annals insomnia

7/29/2019 ANNALS Insomnia

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in the clinic

Insomnia

Screening page ITC1-2

Diagnosis page ITC1-2

Treatment page ITC1-6

Practice Improvement page ITC1-14

CME Questions page ITC1-16

Section EditorsChristine Laine, MD, MPHDavid Goldmann, MD

Science WriterJennifer F. Wilson

The content of In the Clinic is drawn from the clinical information and

education resources of the American College of Physicians (ACP), including

PIER (Physicians Information and Education Resource) and MKSAP (Medical

Knowledge and Self-Assessment Program). Annals of Internal Medicine

editors develop In the Clinic from these primary sources in collaboration with

the ACPs Medical Education and Publishing Division and with the assistance

of science writers and physician writers. Editorial consultants from PIER and

MKSAP provide expert review of the content. Readers who are interested in these

primary resources for more detail can consult http://pier.acponline.org and other

resources referenced in each issue of In the Clinic.

The information contained herein should never be used as a substitute for clinical

judgment.

2008 American College of Physicians

wnloaded From: http://annals.org/ by Jose Roel on 10/04/2012


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Which patient populations have the

highest prevalence of insomnia?

People especially prone to insomniainclude those who are under stress,are depressed or have other emo-tional distress, are working at nightor having frequent major shifts intheir work hours, or are travelinglong distances with time changes(1). Insomnia can occur at any age,but it is particularly prevalent in the

elderly. One large study found thatthe prevalence of insomnia com-plaints ranged between 23% and34% among people 65 years andolder (2). Among this population,sleep complaints are commonly as-sociated with medication use andmedical problems (3). Population-based studies have found an associ-ation between lower socioeconomicstatus and insomnia (4, 5).

Should clinicians screen forinsomnia? If so, how should theyscreen?Clinicians should consider screen-ing for insomnia as part of regularpatient care given its high preva-lence and potential impact on well-being. Insomnia puts people at in-creased risk for poor health, and itcan also reduce work performanceand quality of life (69).

Evidence that screening for insom-nia improves patient outcomes isnot available. However, screeningcan be accomplished in a relativelystraightforward, brief manner byasking patients about trouble initi-ating or maintaining sleep, earlymorning waking, or nonrestorativesleep (10). Further evaluation canbe limited to individuals with thesecomplaints.

2008 American College of Physicians ITC1-2 In the Clinic Annals of Internal Medicine 1 January 2008

People with insomnia have trouble falling or staying asleep, and theresult is poor-quality sleep of insufficient duration. Insomnia is com-mon, affecting 1 in 3 adults intermittently and 1 in 10 adults chroni-

cally, and can seriously affect wellbeing. It typically causes excessive daytimesleepiness, irritability, and lack of energy. Long-term insomnia may lead todepression, inattention, learning and memory problems, and job or schoolunderperformance. Given these substantial health consequences and theprevalence of insomnia, clinicians should be skilled in managing it.

Screening

1. National Heart Lungand Blood Institute.Who is At Risk for In-somnia? U.S. Depart-ment of Health andHuman Services. Na-tional Institutes ofHealth. Accessed atwww.nhlbi.nih.gov/

health/dci/Diseases/inso/inso_whoisatrisk.html on 9 Novem-ber 2007.

2. Foley DJ, Monjan AA,Brown SL, et al.Sleep complaintsamong elderly per-sons: an epidemio-logic study of threecommunities. Sleep.1995;18:425-32.[PMID: 7481413]

3. Maggi S, Langlois JA,Minicuci N, et al.Sleep complaints incommunity-dwelling older per-sons: prevalence, as-sociated factors, and

reported causes. JAm Geriatr Soc.1998;46:161-8.[PMID: 9475443]

4. Gellis LA, Lichstein KL,Scarinci IC, et al. So-cioeconomic statusand insomnia. J Ab-norm Psychol.2005;114:111-8.[PMID: 15709817]

5. Paine SJ, Gander PH,Harris R, Reid P. Whoreports insomnia?Relationships withage, sex, ethnicity,and socioeconomicdeprivation. Sleep.2004;27:1163-9.[PMID: 15532211]

6. Wingard DL, BerkmanLF. Mortality risk as-sociated with sleep-ing patterns amongadults. Sleep.1983;6:102-7.[PMID: 6878979]

