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Home , Automatic behavior, Sleep disorder, Sleep hygiene, Sleep study

Focus on CME at the University of British Columbia

My Patient’s Sleepy, And It’s Not Apnea

Excessive daytime sleepiness is not a benign complaint and always requires careful investigation.

By Jonathan A.E. Fleming, MD

Presented at the 2nd Annual Advances In Respiratory And Critical Care Medicine, Whistler, British Columbia, March 2001.

hen presented with a 45-year-old, moder- asleep in class, at home and anytime he tries to W ately obese, hypertensive male who is study, despite sleeping 10 hours each night. noted by his wife to snore, hold his breath, snort The purpose of this article is to emphasize that, in during the night and fall asleep when driving to the presence of adequate nocturnal sleep, daytime work and during the day, most clinicians would sleepiness is always pathological. It requires further consider a diagnosis of obstructive . investigation to assist the clinician in the systematic Diagnostic certainty may be more elusive, how- assessment of the sleepy patient whose sleepiness is ever, when we change the parameters — our not explained by a respiratory . patient may be a thin, non-, normotensive The clinical assessment begins with a patient his- student, who is on the basketball team yet falls tory supplemented by a sleep diary (ideally complet- ed over a one-week period), a delineation of the sleep complaint (its onset, course and manifestations, both Dr. Fleming is associate day and night), a comprehensive medical and psy- professor, department of chiatric work-up, and the formulation of a differen- , University of British tial diagnosis (see www.sleepfoundation.org/publica- Columbia, and co-director, sleep tions/sleepdiary.html for a sample sleep diary). To program, University Hospital, make an accurate diagnosis, the clinician must be Vancouver. His areas of interest familiar with how sleep disorders are classified, and include the relationship between then make a connection between the clinical find- sleep disorders and psychiatric ill- ings and the available diagnoses within the classifi- ness. cation system.

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Summary My Patient’s Sleepy, And It’s Not Sleep Apnea

• The clinical assessment begins with a patient history supplemented by a sleep diary (ideally completed over a one-week period), a delineation of the sleep complaint (its onset, course and manifestations, both day and night), a comprehensive medical and psychiatric work-up, and the formulation of a differential diagnosis. •Secondary sleep disorders are the most common causes of and, less frequently, or sleepiness. • The most common medical cause of sleep disruption and sleep loss is nocturnal discomfort or pain. • Primary insomnia is viewed as a disorder of hyperarousal, with the physiologic, somatic and cognitive hyperarousal at contributing to the initial and maintenance insomnia. • Daytime sleepiness and are the most consistent symptoms of . • Desynchrony between time and the has important consequences for sleep performance and daytime alertness. • Common experience shows environmental factors, such as noise and light, can significantly influence sleep performance. • Usually and periodic limb will require a sleep laboratory assessment to quantify the extent of the sleep disruption, exclude other sleep pathologies and, where daytime sleepiness is an issue, quantify sleepiness with the multiple sleep latency test.

Classification ders or substance use, or with combinations of all Of Sleep Disorders three. By carefully considering each of these four The Diagnostic of Statistical Manual of Mental major groupings, the physician often can determine Disorders (DSM-IV) provides a user-friendly clas- the correct diagnosis of the patient’s sleepiness by sification system, as it groups sleep disorders into history alone (Figure 1). four major sections according to their presumed In adults, are relatively rare events etiology (Table 1).1 that occur during sleep. They infrequently cause Primary sleep disorders. These are thought to excessive daytime sleepiness, so they can be readily arise from endogenous abnormalities of the sleep- ruled out as causes of hypersomnolence, except in wake or sleep-timing systems and are subdivided two circumstances. First, when parasomnias, such as into (disturbances in the amount, quality , are frequent and distressing, the suffer- or timing of sleep) and parasomnias (characterized er may purposefully ration his/her sleep in the hope by abnormal behavior or physiologic events occur- of decreasing the events, with the resultant daytime ring in association with sleep, specific sleep stages or sleepiness being caused by . The sleep-wake transitions). second circumstance is when the is Secondary sleep disorders. These are the most rapid eye movement (REM) sleep-behavior disorder frequent causes of disrupted sleep, and are associ- (RSBD), which is classified by the DSM-IV as a ated with either mental disorders, medical disor- parasomnia not otherwise specified.2

