination on issues of the day at bedtime. This problem can often be settled with a small amount of extra attention and conversation with a parent at bedtime.

Anxious children are best treated with a combination of therapies, including a cognitive-behavioral approach that empowers them to generate solutions and gain mastery over their worries. For example, the physician might say to the child, “Adults sometimes feel nervous, too. Let’s make a list of the things that could make you feel safe and brave and strong.” In persistent and difficult cases, a 1- to 3-month trial of the short-acting benzodiazepine alprazolam (Xanax) may be indicated, along with referral to a mental health professional.

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Obstructive Sleep Apnea (For more information, see our course on Obstructive Sleep Apnea: An Overview, course #210112)

Obstructive sleep apnea is seen in as many as 3% of preschool and school-age children. Parents often complain that the child snores nightly in all positions, perhaps worse when supine. Parents may also observe choking spells or what they refer to as breath holding or a halting pattern in the snoring. Children may assume a position of neck hyperextension Notes during sleep. Sleep fragmentation caused by obstructive sleep apnea may lead to daytime sleepiness, manifested as increased napping or falling asleep at school or while watching TV. Alternatively, children may show changes in daytime behavior, including hyperactivity, distractibility, and mood changes.

Illustrative Case Report #3 Omar is a 9-year-old who was referred to the sleep disorders clinic from the pediatric otolaryngology clinic prior to tonsillectomy and adenoidectomy for snoring. His parents describe a history of loud snoring and occasional choking or gasping for air during sleep. They report recent worsening in school performance and increased irritability, manifested as verbal fights with his sister and refusal to do chores that he previously did without complaint. Unlike his peers, Omar takes a 1-hour afternoon nap most weekdays and often sleeps on the bus ride to and from school. An older sister also had her tonsils removed because of snoring.

In a recent study, first graders with poor school performance, defined as being in the lowest 10th percentile of their class, were screened for obstructive sleep apnea. Of 297 children, 54 (18%) were found to have a clinical history and gas-exchange abnormalities consistent with obstructive sleep apnea. Academic performance improved in the 24 children who underwent tonsillectomy and adenoidectomy but not in the 30 children whose parents declined the surgery.

Children with obstructive sleep apnea are at increased risk for postoperative respiratory complications. Therefore, they should be observed and monitored as inpatients for at least 24 hours after tonsillectomy and adenoidectomy. This is especially important in those who are under age 2 or have craniofacial abnormalities, failure to thrive, hypotonia, morbid obesity, cor pulmonale, or polysomnographic results indicating an apnea-hypopnea index of more than 40 events per hour or an oxygen-saturation nadir of 70% or less.

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Adolescence (For more information, see our course Contemporary Perspectives of Adolescent Sleep, course #240102)

Sleep disorders to watch for in adolescents are delayed sleep-phase syndrome (a disorder of circadian rhythm) and narcolepsy, which requires differentiation from idiopathic hypersomnolence.

Delayed Sleep-phase Syndrome Notes Delayed sleep-phase syndrome is common (estimated prevalence, 7%) among teenagers, although some delay in sleep phase is considered normal in this age-group (hence, the nationwide advocacy effort toward later high school start times). These teens often describe feeling wide awake in the late-evening hours, with a delay in sleep onset until 3 or 4 AM. When they manage to drag themselves to school, their performance is impaired, and they may fall asleep in morning classes. Accordingly, the young person often presents with academic failure, truancy, or tardiness. Their sleep debt accumulates until the weekend, when they may sleep until early afternoon, further disturbing their circadian clock.

Illustrative Case Report Jordan is a 16-year-old who reluctantly comes to the sleep clinic with his parents. He is on probation for truancy because he missed 67 days of school in the past year. Prior to 2 years ago, he had been an A and B student. He reports that he has always been a night owl, but the summer before last he began staying up later and later, participating in online chat groups. When school began, Jordan could not make the transition back to the 10 PM to 7 AM sleep period needed, and he continued to stay awake until 3 or 4 AM, even when he felt sleep-deprived. On weekends during the school year, he would sleep until late afternoon. Jordan had no history of snoring, and no sleep apnea was observed. According to summertime sleep logs, his sleep requirement appears to be within the normal range, at about 10 hours per night.

Changing a delayed sleep cycle is usually a challenge for both the physician and patient. It consists of setting the morning wake-up time 15 minutes earlier each successive day until the desired target is reached. This procedure is accompanied by exposure to bright natural light or use of a high-intensity (2,500-lux) light box in the morning. Other measures that may be beneficial in resetting the brain clock are minimizing exposure to evening light, a trial of melatonin 4 to 5 hours before desired sleep onset, and a short course of sedative medication in the evening.

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Strict adherence to the new sleep schedule, even on weekends and holidays, is usually necessary to prevent relapse to previous patterns.

Narcolepsy and Idiopathic Hypersomnolence Neurologically based disorders of hypersomnolence often have their onset in adolescence and can have a profound impact on the young person’s academic and social functioning. Such disorders are often

underrecognized and can cause the perception that patients are lazy, Notes unmotivated, or learning-disabled.

Narcolepsy is a genetic condition affecting about 1 of every 2,000 adults. It involves a classic tetrad of symptoms: sleep attacks (i.e., irresistible urges to fall asleep), sleep-onset paralysis, sleep-onset hallucinations, and cataplexy. The “gold standard” for diagnosing narcolepsy is the multiple sleep latency test, which consists of a series of daytime nap opportunities after an overnight sleep study.

In evaluating patients for narcolepsy, other causes of excessive daytime sleepiness need to be ruled out, such as sleep apnea, chronic sleep deprivation, delayed sleep-phase syndrome, and idiopathic hypersomnolence. Idiopathic hypersomnolence is a condition of excessive daytime sleepiness that is not associated with sleep attacks or other symptoms characteristic of narcolepsy.

Illustrative Case Report Kathy is a 17-year-old with a 2-year history of falling asleep in school and missing out on extracurricular activities because of lack of energy and the need for a 1- to 2-hour nap after school. She maintains a B average but feels she is underachieving. A typical night’s sleep for Kathy is 9:30 PM to 6:30 AM on school days and 9:30 PM to 2 PM on weekends. Her understandably worried parents brought her to a neurologist, who reported normal results on brain magnetic resonance imaging. Kathy breathes quietly and comfortably during sleep. She denies recalling sensations of paralysis or hallucinations when falling asleep, and she has never felt weak or fallen down in an emotional context, such as laughter or anger. On overnight polysomnography and a multiple sleep latency test the following day, Kathy slept 16 hours and fell asleep, on average, within 9 minutes during her naps, with no REM sleep on any nap. Sleep logs completed in the summertime indicate that Kathy has a typical nightly sleep requirement of 14 to 15 hours. Idiopathic hypersomnolence was the diagnosis.

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Adolescents who have a long nightly sleep requirement with otherwise restorative sleep may do well if allowed to sleep the full 12 or more hours per night that they need. However, they tend to experience chronic sleep deprivation during the school year when they have to arise early for classes.

Education of school personnel is a critical aspect of clinical management in children and teens with narcolepsy and other sleep disorders. The American Academy of Sleep Medicine, the Narcolepsy Network, the National Sleep Foundation, and Young Adults with Narcolepsy (see Notes below) are valuable sources of information on living with hypersomnolence syndromes.

Summary

Diagnosing sleep disorders in children and adolescents is challenging and rewarding and requires integration of medical, neurodevelopmental, and behavioral histories. Most patients can be successfully treated once a thorough evaluation has been completed and age-appropriate differential diagnosis of common sleep disorders has been considered. With appropriate knowledge and tools, physicians may find that pediatric sleep disorders are some of the most treatable problems in medicine.

References

1. Anders T, Halpern L, Hua J. Sleeping through the night: a developmental perspective. Pediatrics 1992;90(4):554-60 2. Dahl RE. The development and disorders of sleep. Adv Pediatr 1998;45:73-90 3. Ferber R. Solve your child’s sleep problems. New York: Simon & Schuster, 1985 4. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics 1998;102(3 Pt 1):616-20 5. Guilleminault C, Pelayo R. Sleep-disordered breathing in children. Ann Med 1998;30(4):350-6 6. Kryger MH, Roth T, Dement WC, eds. Principles and practice of sleep medicine. 2d ed. Philadelphia: Saunders, 1994:549 7. Pelayo RP, Thorpy M, Glovinsky P. Prevalence of delayed sleep phase syndrome among adolescents. J Sleep Res 1988;17:392 8. Rosen GM, Muckle RP, Mahowald MW, et al. Postoperative respiratory compromise in children with obstructive sleep apnea syndrome: can it be anticipated? Pediatrics 1994;93(5):784-8

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9. Wang RC, Elkins TP, Keech D, et al. Accuracy of clinical evaluation in pediatric obstructive sleep apnea. Otolaryngol Head Neck Surg 1998;118(1):69-73 10. Warwick JP, Mason DG. Obstructive sleep apnea syndrome in children. Anaesthesia 1998;53(6):571-9

Sources of Information on Sleep Disorders

Notes The Narcolepsy Network 10921 Reed Hartman Hwy Cincinnati, OH 45242 513-891-3522 Fax: 513-891-3836 http://www.websciences.org/narnet E-mail: [email protected]

Young Adults with Narcolepsy 1451 W 31st St Minneapolis, MN 55408 612-824-1355 http://www.yawn.org E-mail: [email protected]

Factoids

A sleep disorder that is primarily caused by a physiological abnormality is known as an intrinsic sleep disorder.

The severity of a sleep disorder is most often determined by the patient’s symptoms. Sleep disorders that are related to the timing of sleep within the 24-hour day are classified as Circadian rhythm disorders. A mean sleep latency of less than 5 minutes and two or more sleep onset REM periods seen on a MSLT performed following nocturnal polysomnography which shows severe obstructive sleep apnea syndrome cannot diagnose narcolepsy because of the untreated sleep related breathing disorder. Common symptoms seen in patients with obstructive sleep apnea syndrome include non-continuous loud snoring, daytime sleepiness, and frequent nocturnal urination.

Idiopathic insomnia is a relatively rare disorder, known as childhood onset insomnia, and is present at birth and remains a lifelong disorder.

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The most common cause of obstructive sleep apnea in children is a deviated septum.

A type of apnea that occurs as a result of central respiratory control center malfunction is known as central sleep apnea syndrome. Obstructive sleep apnea events most commonly occur during

Stages II, REM sleep, and I. Disorders of arousal, partial arousal and sleep stage transition are known as parasomnias. Periodic episodes of repetitive and highly stereotyped limb movements that occur during sleep Notes are seen in patients with periodic limb movement disorder. Fever, sleep deprivation, or external stimulation such as noise may increase the frequency of sleep walking episodes.

In order to diagnose impaired sleep related penile erections, polysomnography must document absence of sleep related breathing disorders. Episodes of grinding or clenching the teeth during sleep are seen in patients with sleep bruxism. Polysomnography in patients with primary snoring documents normal respiratory patterns with no evidence of arousals, cardiac arrhythmias or oxygen desaturation. Polysomnography during an episode of sleep enuresis should document involuntary urination during sleep and absence of seizure activity. Sleep disorders which do not meet the criteria for classification under any other category, and are classified as “other parasomnias” include infant sleep apnea, SIDS, and bruxism. Apnea of prematurity (AOP), apnea of infancy (AOI), apparent life threatening events (ALTE), and obstructive sleep apnea syndrome are all components of infant sleep apnea. Nightmares, sleep paralysis, and impaired sleep related penile erections are all parasomnias associated with REM sleep. Repetitive stereotyped movements of the head and neck which occur immediately prior to sleep and into light sleep are characteristic of rhythmic movement disorder.

Myocardial ischemia during sleep may result from oxygen desaturation, bradycardia and decreased blood pressure during slow wave sleep, and/or tachycardia during REM sleep. Chronic impairment of gas exchange and C02 retention are commonly seen in patients with chronic obstructive pulmonary disease. CPAP or oxygen administration in patients with COPD may lead to CO2 retention. Psychosis is characterized by hallucination, delusions, incoherence, and catatonic behavior. Sleep disorders which occur as a result of medical or psychiatric disorders are not primary sleep disorders but have a significant effect on sleep or wakefulness.

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Sleep Updates

January 13, 2004

In an article published in the New York Times on January 13, 2004, Andrew Pollack reported on the topic of sleeping pills and their usage in the United States:

Putting a Price on a Good Night’s Sleep Notes Americans are about to be reminded again how much they need sleep — and sleeping pills. A new effort appears to be developing to expand the use of sleeping pills, which because of their potential for abuse have long had a reputation as being in some ways more dangerous than the insomnia they are meant to treat. Some sleep experts say newer pills are safer than the ones that once caused deaths from overdose. Moreover, some say, there is growing evidence that insomnia is a serious medical condition, not just a nuisance. “Slowly, we are beginning to identify that insomnia does have some risks associated with it, and when that happens there will be more press to treat it aggressively,” said Dr. Michael H. Bonnet, director of the sleep laboratory at the Veterans Affairs Medical Center in Dayton, Ohio. But part of the new push is driven by drug company marketing. Two new sleeping pills are expected to be available by the end of next year and their manufacturers hope to have them approved for broader and longer- term use than recommended for previous pills. And the companies are expected to advertise their products, and the problem of insomnia, heavily. Sepracor, which makes one of the new drugs, recently financed a press seminar on insomnia. The other drug will be marketed by Pfizer, whose vast sales force and ample advertising have helped make best sellers of drugs like Viagra, the cholesterol fighter Lipitor and the painkiller Celebrex. “What Pfizer sees here is a wonderful opportunity for what they’ve done” with those drugs, said Gary A. Lyons, president and chief executive of Neurocrine Biosciences, which developed the drug, indiplon, and licensed it to Pfizer. Only a small fraction of insomniacs now take prescription sleep-inducing drugs, Mr. Lyons said. “This is unquestionably one of the largest potential pharmaceutical markets in the world,” he added. As a hint of what might come, a public relations campaign was mounted a decade ago when Ambien, now the best-selling sleeping pill, was introduced.

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“With a public fearful of sleep medications and reluctant to admit having insomnia, Edelman and client Searle teamed up with the National Sleep Foundation and leading academic institutions to address `Sleep in America,’ “ Edelman, a public relations agency, recounted in a history of its first 50 years. By emphasizing the safety problem of driving and working while sleepy, “Edelman helped Searle revitalize a flagging sleep market,” the company wrote. Dr. Daniel F. Kripke, professor of psychiatry at the University of California at San Diego, said that drug companies and some sleep doctors, many of them consultants for drug companies, were Notes exaggerating the seriousness of insomnia. “Frankly, worrying people about sleep is good for the drug companies, it’s good for the sleep clinics and maybe it helps people get research funding too,” said Dr. Kripke, who runs a Web site, the Dark Side of Sleeping Pills, at www.darksideofsleepingpills.com. There is little evidence that sleeping pills meaningfully improve sleep over the long run, he said. There is even evidence from a survey in the 1980’s that regular users of sleeping pills tend to die younger than non- users. But most experts dismiss that evidence. “He’s about the only person I know of who supports that view,” said Dr. Andrew D. Krystal, associate professor of psychiatry and director of the sleep research laboratory at Duke who has consulted for Sepracor. He said the consensus was that insomnia is a serious condition and that pills were becoming safer. “I believe we’ll see a shift toward people having effective treatments available that doctors are willing to prescribe and patients are willing to take,” Dr. Krystal said. Estimates of the number of people with insomnia vary widely. About 40 percent of adult Americans have at least occasional trouble sleeping, according to the National Sleep Foundation, which promotes understanding of sleep disorders and research on them. Some insomnia is temporary, caused by job worries, for instance. But an estimated 10 to 15 percent of adults have severe or chronic insomnia. Many cases appear to be caused by an underlying condition like depression or painful arthritis, and the best approach is to treat that underlying condition. But for perhaps 15 to 30 percent of those with chronic insomnia, no known underlying disorder can be found. Several studies have shown that people with insomnia are more likely than others to become depressed. Lack of sleep, though not always caused by insomnia, can interfere with social life, job performance and driving. At least one study has shown that sleep deprivation results in poor glucose metabolism, a hallmark of diabetes.