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RSBD is more commonly seen in older men and Table 1 is characterized by a loss of the atonia ( of the antigravity muscles) normally accompanying DSM-IV Sleep Disorders REM sleep, which permits the physical acting out of content, with disruptive and potentially Primary sleep disorders violent behavior. In its early stages RSBD is usual- • Dyssomnias ly not associated with sleepiness, but as it is associ- - Primary insomnia ated with a variety of neurologic conditions, sleepi- - Primary hypersomnia ness may be seen in later stages as secondary to the - Narcolepsy sleep disruption associated with the primary condi- - Breathing-related sleep disorder - Circadian rhythm sleep disorder tion (e.g., or Lewy body ) or - Delayed sleep phase type 3 its treatment. The characteristic clinical history of - type dream enactment, with clear recall of the dream, - type helps distinguish sleepiness caused by RSBD or its - Unspecified type treatment from other causes of sleepiness. - not otherwise specified - Environmental factors - Sleep deprivation Secondary Causes Of - Restless legs syndrome Hypersomnolence - Periodic limb movements Secondary sleep disorders are the most common - Dyssomnia of indeterminate causes of insomnia and, less frequently, hypersom- origin nia or sleepiness. In assessing the sleepy patient, a • Parasomnias complete consideration of possible etiologies - disorder requires a careful diagnostic work-up, which should - Sleep terror disorder include a detailed medical and psychiatric evalua- - disorder - Parasomnia not otherwise specified tion, as well as documentation of all medications, non-prescription medication and recreational drug Secondary sleep disorders use by the patient. • Sleep disorders related to another mental The most common medical cause of sleep dis- disorder ruption and sleep loss is nocturnal discomfort or - Hypersomnia pain. For example, in patients with osteoarthritis, - Insomnia physical distress during sleep causes significant • Sleep disorder related to a general medical sleep disruption and daytime impairment that is condition improved by the judicious use of analgesia.4 In - Insomnia type - Hypersomnia type addition to the direct effects of a on the - Parasomnia type sleep process, medications used to treat chronic dis- • Substance-induced sleep disorder eases also can induce (Table 2). - Insomnia type Sleepiness associated with the newer anti- - Hypersomnia type Parkinsonian agents, for example, has been a recent - Parasomnia type focus of concern, although it is likely that somno- - Mixed type lence is a side effect of most agents used to treat this disease.5

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EXCESSIVE DAYTIME SLEEPINESS

YES If history suggests a Respiratory sleep disorder ruled out? respiratory sleep NO disorder, refer for further assessment YES NO Ensure regular, Adequate night-time sleep? adequate sleep time YES Slow withdrawal Refer to sleep center followed by a Unusual nocturnal behaviors YES for further reassessment to (parasomnias)? evaluation and exclude medical, treatment psychiatric NO and/or sleep Physical symptoms, medical illness or treatments disorders YES Rigorous causing sleep disruption? treatment of primary NO Substance- condition; induced sleep practise good Prominent psychiatric illness causing sleep disruption? disorder YES sleep

NO

YES Alcohol, recreational drug or non-prescription drug use, intoxication or withdrawal? Refer to sleep center for NO Consider jet further lag, shiftwork Is there a sleep timing issue or YES evaluation intolerance, circadian rhythm disorder? and delayed treatment NO sleep-phase syndrome YES Is there a history of cataplexy, hypnagogic or ?

NO Refer to Is there a history of long sleep times, sleep drunkenness, sleep center and unrefreshing ? for further evaluation Primary and YES hypersomnia treatment

Figure 1. Diagnosis of patient sleepiness.

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Recreational drugs, such as marijuana and alco- hol, are sedating and can induce sleepiness in good Table 2 sleepers and exacerbate it in sleep-deprived sub- Medications Causing Daytime jects.6,7 Obviously, due to the risk of dependence Sleepiness and abuse and because of adverse side-effects, recreational drugs and alcohol should not be used Anticonvulsants as . •Barbiturates The abrupt withdrawal of causes an •Carbamazepine acute sleep disturbance and periods of hypersom- • •Topiramate nia.8 users commonly abuse sedative •Valproate sodium drugs to promote sleep during the time they are using the stimulant. The associated mood changes Antidepressants of withdrawal may further complicate the picture. • Serotonin reuptake inhibitors (e.g., fluoxetine) •Tricyclics (e.g., amitriptyline, trimipramine) , such as diphenhydramine, are •Trazodone common, self-directed treatments for insomnia.9 They are effective hypnotics, but because of their Antihistamines • Diphenhydramine psychomotor effects, antihistamines compare • Loratadine unfavorably with the short-acting benzodiazepine, •Terfenadine cyclopyrrolone and pyrazolopyrimidine hyp- Antihypertensives notics. This unfavorable comparison is solidified •Beta blockers by the fact that antihistamines are associated with • significant daytime sedation or sleepiness.10 As • Methyldopa they are available “over the counter,” patients do not view antihistamines as potent medications and • Chlorpromazine may forget to tell their doctor they are taking • Loxapine them. Furthermore, it is not uncommon for •Trifluperazine patients to double or triple the dose to either get a • Haloperidol more restful sleep or to manage the loss of effect Dopamine agonists (tolerance) seen with chronic use of the drug. • Levodopa Psychiatric disorders are the most common •Pramipexole cause of secondary insomnia and, as disrupted • Pergolide sleep is usually associated with daytime sleepi- • Ropinirole ness, they may cause excessive daytime sleepiness Sedative hypnotics (EDS). Additionally, because of symptoms associ- • Benzodiazepines (especially long half-life ated with their psychiatric illness (i.e., , drugs, such as flurazepam) • Chloral hydrate phobic avoidance, ), • patients may not practise good , keep regular sleeping times or receive adequate expo- Opiates •Morphine sure to bright light. Patients with mood disorders, • Codeine particularly those afflicted with the atypical or • Oxycodone seasonal variant, complain of EDS. Objective

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measures of their daytime sleep propensity, how- In primary hypersomnia, the patient has expe- ever, shows that, although they are impaired, they rienced excessive sleepiness, with impairment in are less sleepy than patients with primary hyper- daytime functioning for at least one month. somnia or normal controls.11 As for the hyper- Despite a nocturnal sleep period of eight to 12 somnias secondary to medical disorders, rigorous hours, the patient usually will complain of diffi- treatment of the primary cause of sleep disruption culty arising in the morning, exhibit sleep and maintenance of good sleep hygiene practices drunkenness or automatic behavior upon awak- usually result in a significant improvement in day- ening, battle episodes of sleepiness and usually time functioning. take unrefreshing naps of one or more hours. Because of their lack of alertness, patients with Primary Causes primary insomnia also complain of lowered Of Hypersomnolence occupational efficiency, impaired concentration and memory, and difficulty in performing tasks, Primary hypersomnia. Having ruled out the para- such as driving. somnias and the secondary causes of sleep disrup- Also in primary hypersomnia, the quality of tion (psychiatric illness, medical illness and/or nocturnal sleep is normal, yet the objective mea- substance use), the physician should consider the surement of sleepiness in the day via the multi- primary causes of insomnia and daytime sleepi- ple sleep latency test (MSLT) shows increased ness. Primary insomnia is viewed as a disorder of physiologic sleepiness without the disturbances hyperarousal, with the physiologic, somatic and in REM sleep, which are characteristic of nar- cognitive hyperarousal at bedtime contributing to colepsy.13 Confirmation of a diagnosis of prima- the initial and maintenance insomnia. This same ry hypersomnia usually requires further evalua- hyperarousal prevents drowsiness or sleepiness in tion at a sleep center, as well as treatment with the daytime and, although primary insomniacs stimulants during the day.11 complain of being tired and fatigued, they are usu- Narcolepsy. Narcolepsy is a syndrome affect- ally not sleepy and are rarely able to during ing 0.02% to 0.18% of the general population, the daytime.12 Therefore, when the sleep diary of characterized by EDS, disturbed nocturnal sleep a patient with suspected primary insomnia shows and abnormalities in REM sleep, such as cata- significant and sustained daytime sleeping, other plexy, sleep paralysis and hypnagogic hallucina- conditions like poor sleep hygiene, a psychiatric tions. It is diagnosed using nocturnal disorder causing hypersomnolence or a circadian with the demonstration of rhythm sleep disturbance, should be considered. EDS (average sleep latencies of less than five Approximately 10% to 15% of patients seen at minutes) and REM transitions (two or more sleep disorder clinics receive either a diagnosis of REM periods in the daytime sleep recording) primary hypersomnia or hypersomnia related to a during the MSLT. . Primary hypersomnia is a poorly Daytime sleepiness and cataplexy are the understood condition or, more likely, group of most consistent symptoms of the syndrome, conditions. Differentiating it from psychiatric although about 30% of narcoleptics will never hypersomnia is difficult, often requiring a sleep experience cataplexy during the lifelong course expert and a to help delineate the prob- of their illness. Chronic sleepiness is the most lem. disabling symptom. Cataplexy is the most dra-