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Still, scientists cannot yet point to any study showing that treating insomnia with sleeping pills staves off depression or other diseases. Yet some experts say understanding the dangers of insomnia is only a matter of time. “Some day we’ll see that like smoking, this isn’t good for you,” said Dr. Michael L. Perlis, associate professor of psychiatry and director of the sleep research laboratory at the University of Rochester. Sleeping pills, technically called hypnotics, have gone through several generations. Decades ago, the common pills were barbiturates, which were addictive and led to many deaths from accidental or deliberate overdoses. By the Notes 1970’s, they were largely displaced by drugs called benzodiazepines, which included the sleeping pills Halcion and Restoril and the tranquilizer Valium. With these drugs it was much more difficult to die from an overdose, though they could still be dangerous if paired with alcohol. Halcion was taken off the market in some European countries and the recommended dose in the United States was reduced after some users suffered amnesia, hallucinations and other side effects. There is evidence that benzodiazepines can be addictive and that people develop a tolerance, so the pills eventually lose effectiveness. In 1983, the National Institutes of Health issued a consensus statement from experts urging doctors not to prescribe such pills for more than three or four months. The Drug Enforcement Administration considers the drugs Schedule IV controlled substances because of a limited potential for abuse. In the 1990’s, drugs known as non-benzodiazepines, exemplified by Ambien and Sonata, entered the market. Because many doctors perceive it as safer than the older drugs, Ambien, now sold by Sanofi-Synthelabo of France, accounts for two-thirds of prescriptions of nonbarbiturate hypnotics, according to IMS Health, a market research firm. Though chemically different from the older drugs, Ambien works in a similar way. All the drugs bind to receptors in the nervous system meant for a neurotransmitter called GABA. The binding enhances the transmitter’s effects, which slow the nervous system. Though the older drugs bind to all three of the main types of GABA receptors, Ambien, known generically as zolpidem, binds mainly to the one type thought to promote sleep. Though some studies in animals have suggested that this causes fewer side effects, Ambien has never been tested in clinical trials lasting more than a few weeks. So its label recommends use for only 7 to 10 days, with prescriptions not to exceed 30 days. Like the older drugs, it is still a controlled substance and its label mentions the potential for dependence and tolerance. Dr. James K. Walsh, president of the National Sleep

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Foundation and head of a sleep research center affiliated with two hospitals in St. Louis, said newer drugs were being unfairly tarnished by “some myths and regulatory restraints that have evolved over the years.” Those restraints have “led patients to be fearful of medications that they don’t need to be fearful about, in my opinion,” said Dr. Walsh, who is a consultant to many drug companies.

The labeling of the drugs for only short-term use is a problem, some doctors say, because those most in need of treatment are chronic insomniacs. “There’s a real logical inconsistency between what we know Notes about insomnia and how we treat it,” said Dr. Daniel J. Buysse, professor of psychiatry at the University of Pittsburgh. While some people do take the sleeping pills for months at a time, others use over-the-counter antihistamines or prescription antidepressants that have sedation as a side effect. But those drugs have not been approved for insomnia, Dr. Walsh said, so scientists know less about their effects on sleep than they do for sleeping pills. Some sleep specialists have been urging the National Institutes of Health to develop a new consensus statement about insomnia and its treatment, and that is expected to happen in the next year or two. The N.I.H. has already stamped the 1983 statement obsolete. The move toward longer use of sleeping pills could be spurred by the new pills coming to market, which for the first time are being tested for months instead of weeks. Sepracor, which is based in Marlborough, Mass., sponsored a clinical trial showing that its drug, Estorra, worked for six months without loss of effectiveness, providing about 35 minutes more sleep per night than a placebo. The Food and Drug Administration is expected to decide whether to approve Estorra by the end of February, after postponing its deadline of last November. Indiplon, the Neurocrine and Pfizer drug, is in the final stages of clinical trials and could reach the market next year. Estorra and indiplon work the same way as Ambien. Estorra, known generically as eszopiclone, is a derivative of zopiclone, a non-benzodiazepine sold outside the United States. “These are quantitative not qualitative differences,” said Dr. Thomas Roth, director of the sleep center at Henry Ford Hospital in Detroit. “We’re not talking about a new chemical class.” So besides seeking approval for longer-term use, the newcomers will try to distinguish their drugs from Ambien by how long their drugs last in the body. If a drug does not last long enough, people can wake up again, a problem that has hurt sales of Sonata. If the drug lasts too long, people can feel groggy when they are supposed to be awake, a side effect that

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increases the risk of accidents. Estorra lasts somewhat longer than Ambien so perhaps could provide longer sleep. Sepracor says the drug does not cause hangovers. Neurocrine Biosciences, based in San Diego, is developing two forms of indiplon. A short-acting form would be for people who wake up in the middle of the night or too early in the morning and want to go back to sleep without oversleeping.

The other version of indiplon will have a coating that releases some drug Notes immediately to induce sleep at bedtime and a core that will release more later to keep people sleeping through the night. Sanofi-Synthelabo is developing a similar pulsed-release version of Ambien, which it hopes to have on the market by the end of 2005, to fend off not only the new rivals but also generic versions of Ambien that will be allowed in 2006. Some scientists say true breakthroughs will require drugs that work through new mechanisms, like adjusting the body’s natural sleep-wake cycle. Takeda Chemical Industries, Japan’s largest pharmaceutical company, is in late-stage trials of a drug, Ramelteon, that mimics melatonin, a hormone released in the brain in response to darkness that helps induce sleep. Many people take nutritional supplements containing melatonin, though experts say it is not clear they are effective. Dr. Stephen M. Sainati, vice president at Takeda Global Research and Development, says that while melatonin binds to three receptors and had multiple effects, Ramelteon binds to only the one connected with sleep. He said the drug should have “absolutely no abuse liability whatsoever.” Takeda hopes to file for approval by early 2005, he said. Drugs working through yet other mechanisms are further back in development. Dr. Bonnet, of Dayton, who is also a professor of neurology at Wright State University, said that even with improvements in sleeping pills, doctors might be cautious about prescribing them. “We’ve forgotten the mistakes of the past so now we can go back and repeat them,” Dr. Bonnet said. “People are going to pause and think, `Are we really beyond those problems?’ “

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http://www.latimes.com/news/local/la-me- tjcommute2jan02,0,4930244.story?coll=la-home-headlines

For this commute, set it on snooze control Drivers with jobs in the U.S. form an unusual bedroom community at the Tijuana border. Notes By Richard Marosi Times Staff Writer

January 2, 2007

TIJUANA — It’s 2 in the morning, and the lines of cars waiting to cross the border have already grown so long that they are snarling the streets of this city’s downtown nearly half a mile away.

The cars keep coming, clogging ramps and overpasses, snaking around tamale vendors, traffic-circle monuments and the plaza outside City Hall.

But most of the lines at the border crossing aren’t moving. Car engines are turned off. Motorists are literally asleep at the wheel. Some rest their heads on their steering wheels, others against the glass of the car windows. A chorus of snorts and whistles drifts out the open windows of a Volkswagen Jetta in which four men snooze. In a Toyota Corolla, a man has tied a towel around his eyes to block out light.

The slumberers don’t have to be in San Diego until the workday begins hours from now. But night after night, they queue up in the area leading to the border inspection lanes — with pillows and blankets as well as packed lunches — because of a twisted sort of logic.

If they show up at 4 a.m., when 20 of the lanes leading to the San Ysidro Port of Entry open for the day, they could find themselves in stop-and- go traffic for up to two hours. Four other lanes are always open, but if the crossers try to get through those lanes at this hour, they’ll have to stay awake in line for at least half an hour — and then find somewhere to sleep in San Diego before work starts.

This way, they can count on crossing the border reasonably quickly after sleeping fairly safely — if far from comfortably.

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“That’s why we get old here in line,” said Librado Garcia, who paints mansions in Rancho Santa Fe. “We don’t sleep well.”

This snoozer of a commute is one of the unwelcome byproducts of a booming metropolitan area sliced by an international border. Most high- paying jobs in the border region are in the San Diego area, but an ever- increasing number of workers comes from Tijuana. Most of the overnight commuters — the sleepers number in the hundreds and possibly thousands — are either U.S. citizens or Mexican nationals who Notes are legal U.S. residents. Many have moved to Tijuana after being forced out of San Diego’s pricy housing market.

Federal authorities and regional planners have long wrestled with how to balance national security concerns with the needs of a regional economy in which all sorts of people (construction crews, delivery truck drivers, stock clerks, painters, students, shoppers) cross back and forth each day.

About 47,000 cars pass through the port on an average day. And more rigorous inspections of cars for evidence of drug or human smuggling have slowed their speed.

Congestion at the three border crossings into San Diego County cost the U.S. and Mexican economies an estimated $6 billion in 2005 in such areas as lost wages and spending, according to a report by the San Diego Assn. of Governments.

During morning rush hour, from about 7 to 10 a.m., the wait to cross can reach three hours. But in recent years, the commuter crush has grown steadily worse at all times of day, creating a 24-hour traffic nightmare.

The San Ysidro Port of Entry is the world’s busiest border crossing. “You do the math,” said Guadalupe Angeles, 48, a landscaper who showed up so early one recent morning — 1:15 — that he parked his car at the double yellow lines marking the border. He said the extra lanes open at 4 a.m., and “If I leave home at that time, it’ll take two hours to cross. I’m here so that when they open, I’ll be the first to get across.”

Using Angeles’ formula, the Tijuana to San Diego early morning drive is perhaps the world’s longest short commute. For many people, it is the central fact in their day-to-day lives, around which everything else has to be juggled.

Take the case of Alberto Estrada, 46, a construction worker. He goes to sleep at home at 10 p.m. and wakes at 1:30 a.m. His wife makes him a burrito lunch and he’s out the door. By 2 a.m. he’s parked in the ocean of

Sleep Disorders cars, sleeping away the next two hours with his stockinged feet up on the dashboard.

After he crosses the border, Estrada catches another hour of sleep at a parking lot, then goes to work in National City, a San Diego suburb. Total distance: 20 miles. Total commute time: five hours.

“If I don’t come here now, I won’t get to work on time,” said Estrada.

Although the evening southbound commute back to Tijuana is faster Notes because there are no inspections, that’s does little to make up for the early morning routine.

Garcia, the painter, said he hadn’t had a full night’s sleep in years. Even on weekends, he wakes up in the middle of the night. He ends up channel surfing the night away.

Some people in the standstill of cars can’t sleep at all. There’s the glare of the stadium lights that illuminate the port area. The flashing Jumbotron advertising oceanfront homes in Baja California. The shouts of the coffee and empanada vendors who never stop trying to make sales. One has a bullhorn, but he wisely saves it for when people start waking up at 4 a.m.

Enrique Duco, 55, stays up in his car watching the early news on a portable television.

College student Michael Gonzalez, 23, does homework while his sister Sarah, 10, sleeps in the back seat. Both are U.S. citizens who moved to Tijuana five years ago to be closer to an ailing relative. When they first began this routine, drowsiness would overcome Sarah at school, Gonzalez said. But she adjusted and now slumbers soundly in the car until they arrive at a friend’s house, where she sleeps an additional hour before her fifth-grade class.

Another worker, Alex Gonzalez, is one of those who moved south of the border to escape high housing costs.

Gonzalez, 37, a delivery driver, moved his family to Tijuana to rent a two-bedroom house for $500, a fraction of what he would have to pay in San Diego.

Garcia, the painter, said he moved to Tijuana two years ago from the San Diego suburb of Imperial Beach. With the savings, he can make the $500 car payment for a new SUV.

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He and other longtime commuters can’t help but think that if the port kept all the inspection lanes open around the clock, wait times would drop. Port authorities, however, say budget constraints prevent expanded staffing.

The veterans seem resigned to their sleepy fate. It’s mostly the ones new to the strange routine who react with amazement or anger.

Manuel Robles, a West Covina resident, said being caught in the Notes congestion made him realize that there are actually worse experiences than a Los Angeles traffic jam.

“I can’t imagine doing this every day,” he said. “Thank God I don’t live here.” * [email protected]

January 9, 2007

Mysteries of the Brain and the Science of Sleep, Brought to Life in a Barn

By KATIE ZEZIMA

EAST BURKE, Vt. — Amber Powers, 13, thought about sleep only when she didn’t get enough, which was most of the time. A trip to a remote barn here, however, left her spending many of her waking hours mulling over the time she spends sleeping.

The barn’s owner, Dr. J. Allan Hobson, a psychiatry professor and sleep researcher at Harvard Medical School, has converted part of it into a small, interactive sleep museum that students visit after four weeks of lessons on brain function and sleep. Dr. Hobson is working with the Caledonia North school district in the northeast corner of the state to develop a sleep curriculum that he hopes to eventually distribute nationwide to different grade levels.

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The museum is a resurrection of Dreamstage, a multimedia exhibition on sleep and dreams that Dr. Hobson took on an international tour from 1977 to 1982.

The museum includes a sleep chamber, a small, windowed room where subjects sleep as their brain rhythms are recorded; a preserved brain; and multimedia presentations about the brain and dreams. It is also, in many ways, a showcase for the brain as a work of art, with scientists’ detailed sketches and a framed painting of a human brain. Dr. Hobson, 73, said the museum “won’t truly be a public institution,” Notes but rather an opportunity for students to supplement classroom lessons with a three-dimensional view of the brain and its activities, helping them grasp its complexity and its functions.

The idea of preparing students with lessons before they visit came during Dreamstage. Dr. Hobson said most students arrived with minimal knowledge of the brain and left without a full appreciation of it.

“The school visits were all poorly organized,” he said. “They’d get out of the yellow buses like locusts and push every button to see if things moved. They didn’t understand everything. I said, ‘These kids should be coming to the museum after they’ve had a unit on a subject like sleep.’ ”

About two years ago, Dr. Hobson, who bought a farm in Caledonia County in the 1960s, took the idea to Scott Graham, the superintendent of the Caledonia North school district. Mr. Graham immediately agreed to go along with the experiment and allowed two middle school science teachers, Lois Michaud and Alison Chadboard, to develop a curriculum with Dr. Hobson.

“Our kids hadn’t had anything about the brain previous to this,” Ms. Michaud said. “The question was, how do we have them experience what Allan is trying to get them to understand, that during sleep there is a lot of stuff going on in your brain?

“There is a lot going on,” she added, “and so we had them do activities like keep a sleep log, but with no dream stuff because it might not be appropriate to talk about in school. They could say they had a dream but not talk about the content, and how they went to sleep, whether they stayed asleep and how they felt the next day.”

The goal was to get students to demonstrate an understanding of how bodily systems are connected and how that plays out during sleep. Students were also expected to learn what happens when the sleep cycle

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is disrupted and how the body adapts to changes in its equilibrium, like sleep deprivation.

The four-week lesson starts with a two-week introduction to the brain and its structure and what functions are controlled by different parts of the brain. Students become familiar with neurotransmitters and how they affect mood and hunger, and with dendrites, fibers that receive and transfer information.

Notes The following weeks focus on the sleep cycle. Students learn that they sleep so much because growth hormone is secreted during sleep, and if they do not sleep they will have shorter attention spans and use calories less efficiently. The lesson also covers disorders like narcolepsy and sleep apnea and their consequences.

Students also learn about dreams, and they are encouraged to discuss three theories about why people dream: to reorganize and refresh the brain; to help people remember things; and, Freud’s notion, to help people work out unsolved problems. Students also explore the psychology of dreams, including possible reasons for nightmares and dream content, but they are urged not to analyze one another’s dreams.

Ms. Michaud and Ms. Chadboard selected students to visit the barn, where they climbed into the sleep chamber and viewed sketches of the brain and frame-by-frame photos of people sleeping. They peppered Dr. Hobson with questions at a discussion in a silo he has converted into a five-story library that holds thousands of slides and books.