106 The Canadian Journal of CME / December 2001 Non-respiratory Sleep Disorders

VANCOUVER 12:00 16:00 20:00 00:00 04:00 08:00 12:00 TIME

HALIFAX 16:00 20:00 00:00 04:00 08:00 12:00 16:00 TIME

The sleeper is trained to a 23:00 – 07:00 sleep period on his local (Vancouver) time (yellow rectangle). Following an eastern flight across four time zones, to maintain the same sleep period he must now retire at 19:00 and arise at 03:00 (Vancouver time) [23:00 – 07:00 Halifax time]. This represents a phase advance of the circadian rhythm. Predictably, he will have difficulty falling asleep (red rectangle) until his usual time (23:00 Vancouver time; 03:00 Halifax time) and the total sleep time will be shortened (turquoise rectangle), resulting in daytime sleepiness.

Figure 2. Sleep disturbance following an eastward flight across four time zones. matic symptom, with the sudden occurrence of interest in the role of immune mechanisms in the muscle atonia during emotional arousal (com- etiology of human narcolepsy.14 monly laughter or anger) being pathognomonic Circadian rhythm disorders. The sleep-wake for the disorder. cycle is a circadian rhythm, which has a slightly Narcolepsy typically presents between 15 and 25 longer period than the 24 hours of clock time. To years of age, but may be seen in children as young remain in sync with the 24-hour, light-dark cycle, a as five or six years old. There is an unacceptable daily adjustment must be made to keep the sleep- delay (usually 10 or more years) associated with sig- wake rhythm constant.15 Important zeitgebers, or nificant psychosocial impairment between the man- time givers, for the human sleep-wake cycle include ifestation of the first symptoms, the correct diagno- arising time, light exposure and social interaction. sis and the institution of symptomatic treatment. Desynchrony between clock time and the circadi- Narcolepsy usually occurs sporadically, but an rhythm has important consequences for sleep familial clustering is reported in approximately 10% performance and daytime alertness, with changes in of cases. An association between narcolepsy and the functioning being apparent following relatively major histocompatibility complex genes (HLA-DR2 small time shifts, such as when we lose an hour of and DQ1) was demonstrated in 1983. This suggests sleep in the spring. The effects are more obvious a possible autoimmune mechanism which, with the when we rapidly cross two or more time zones and recent discovery that human narcolepsy may be experience jet lag. For example, a businessman fly- associated with the immune destruction of a small ing from Vancouver to Halifax (four-hour time dif- number of hypothalamic neurons containing the ference) will attempt to replicate his usual sleep peptide hypocretin (), has inspired renewed period of 23:00 to 07:00 hours, which, in his new