Dr. Hobson said the visit was exactly what he had imagined — students with a working knowledge of the brain, sleep and dreams excited to watch interviews of sleep subjects and analyze their dreams. They asked dozens of questions, including the theoretical, like how animals dream, and the personal, like how Dr. Hobson got into the field.

“Allan gave them permission to just take out of it whatever they could,” Ms. Michaud said, “and I think each kid did in their own way take something very different out of it.”

Amber Powers said she enjoyed learning about the intricacies of the brain.

“The thing I found interesting was that I saw a lot of pictures of different brain stems, things done by hand, very detailed drawings done with a camel-hair brush. A couple of them almost looked like frogs, they were so detailed,” she said. “It was really cool to see the sleep chamber where

Sleep Disorders these experiments took place and the monitors that showed the waves of the brain in different stages of sleep. You could really see how they differed.”

She said the lessons showed her that she was sleeping a few hours less than the 11 hours recommended for a 13-year-old. Her sleep journal showed that she played with her cats, getting hyped up before bed, or watched television and was unable to turn it off. She has since started reading or doing other relaxing activities to help her slow down before bedtime. Notes

School officials said Dr. Hobson was giving students in this rural part of the state an opportunity to see in their backyard things that usually require a trip to a city. “It was kind of like, wow, this kind of thing is going on right here; I thought this kind of thing happened in big cities,” Amber said. “It was really neat that all of this is in a barn.”

February 15, 2007

Fighting Snoring, and Its Dangers, Together

By LAURA RIVERA

MORRISTOWN, N.J., Feb. 13 — After canceling a planned romantic dinner, Dan Hajjar and Anne Marie Jarka-Hajjar, who have been married 17 years, spent Valentine’s eve in separate beds, tossing and turning amid a tangle of electrode wires and sensors stuck all over their bodies.

In a last-ditch bid for bedtime bliss, the couple checked into the sleep disorder clinic of Morristown Memorial Hospital, hoping its medical staff would deliver a respite from nearly two decades of uninterrupted snoring.

Mr. Hajjar, 42, an executive at Aon Corporation, has long been plagued by sleep apnea, which can disrupt breathing hundreds of times a night. Then, starting 18 months ago, Ms. Jarka-Hajjar, 41, a college professor and theater producer, turned their bedroom in Convent Station, N.J., into a nighttime chorus.

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“He would have 100 percent pushed this off until another time if he was doing it alone,” said Ms. Jarka-Hajjar, who blames sinus problems for her muffled snores. “So I’m hoping that by me being there and going through the same thing, it’s really going to help him, which will help me.”

As with so many newlyweds, snoring was a source of friction from the outset. For years, Ms. Jarka-Hajjar said, she dealt with it by taking a sleeping pill — or by taking her pillow to a couch in the den.

Notes But a few months ago, Mr. Hajjar’s condition took a turn for the worse. “I wake up in a panic like someone is suffocating me,” he said. “You’re gasping for air and your adrenaline starts pumping, and it’s more and more difficult to get back to sleep.”

Mr. Hajjar, an executive vice president of human resources at Aon, the insurance brokerage, admitted that his stressful work schedule had tempted him to cancel the appointment at the sleep clinic, but fear for his health won out.

The couple arrived at the hospital at 7 p.m. on Tuesday and settled into the hotel-like wing where the sleep lab is housed (their 5-year-old son spent the night at a relative’s). A crew of sleep technicians scurried from room to room, monitoring the placement of the myriad cords and tubes. Two consoles allow sleep experts to watch sleepers from a video feed, listen to their snoring, and check on vital signs they keep track of, including eye movement, muscle tension, heart rate and oxygen level.

The lab, founded in 1990, was rated the No. 1 sleep center in the nation by Advance for Managers of Respiratory Care, a medical journal, in 2005. It treats more than 2,600 patients a year, including perhaps a dozen couples, tops. More than 12 million Americans suffer from sleep apnea, a potentially dangerous disease that affects mostly men and overweight people and can increase the risk of stroke, heart attack and high blood pressure, according to the National Institutes of Health. In most cases, the sleeper’s throat muscles relax too much, obstructing the air passage and making breathing difficult.

Patients like Mr. Hajjar, who is physically fit, are often prescribed a continuous positive airway pressure machine, a masklike device that drives air into the collapsed passage. Mr. Hajjar has used such a machine sporadically since 2004, but he does not like it one bit. “It’s like someone is sticking an air hose up your nose,” he said. “My son, who is into Star Wars, said, ‘Dad, you sound like Darth Vader.’ ”

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During his evening at the clinic, Mr. Hajjar wore the awkward contraption, which consists of a tube placed below the nostrils, a strap around the head, and a bedside box that produces a steady whirring sound. The point of the exam was to adjust the machine to give Mr. Hajjar the air he needed to get some rest, and quiet the snoring that bothers his wife.

It will take a week or so before doctors fully analyze the results of the couple’s sleep test, but Neil Friedman, a registered nurse who runs the clinic, said Mr. Hajjar suffers from sleep apnea and will probably be Notes invited back for training on how to manage the problem, including simple tips like sleeping on his side instead of his back.

Because each partner’s snoring, shifting and occasional kicking would interrupt the other’s test, Mr. Hajjar and Ms. Jarka-Hajjar were asked, after initial testing, to retire to different rooms.

“We do let them stay together until the very end,” said Mr. Friedman, the center’s coordinator. “And they can actually kiss good night.”

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Glossary of Terms Used in Sleep Disorders

A Alpha activity The presence of alpha waves or alpha rhythm (i.e., electrical Notes oscillations in the alpha frequency) in the EEG of humans. See Alpha rhythm. Alpha intrusion (-infiltration, -insertion, -interruptions “riddled with” alpha) A brief interposition of alpha activity during a stage of sleep. Alpha rhythm (-activity, -frequency) EEG oscillations with a frequency of 8-13 Hz in adults, prominent over the occipital cortex: indicative of the awake state in humans; present in most, but not all, normal individuals most consistent and predominant during relaxed wakefulness, particularly with reduction of visual input. The alpha frequency has a range in each individual: the low end is exhibited in drowsiness or sleep and the upper end with alertness. The frequency range also varies with age; it is slower in children and older age groups relative to young and middle-aged adults. Arousal An abrupt change from a “deep” stage of NREM sleep to a “lighter” stage, or from REMS to awake, with the possibility of awakening as the final outcome. Arousal may be accompanied by increased tonic EMG activity and heart rate, as well as body movements. Awakening (full arousal) The return to the polysomnographically defined awake state from any of the NREM stages or REMS: characterized by alpha and beta waves, rise in tonic EMG, voluntary REMS, and eye blinks. This definition of awakening is valid only insofar as the polysomnogram is matched by a resumption of a reasonably alert state of consciousness.

B Base line The normative (i.e., typical) state of an individual or of an investigative parameter prior to an experimental manipulation.

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Bedtime Defined as the time when one attempts to fall asleep (as distinguished from the time when one gets into bed). Beta rhythm (-waves, -activity) EEG frequency in the range of 13-35 Hz; when the predominant frequency, beta rhythm is usually associated with alert wakefulness or vigilance and is accompanied by a high tonic EMG.

Notes

C Cataplexy A sudden, dramatic decrement in muscle tone and loss of deep reflexes leading to muscle weakness, paralysis, or postural collapse: usually precipitated by an outburst of emotional expression-notably laughter, startle, or sudden physical exercise; one of the tetrad of symptoms of narcolepsy. During cataplexy, respiration is not compromised. Cheyne-Stokes respiration A breathing pattern characterized by regular “crescendo- decrescendo” fluctuations in respiratory rate and tidal volume. Circadian rhythm An innate, daily, fluctuation of physiological and behavioral functions, including sleep waking, generally tied to the 24 hour day-night cycle but sometimes to a measurably different (e.g., 23 or 25 hour) periodicity when light/dark and other time cues are removed. Conditioned insomnia An easily overlooked form of chronic insomnia (sometimes a component of psychophysiological DIMS) caused by the development-during an earlier experience of sleeplessness --of a negative association between characteristics of the customary sleep environment and sleeping.