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TIME 12:00 16:00 20:00 00:00 04:00 08:00 12:00

TIME 12:00 16:00 20:00 00:00 04:00 08:00 12:00

During his summer vacation, this student found he drifted to sleep later and arose later over a number of months, eventually settling on an 2:30 to 12:30 schedule (blue rectangle). Prior to the drift, he was on a 23:00 to 07:30 schedule (black rectangle). In September, he wishes to revert to his school-time schedule, but as this requires a difficult-to-complete phase advance of his sleep, he experiences difficulty falling asleep until his usual (summer) sleep onset time (red rectangle). As a result, he has a short sleep period (brown rectangle) as he has difficulty getting up at 07:30. Even if he makes it, he will be sleepy during the day.

Figure 3. Delayed sleep phase.

time zone, will require him to attempt sleep at ers will, on average, sleep eight hours less each 19:00 and arise at 03:00 Vancouver time (Figure week than will day workers.17 Sleep deprivation 2). Without using sedatives, he will have difficulty often has calamitous results and has been impli- in getting to sleep at such an early time. He also cated in dramatic major disasters (i.e., the will have a short sleep period and will be arising at spaceshuttle Challenger and Chernobyl nuclear a time when his core temperature will be close to disasters), tragic medical errors and frequent its nadir. Both the sleep loss and the circadian motor vehicle accidents. Both the nature of the desynchrony will affect his performance through shift (i.e., more than four 12-hour shifts in a row) effects on cognitive ability, mood and psychomotor and individual differences (i.e., age, presence of performance.16 psychiatric illness, presence of heart disease) Although travelers slowly adjust to local time affect one’s ability to cope with shift work.18 cues, shift workers are constantly living at odds The delayed sleep phase type of circadian with them. For most night-shift workers, true syn- rhythm sleep disorder is a chronic condition, char- chrony between their internal clocks and local acterized by sleep onset and wake times that are time rarely develops. In both jet lag and shift work delayed three to six hours relative to conventional intolerance, daytime sleepiness is caused by acute sleep-wake times (Figure 3). The condition usual- or chronic sleep loss. About 20% of our workforce ly follows a period of unencumbered sleep (as dur- is employed on a shift-work basis, and these work- ing summer vacations), with the preferred retiring

110 The Canadian Journal of CME / December 2001 Non-respiratory Sleep Disorders

Awakening

10 secs

Figure 4. Periodic limb movements. A 90-second recording of a patient with periodic limb movement disorder. The elec- troencephalogram shows Stage 2 sleep (top tracing; blue). The fifth leg movement (anterior tibialis electromyogram in black) causes an awakening. and arising times becoming later and later, and Treatment, usually at a sleep disorder center, eventually consolidating around a significantly involves the use of interventions, such as mela- delayed period (for example 03:00 hours to 11:00 tonin and bright light, which can help reset circa- hours). Attempts to go to earlier are met with dian rhythms.19 sleeplessness, even when large doses of sedative Other dyssomnias. The last group of conditions hypnotics are used. Attempts to arise at a reason- we need to consider are the dyssomnias not other- able time will be almost impossible due to sleep wise specified. Common experience shows that deprivation and circadian effects. environmental factors, such as noise and light, can The diagnosis is confirmed by examining a significantly influence sleep performance. Sleeping sleep diary completed over a week. The tell-tale in hospitals and in intensive-care settings are partic- late sleep onset and arising times will be obvious, ularly difficult. Under these circumstances, patients with the patient only obtaining normal sleep on the will complain of both disrupted sleep and daytime weekends when he/she sleeps according to the sleepiness. new, but delayed, phase schedule. Sleep deprivation from any cause is inevitably This disorder is more common in adolescents associated with daytime sleepiness and impair- and young adults and has a reported prevalence of ment. The most common cause of EDS in modern 7%. The patient may complain he/she cannot fall society is elective, chronic sleep deprivation. Over asleep before 02:00 to 06:00, and may prefer to the last century, sleep times have been curtailed by arise between 10:00 and 14:00. Despite attempts 25%. This is not because we need less sleep, but to go to sleep earlier, patients with this condition because more activities, including work, are com- cannot advance their sleep times and hypnotics or peting for our wake time. It is important to remem- other sedatives have no effect. Rigid enforcement ber sleep requirements are highly individualistic, of conventional sleep times is ineffective and may although most people need 7.5 hours to eight result in sleep deprivation and daytime sleepiness. hours of sleep within 24 hours. Sleep requirements

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The last two conditions, classified in the DSM-IV Table 3 as dyssomnias not otherwise specified that are caus- Conditions Associated With es of hypersomnia, are restless legs syndrome (RLS) Restless Legs Syndrome And and periodic limb movement disorder (PLMD). (The Periodic Limb Movement Disorder Restless Legs Syndrome Foundation [www.rls.org] is an excellent electronic resource on these two con- Neurologic ditions for both physicians and patients.) RLS and • Neuropathy PLMD are related both in their pathophysiology and • Radiculopathy in their clinical expression. Patients with RLS often have PLMD, although patients can have PLMD •Head injury without experiencing symptoms of RLS. • Parkinson’s disease RLS has been described for centuries and iden- • tified as a clinical entity by K.A. Ekbom in 1945. Medical Surveys show that about 15% of the population are • Anemia afflicted. Patients with RLS experience difficult to •Uremia define dysesthetic sensations, usually in their lower •Pregnancy limbs and sometimes in their arms. This may inter- fere with the initiation of sleep. The sensations • Diabetes have a circadian rhythm, building up in the after- • Low iron stores noon and peaking prior to the sleep period. • Characteristically, the sensations are relieved by • Rheumatoid arthritis movement, but recommence once activity stops. • Attention deficit hyperactivity disorder Most patients experience difficulty falling asleep, Sleep disorders but some are woken during the night, experience • the dysesthesias and are compelled to move their • Narcolepsy legs in bed or to get up and walk off the discomfort. The condition waxes and wanes, but usually gets • REM sleep behavior disorder worse with age. A significant proportion of suffer- Treatment ers complain of excessive daytime or som- • Serotonin reuptake inhibitors nolence (46.2% of men and 22.2% of women). • Lithium The movements in PLMD are stereotyped •Tricyclics (extension of the big toe and dorsiflexion of the • Hemodialysis ankle, with occasional flexions of the knee and hip) • Sedative withdrawal and repetitive. They are about 0.5 to five seconds in duration and occur with a frequency of one every 20 to 40 seconds. The limb movements cause arousals and awakenings (Figure 4) and tend to range from four hours to 14 hours. Obviously, an predominate in the first third of the night. They individual who needs 14 hours of sleep, but is only commonly cause initial and maintenance insomnia, obtaining seven hours, will develop a significant but can cause sleepiness in about 17% of sleep deficit and will be chronically sleepy.17 patients.20 The limb movements occur in a prima-