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D “Deep” sleep stage Common term for NREM stages 3 and 4 sleep. In some European sleep literature, “deep” sleep is applied to REM sleep

because of its high awakening threshold. Set, “Intermediary” Notes sleep stage: “Light” sleep stage.

Delayed sleep phase A condition that occurs when the clock hour at which sleep normally occurs is moved back in time in a given, 24-hour sleep- wake cycle. This results in a temporarily displaced (delayed) occurrence of sleep within the 24-hour cycle. The same term denotes a chronic sleep schedule disturbance. Delta sleep stage(s) Indicative of the stage(s) of sleep in which EEG delta waves are prevalent or predominant (sleep stages 3 and 4, respectively). See Slow wave sleep. Delta waves EEG activity with a frequency of less than 4 Hz. In human sleep scoring, the minimum characteristics for scoring delta waves is conventionally 75 uV (peak-to-peak) amplitude, and 0.5 second duration (2 Hz). Dyssomnia Any disorder of sleep or wakefulness per se; not a parasomnia.

E Early a.m. arousal Synonymous with premature morning awakening. Electroencephalogram (EEG) A recording through the scalp of the electrical potentials from the brain and the moment-to-moment changes in these potentials. With the EMG and EOG, the EEG is one of the three basic variables used to score sleep stages and waking. Sleep recording in humans utilizes surface electrodes to record potential differences between brain regions and a neutral reference point, or simply between brain regions. Either the C3 or C4, central

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region, placement in the International 10-20 system is the standard electrode from which stage scoring is done. Electromyogram (EMG) A recording of electrical activity from the muscular system; in sleep recording, synonymous with resting muscle activity or potential. The chin/cheek EMG, along with EEG and EOG, is one of the three basic variables used to score sleep stages and waking. Sleep recording in humans utilizes surface electrodes to measure activity from the submental or masseter muscles. These reflect maximally the changes in resting muscle activity. The Notes chin/cheek EMG is tonically inhibited during REM sleep. Electro-oculogram (EOG) A recording of voltage changes resulting from shifts in position of the eyeball-possible because each globe is a positive (anterior) and negative (posterior) dipole; along with the EEG and the EMG, one of the three basic variables used to score sleep stages and waking. Sleep recording in humans utilizes surface electrodes placed near the eyes to record the movement (incidence, direction, and velocity) of the eyeballs. Rapid eye movements in sleep indicate a certain stage of sleep (REM sleep). Excessive daytime sleepiness or somnolence A subjective report of difficulty in maintaining the awake state, accompanied by a ready entrance into sleep when the individual is sedentary; may be quantitatively measured by use of subjectively defined rating scales of sleepiness.

F Fragmentation (pertaining to sleep architecture) The interruption of any stage of sleep due to appearance of another stage or waking, leading to disrupted NREMS-REMS cycles; often used to refer to the interruption of REMS by movement arousals or stage 2 activity. Sleep fragmentation connotes repetitive interruptions of sleep by arousals and awakenings.

H Hertz (Hz) A unit of frequency; synonymous with cycles per second (cps).

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Hypercapnia Elevated carbon dioxide level in blood Hypersomnia Excessive or prolonged sleep. Sometimes associated with difficulty in awakening or sleep drunkenness. Hypnagogic imagery (-hallucinations) Vivid sensory images occurring at sleep onset but particularly vivid with sleep-onset REMS periods. A feature of narcoleptic REMS naps. Notes Hypnagogic startle A “sleep start” or sudden body jerk, observed normally just at sleep onset and resulting in at least momentary awakening.

I Insomnia Difficulty in sleeping. A confusing term-though ubiquitously employed because it is used to indicate any and all gradations and types of sleep loss.

K K complex A sharp, negative, high-voltage EEG wave, which is followed by a slower, positive component. K complexes occur spontaneously during NREM sleep, beginning in (and defining) stage 2. They are thought to be CNS-evoked responses to internal stimuli. They can be elicited during sleep by external (particularly auditory) stimuli as well.

L “Light” sleep stage Common term for NREMS stage I (and sometimes stage 2). See “Deep” sleep stage.

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M Microsleep(s) A period lasting up to a few seconds during which the polysomnogram suddenly shifts from waking characteristics to sleep and external stimuli are not perceived; associated with

excessive daytime sleepiness and automatic behavior, which are symptoms of DOES. Notes Movement arousal A body movement associated with arousal or awakening; a sleep scoring variable. Movement time The term used in sleep record scoring to denote when EEG and EOG tracings are obscured for more than 15 seconds because of movement. Usually combined with awake time. Multiple sleep latency test (MSLT) A series of measurements of the interval from “lights out” to sleep onset that is utilized in the assessment of excessive daytime sleepiness. Subjects are allowed a fixed number of opportunities to fall asleep during their customary awake period. Long latencies are helpful in distinguishing physical tiredness or fatigue from true sleepiness. Muscle tone A term sometimes used for resting muscle potential or resting muscle activity. See Electromyogram (EMG). Myoclonus Muscle contractions in the form of “jerks” or twitches. In sleep- related (nocturnal) myoclonus, the jerks are primarily of the flexor groups in the lower extremities and have a characteristic frequency of 20-40 seconds.

N Nightmare Used to denote a dream anxiety attack, not a sleep (night) terror. In the past-and still in the European sleep literature-nightmare is used to indicate both sleep terror and anxiety dream. Nocturnal confusion Episodes of delirium and disorientation close to or during nighttime sleep; often seen in the elderly and indicative of organic CNS deterioration.

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Nocturnal dyspnea Respiratory distress, minimal during the day but becoming quite disturbing in sleep. Nocturnal sleep Indicative of the typical “nighttime,” or major, sleep period dictated by one’s circadian rhythm of sleep and wakefulness; the conventional time for sleeping. Non-rapid eye movement sleep (NREMS, also written as non-REMS) See Sleep stages. Notes NREMS intrusion An interposition of NREM sleep, or a component of NREMS physiology (e.g., elevated EMG, K-complex, sleep spindle, delta waves), in REMS; a portion of NREMS not appearing in its usual sleep cycle position. NREMS period The NREMS portion of NREMS - REMS cycle; such a period consists primarily of sleep stages 3/4 early in the night and of sleep stage 2 later. See Sleep cycle; Sleep stages. NREMS-REMS cycle (synonymous with sleep cycle) A period during sleep composed of a NREMS period and the subsequent REMS period; each NREMS-REMS couplet is equal to one cycle. Any NREM sleep stage suffices as the NREMS portion of a cycle. A sleep period of 6.5-8.5 hr generally consists of four to six cycles.

P Parasomnia Not a disorder of sleep or wakefulness per se; rather, an event happening during sleep, or induced or exacerbated by sleep, such as sleepwalking or asthma; not a dyssomnia. Paroxysmal nocturnal dyspnea (PND) Respiratory distress and shortness of breath due to pulmonary edema, which appear suddenly and often awaken the sleeping individual. Period length The duration of time encompassed by an individual’s full, daily sleep-wake cycle; conventionally, but not always, 24 hours. See Circadian rhythm. Phase advance The movement to a position earlier in the 24 hour sleep - wake cycle of a period of sleep or wake; for example, a shift of the

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sleep phase from 11 p.m. - 7 a.m. to 8 p.m. - 4 a.m. See Phase delay. Phase delay Phase delay is exactly the opposite of phase advance, i.e., a shift later in time. (Confusion is sometimes introduced into these concepts because clock language is reversed; to effect a phase delay, the clock is moved ahead or advanced. Contrariwise, as in the example in phase advance, the change from the 11 p.m. - 7 a.m. to the 8 p.m. - 4 a.m. position requires a movement of the clock backward.) See Phase advance. Notes Phase transition One of the two junctures of the major sleep and wake phases in the 24 hour sleep-wake cycle. Phasic event (-activity) Brain, muscle, or autonomic events of an episodic or fluctuating nature occurring in sleep; characteristic of REMS (e.g., eye movements, muscle twitches); usually enduring for milliseconds to 1 -2 seconds. Polysomnogram The continuous and simultaneous recording of physiological variables during sleep, i.e., EEG, EOG, EMG (these are the three basic stage scoring parameters), EKG, respiratory air flow, respiratory excursions, lower limb movement, and other electrophysiological variables. Premature morning awakening Early termination of the sleep period in a sleep maintenance DIMS due to inability to return to sleep after the last of several awakenings, typifies the failure to accomplish a normal length of nocturnal sleep because of interference at the end rather than at the commencement of sleep: the DIMS characteristic of depressed individuals.

R Rapid eye movement sleep (REMS) See, Sleep stages. REM density (-intensity) A function that expresses the frequency of eve movements during sleep stage REM. REMS intrusion A brief interval of REMS appearing out of its usual position in the NREMS-REMS cycle, an interposition of REMS in NREMS; sometimes appearance of a single, dissociated component of

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REMS (e.g., eye movements, or “drop out” of muscle tone) rather than all REMS parameters. REMS latency The period of time in the sleep period from sleep onset to the first appearance of stage REMS. REMS onset The designation for commencement of a REMS period. Sometimes also used as a shorthand term for a sleep-onset REMS period. See Sleep onset: Sleep-onset REMS period. Notes REMS percent The proportion of total sleep time constituted by the REM stage of sleep. REMS period The REMS portion of a NREMS-REMS cycle; early in the night it may be as short as a half-minute, whereas in later cycles longer than an hour. See Sleep stage REM. REMS rebound or recovery Lengthening and increase in frequency and density of REMS periods, which results in an increase in REMS percent above base line. REMS rebound follows REMS deprivation once the inhibitory influence is removed. Restlessness (referring to a quality of sleep) Persistent or recurrent body movements, arousals, and brief awakenings in the course of sleep.

S Sleep architecture The NREMS/REMS stage and cycle infrastructure of sleep understood from the vantage point of the quantitative relationship of these components to each other. See Sleep structure. Sleep cycle Synonymous with NREMS-REMS cycle. Sleep efficiency (or sleep efficiency index) The proportion of sleep in the period potentially filled by sleep-, that is, the ratio of total sleep time to time in bed. Sleep hygiene The conditions and practices that promote continuous and effective sleep. These include regularity of bedtime and arise time: conformity of time spent in bed to the time necessary for sustained and individually adequate sleep (i.e., the total sleep time sufficient to avoid sleepiness when awake); restriction of alcohol

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and caffeine beverages in the period prior to bedtime; employment of exercise, nutrition, and environmental factors so that they enhance, not disturb, restful sleep. Sleep interruption Breaks in the sleep architecture resulting in arousal and wakefulness. See Fragmentation; Restlessness. Sleep latency The period of time measured from “lights out,” or bedtime, to the commencement of sleep. Sleep log (-diary) Notes A daily, written record of an individual’s sleep-wake pattern containing such information as time of retiring and arising, time in bed, estimated total sleep period, number and duration of sleep interruptions, quality of sleep, daytime naps, use of medications or caffeine beverages, nature of waking activities, and other data. Sleep-maintenance DIMS or insomnia A disturbance in maintaining sleep once achieved; persistently interrupted sleep without difficulty falling asleep. Synonymous with sleep continuity disturbance. Sleep mentation The imagery and thinking (and emotion) experienced during sleep. Sleep mentation consists of individual representations-but usually combinations of-images and thoughts. Imagery is vividly expressed in dreams during REMS in all the senses in approximate proportion to their waking representations. Mentation is experienced generally less distinctly in NREM sleep, but it may be quite vivid in stage 2 sleep, especially toward the end of the sleep period. Sleep onset The transition from the awake to the sleep state, normally into NREM stage I (but in certain conditions, such as infancy and narcolepsy, into stage REMS). Most polysomnographers accept EEG slowing, reduction, and eventual disappearance of alpha activity, presence of EEG vertex spikes, and slow rolling eye movements (the components of NREM stage 1) as sufficient for sleep onset. others require appearance of stage 2 wave forms. Consciousness has been shown to be lost as alpha activity fragments. See Sleep latency, Sleep stages. Sleep-onset REMS period The atypical beginning of sleep by entrance directly into stage REMS. Sleep pattern (24 hour sleep-wake pattern) An individual’s clock hour schedule of bedtimes and rise times as well as nap behavior: may also include time and duration of sleep

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interruptions. See Sleep-wake, 24-hour cycle; Circadian rhythm; Sleep log. Sleep spindle An episodically appearing, spindle-shaped aggregate of 12-14 Hz waves with a duration of 0.5-1.5 seconds, one of the identifying EEG phenomena of NREM stage 2 sleep; may persist into NREM stages ¾: not seen in REMS. Sleep stage demarcation The significant polysomnographic characteristics that distinguish Notes the boundaries of the sleep stages. In certain conditions and with drugs, sleep stage demarcations may be blurred or lost, making it difficult to identify certain stages with certainty or to distinguish the temporal limits of sleep stage lengths. Sleep stage period A sleep stage interval that represents the stage in a NREMS - REMS cycle; easiest to comprehend in relation to REMS, which is a homogeneous stage, i.e., the fourth REMS period is in the fourth sleep cycle. If one interval of REMS separated from another by more than 20 minutes, they constitute separate REMS periods (and are in separate sleep cycles); a sleep stage period may be any duration. Sleep stages: Sleep stage NREM (NREMS) The other major sleep state apart from REMS; comprises sleep stages 1-4, which constitute areas in the spectrum of NREMS “depth” or physiological intensity. Sleep stage I (NREMS stage 1) A stage of NREM sleep that ensues directly from the awake state. Its criteria consist of a low-voltage EEG with slowing to theta frequencies, alpha activity less than 50%, EEG vertex spikes, and slow rolling eye movements; no sleep spindles, K complexes, or REMS. Stage I normally assumes 4-5% of total sleep. Sleep stage 2 (NREMS stage 2) A stage of NREM sleep characterized by the advent of sleep spindles and K complexes against a relatively low- voltage, mixed-frequency EEG background; high-voltage delta waves may comprise up to 20% of stage 2 epochs; usually accounts for 45-55% of total sleep time. Sleep stage 3 (NREMS stage 3) A stage of NREM sleep defined by at least 20 and not more than 50% of the period consisting of EEG waves less than 2 Hz and more than 75 uV (high-amplitude delta waves); a “delta” sleep stage; with stage 4, it constitutes “deep” NREM sleep; often combined with

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stage 4 into NREMS stage 3./4 because of the lack of documented physiological differences between the two; appears usually only in the first third of the sleep period; usually comprises 4-6% of total sleep time. Sleep stage 4 (NREMS stage 4) All statements concerning NREMS stage 3 apply to stage 4 except that high-voltage, slow EEG waves, cover 50% or more of the record: NREMS stage 4 usually takes up 12-15% of total sleep time. Somnambulism, sleep terror, and sleep-related enuresis episodes generally start in stage Notes 4 or during arousals from this stage. See Sleep stage 3. Sleep stage REM (REMS) The stage of sleep (i.e., state of the CNS) found in all mammals studied, including man, in which brain activity is extensive, brain metabolism is increased, and vivid hallucinatory imagery, or dreaming occurs (in humans). It is also called “paradoxical sleep” because, in the face of this intense excitation of the CNS and presence of spontaneous rapid eye movements, resting muscle activity is suppressed. The EEG is a low-voltage, fast-frequency, nonalpha record. Stage REMS is usually 20-25% of total sleep time. Sleep structure Similar to sleep architecture. However, sleep structure-in addition to encompassing sleep stage and cycle relationships-assesses the within-stage qualities of the EEG and other physiological attributes. Sleepiness (somnolence, drowsiness) Difficulty in maintaining the wakeful state so that the individual falls asleep if not actively kept aroused-, not simply a feeling of physical tiredness or listlessness. See Excessive daytime Sleepiness. Sleep talking Talking in sleep takes place during stage REMS, at which time it represents a motor breakthrough of dream speech, or in the course of transitory arousals from NREMS and other stages. Full consciousness is not achieved and no memory of the event remains. Sleep-wake, 24 hour cycle Basically, the clock hour relationships of the major sleep and wake phases in the 24 hour cycle: similar to sleep pattern. See Phase transition; Circadian rhythm. Sleep-wake shift (-change, -reversal) When sleep-wholly or partially-is moved to a time of customary waking activity, and the latter is moved to the habitual sleep period; common in jet lag and shift work.