112 The Canadian Journal of CME / December 2001 Non-respiratory Sleep Disorders

groups of Parkinson’s disease patients taking pramipexole, ry idiopathic form and are associated with a variety cabergoline and levodopa mono and combination therapy. J of medical conditions, treatments and other sleep Neural Transm 2001; 108(1):71. 6. Robson P: Therapeutic aspects of cannabis and cannabi- disorders (Table 3). Usually RLS and PLMD will noids. Br J Psychiatry 2001; 178:107. require a sleep laboratory assessment to quantify 7. Zwyghuizen-Doorenbos A, Roehrs T, Timms V: Individual the extent of the sleep disruption, exclude other differences in the sedating effects of alcohol. Alcohol Clin sleep pathologies and, where daytime sleepiness is Exp Res 1990; 14:400. 8. Gillin JC, Drummond SPA: Medication and . an issue, quantify sleepiness with the MSLT. In: Kryger MH, Roth T, Dement WC (eds): . Third Edition. W.B. Saunders, St. Louis, 2000, p. 1176. Conclusion 9. Monti JM, Monti D: Histamine H-1 receptor antagonists in EDS is not a benign complaint and always requires the treatment of insomnia — Is there a rational basis for use? CNS Drugs 2000; 13(2):87. careful investigation. Sometimes the cause can be as 10. Weiler JM, Bloomfield JR, Woodworth GG, et al: Effects of simple as insufficient sleep, but usually it is more fexofenadine, diphenhydramine, and alcohol on driving per- complicated, often with comorbid contributions formance. A randomized, placebo-controlled trial in the Iowa driving simulator. Ann Intern Med 2000; 132(5):354. from medical, sleep and psychiatric disorders and/or 11. Vgontzas AN, Bixler EO, Kales A, et al: Differences in noc- their treatments. A careful evaluation of the sleepy turnal and daytime sleep between primary and psychiatric patient will address all of these possible etiologies hypersomnia: Diagnostic and treatment implications. and quantify the daytime impairments associated Psychosom Med 2000; 62(2):220. 12. Bonnet MH, Arand DL: The consequences of a week of with sleepiness. Often with the secondary hyper- isnomnia. Sleep 1996; 19(6):453. somnias, rigorous treatment of the primary distur- 13. Mitler MM, Miller JC: Methods of testing for sleepiness. bance, combined with good sleep hygiene practices, Behavioral Medicine 1996; 21(4):171. will be sufficient to return the patient to normal 14. Overeem S, Mignot E, van Dijk JG, et al: Narcolepsy: Clinical features, new pathophysiologic insights, and future functioning. Sometimes, however, a referral to a perspectives. J Clin Neurophysiol 2001; 18(2):78. sleep center may be required to delineate the condi- 15. Waterhouse J: Jet-lag and shift work: Circadian rhythms. tion and find the optimal treatment. J R Soc Med 1999; 92(8):398. 16. Cho K, Ennaceur A, Cole JC, et al: Chronic jet lag produces cognitive deficits. J Neurosci 2000; 20(6):RC66. CME 17. Mahowald MW: What is causing excessive daytime sleepi- ness? Evaluation to distinguish sleep deprivation from sleep References disorders. Postgrad Med 2000; 107(3):108. 1. American Psychiatric Association: Diagnostic and 18. Tepas DI, Monk TH: Work schedules. In: Salvendy G (ed.): Statistical Manual of Mental Disorders. Fourth Edition. Handbook of Human Factors. John Wiley and Sons. New American Psychiatric Association, Washington, DC, 1994. York, 1987, p. 819. 2. Schenk CH, Mahowald MR: REM sleep parasomnias. 19. Kayumov L, Brown G, Jindal R, et al: A randomized, dou- Neurol Clin 1996; 14:697. ble-blind, placebo-controlled crossover study of the effect of 3. Boeve BF, Silber MH, Ferman TJ, et al: REM sleep behavior exogenous on delayed sleep phase syndrome. disorder and degenerative dementia: An association likely Psychosom Med 2000; 63(1):40. reflecting Lewy body disease. 1998; 51:363. 20. Coleman RM, Pollak CP, Weitzman ED: Periodic move- 4. Caldwell JR, Hale ME, Boyd RE, et al: Treatment of ments in sleep (nocturnal ): Relation to sleep dis- osteoarthritis pain with controlled release oxycodone or orders. Ann Neurol 1980; 8(4):416. fixed combination oxycodone plus acetaminophen added to nonsteroidal anti-inflammatory drugs: A double-blind, ran- domized, multicenter, placebo controlled trial. J Rheumatol 1999; 26(4):862.

5. Pal S, Bhattacharya KF, Agapito C, et al: A study of exces- sive daytime sleepiness and its clinical significance in three

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