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Slow wave sleep (SWS) Synonymous with sleep stages 3 and 4. See Delta sleep stage(s). Snoring A noise produced primarily with inspiratory respiration during sleep owing to vibration of the soft palate and the pillars of the oropharyngeal inlet. Many snorers have incomplete obstruction of the upper airway, and may in time develop frank obstructive sleep apnea. Spindle REMS Notes A condition in which sleep spindles persist atypically in REMS; seen in chronic DIMS conditions. Subwakefulness syndrome A syndrome postulated as a defect in the CNS support system for waking. The few individuals reported with subwakefulness syndrome have daytime drowsiness and daytime sleep episodes that are always composed of NREMS stages I or 2. The naps occur repetitively.

T Theta waves EEG activity with a frequency of 4-8 Hz, maximal over temporal cortex. Total sleep period The period of time measured from sleep onset to final awakening. In addition to total sleep time, it is comprised of the time taken up by arousals and movement time until wake-up. See Sleep efficiency. Total sleep time The amount of actual sleep time in a sleep period; equal to total sleep period less movement and awake time. Total sleep time is the total of all REMS and NREMS in a sleep period. Tumescence (penile) Hardening and expansion of the penis: penile erection. Commonly referred to as nocturnal penile tumescence (NPT) in sleep recordings. Twitch (body twitch) A very small body movement such as a facial grimace or finger jerk: not usually associated with arousal.

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W Wake time The total time that is scored awake in a polysomnogram occurring between sleep onset and final wake-up.

List of Abbreviations Notes

CNS Central nervous system cps Cycles per second DIMS Disorders of initiating and maintaining sleep DOES Disorders of excessive somnolence EEG Electroencephalogram EMG Electromyogram EOG Electro-oculogram Hz Hertz NPT Nocturnal penile tumescence NREMS Non-rapid eye movement sleep PND Paroxysmal nocturnal dyspnea REM(S) Rapid eye movement(s) REMS Rapid eye movement sleep SWS Slow wave sleep

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Notes

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Sleep Disorders Exam

1. A sleep disorder that is primarily caused by a physiological abnormality is known as: a. an intrinsic sleep disorder. b. an extrinsic sleep disorder. c. a parasomnia. d. a circadian rhythm disorder. Notes 2. The severity of a sleep disorder is most often determined by: a. the patient’s symptoms. b. the duration of the complaint. c. the bedpartner’ observations. d. all of the above.

3. Sleep disorders that are related to the timing of sleep within the 24 hour day are classified as: a. Circadian rhythm disorders. b. parasomnias. c. insomnias. d. hypersomnias.

4. A mean sleep latency of less than 5 minutes and two or more sleep onset REM periods seen on a MSLT performed following nocturnal polysomnography which shows severe obstructive sleep apnea syndrome: a. is diagnostic of narcolepsy. b. indicates idiopathic hypersomnia. c. cannot diagnose narcolepsy because of the untreated sleep related breathing disorder. d. is diagnostic of recurrent hypersomnia.

5. Common symptoms seen in patients with obstructive sleep apnea syndrome include: a. non-continuous loud snoring. b. daytime sleepiness. c. frequent nocturnal urination. d. all of the above.

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6. Idiopathic insomnia is: a. a relatively rare disorder. b. also known as childhood onset insomnia. c. present at birth and a lifelong disorder. d. all of the above.

7. The most common cause of obstructive sleep apnea in children is: a. a deviated septum. Notes b. enlarged tonsils and adenoids. c. poor respiratory muscle tone. d. hypothyroidism.

8. A type of apnea that occurs as a result of central respiratory control center malfunction is known as: a. central sleep apnea syndrome. b. central alveolar hypoventilation. c. obstructive sleep apnea syndrome. d. obstructive alveolar hypoventilation.

9. Obstructive sleep apnea events most commonly occur during: a. Stage I and II sleep. b. Stages I, II, and REM sleep. c. Stage IV sleep. d. Stage III sleep.

10. Periodic episodes of repetitive and highly stereotyped limb movements that occur during sleep are seen in patients with: a. rhythmic movement disorder. b. restless movements syndrome. c. periodic limb movement disorder. d. sleep bruxism.

11. Disorders of arousal, partial arousal and sleep stage transition are known as: a. circadian rhythm disorders. b. parasomnias. c. sleep state misperception. d. insomnias.

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12. Fever, sleep deprivation, or external stimulation such as noise may increase the frequency of: a. sleep terrors. b. confusional arousals. c. sleep walking episodes. d. all of the above.

13. In order to diagnose impaired sleep related penile erections, polysomnography must document: a. the absence of sleep related breathing disorders. Notes b. normal sleep architecture and adequate REM sleep. c. the absence of periodic limb movements and sleep fragmentation. d. all of the above.

14. Episodes of grinding or clenching the teeth during sleep are seen in patients with: a. sleep bruxism. b. sleep enuresis. c. nocturnal eating (drinking) syndrome. d. all of the above.

15. Polysomnography in patients with primary snoring documents: a. repetitive central apnea events. b. obstructive hypopnea events with arousals, but no evidence of oxygen desaturation. c. normal respiratory patterns with no evidence of arousals, cardiac arrhythmias or oxygen desaturation. d. all of the above.

16. Polysomnography during an episode of sleep enuresis should document: a. urination occurring upon arousal from sleep. b. the presence of seizure activity during the episode. c. bursts of masseter muscle activity during the episode. d. involuntary urination during sleep and absence of seizure activity.

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17. Sleep disorders which do not meet the criteria for classification under any other category, and are classified as “other parasomnias” include: a. limit setting disorder and hypnotic dependent sleep disorder. b. infant sleep apnea, SIDS, and bruxism. c. REM sleep behavior disorder and sleep walking. d. recurrent hypersomnia and environmental sleep disorder. Notes 18. Apnea of prematurity (AOP), apnea of infancy (AOI), apparent life threatening events (ALTE), and obstructive sleep apnea syndrome are all components of: a. infant sleep apnea. b. congenital central hypoventilation. c. cerebral degenerative disorders. d. central sleep apnea syndrome.

19. Nightmares, sleep paralysis, and impaired sleep related penile erections are all: a. arousal disorders. b. parasomnias associated with REM sleep. c. sleep wake transition disorders. d. circadian rhythm sleep disorders.

20. Repetitive stereotyped movements of the head and neck which occur immediately prior to sleep and into light sleep are characteristic of: a. periodic limb movement disorder. b. REM behavior disorder. c. rhythmic movement disorder. d. sleep bruxism.

21.Myocardial ischemia during sleep may result from: a. oxygen desaturation. b. bradycardia and decreased blood pressure during slow wave sleep. c. tachycardia during REM sleep. d. all of the above.

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22. Chronic impairment of gas exchange and C02 retention are commonly seen in patients with: a. nocturnal cardiac ischemia. b. chronic obstructive pulmonary disease. c. sleep related gastroesophageal reflux. d. all of the above.

23. CPAP or oxygen administration in patients with COPD may lead to: a. an increase in obstructive apnea events. Notes b. CO2 retention. c. a significant increase in slow wave sleep. d. REM rebound.

24. ______is characterized by hallucination, delusions, incoherence, and catatonic behavior. a. Psychosis b. Narcolepsy c. Dementia d. Nocturnal cardiac ischemia

25. Sleep disorders which occur as a result of medical or psychiatric disorders: a. are classified as primary sleep disorders. b. include sleep enuresis and sleep bruxism. c. are not primary sleep disorders but have a significant effect on sleep or wakefulness. d. include inadequate sleep hygiene and environmental sleep disorders.

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Notes