7. Suka M, Yoshida K,Sugimori H. Persist-ent insomnia is apredictor of hyper-tension in Japanesemale workers. J Oc-cup Health.2003;45:344-50.[PMID: 14676413]

Screening... Given the high prevelance of insomnia and its potential impact onhealth and quality of life, clinicians should consider incorporating screening for

insomnia as a regular part of patient care. It can be done in a relatively straight-

forward way that does not take long by asking patients about difficulty initiating

or maintaining sleep, early morning awakening, or nonrestorative sleep. People

prone to insomnia are those who are under a lot of stress; who are depressed or

have other emotional distress; and those who work nights, have frequent major

shifts in their work hours, or travel long distances with time changes.

CLINICAL BOTTOM LINE

DiagnosisWhat are the components of a

comprehensive sleep history?

A consensus paper from the Amer-ican Academy of Sleep Medicinerecommends detailed historical in-formation, as well as medical, psy-chological, and psychiatric assess-ment to evaluate insomnia (11).

Comprehensive assessment enablesclinicians to establish the cause ofinsomnia and to plan effectivetreatment.

Clinicians should ask about spe-cific sleep complaints and duration,sleep hygiene, mood disorders,



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8. Studio Morfeo Com-mittee. Studio Mor-feo: insomnia in pri-mary care, a surveyconducted on theItalian population.Sleep Med.2004;5:67-75.[PMID: 14725829]

9. Ohayon MM, Roth T.Place of chronic in-somnia in the courseof depressive andanxiety disorders. JPsychiatr Res.2003;37:9-15.[PMID: 12482465]

10. Chesson A Jr, HartseK, Anderson WM, etal. Practice parame-ters for the evalua-tion of chronic in-somnia. AnAmerican Academyof Sleep Medicinereport. Standards ofPractice Committeeof the AmericanAcademy of SleepMedicine. Sleep.2000;23:237-41.[PMID: 10737341]

11. Sateia MJ,Doghramji K, HauriPJ, Morin CM. Evalu-ation of chronic in-somnia. An Ameri-can Academy ofSleep Medicine re-view. Sleep.2000;23:243-308.[PMID: 10737342]

12. Hohagen F, Rink K,Kppler C, et al.Prevalence andtreatment of insom-nia in general prac-tice. A longitudinalstudy. Eur Arch Psy-chiatry Clin Neurosci.1993;242:329-36.[PMID: 8323982]

13. American Sleep Dis-orders Association.International classifi-cation of sleep disor-ders, revised: Diag-nostic and codingmanual. Westchester,IL: American Acade-my of Sleep Medi-cine; 1997.

14. Reite M, Buysse D,Reynolds C, Mendel-son W. The use ofpolysomnography i nthe evaluation of in-somnia. Sleep.1995;18:58-70.[PMID: 7761745]

2008 American College of PhysiciansITC1-3In the ClinicAnnals of Internal Medicine1 January 2008

underlying medical disorders, med-ication use, and substance use.Patient sleep diaries can supple-ment history by helping to obtain amore accurate record of sleep habitsthan general questioning alone andto assess total sleep time. If askingpatients to keep a sleep diary, clini-cians should instruct them to

record bedtime, sleep time, noctur-nal waking, and rising time in sleepdiaries daily for at least 1 to 2weeks. Standardized sleep ques-tionnaires are primarily used in re-search settings, but their utility inclinical settings is uncertain.

Which conditions should clinicians

consider as potential secondary

causes of insomnia?

The most common type of insom-nia is secondary insomnia, meaningthat it is attributable to an underly-ing condition, poor sleep environ-ment, or use of medications or othersubstances that interfere with sleep.A longitudinal study of more than200 general medical patients founda strong linkage between severeinsomnia and chronic medical andpsychiatric disorders (12). A studyof 2398 community-dwelling indi-viduals aged 65 years and olderfound that sleep complaints werecommon and associated with arange of medications and medicalproblems (3). The American SleepDisorders Association released aninternational classification of sleepdisorders manual to better definethese various causes (13). Tables 1and 2 summarize the main consid-erations in the differential diagnosisof potential causes of secondaryinsomnia.

What is the role of physicalexamination in the evaluation of

patients with insomnia?

The physical examination can iden-tify signs that suggest a specific dis-order underlying insomnia. Under-lying causes include obstructivesleep apnea syndrome (OSAS),obesity, hypertension, thyroiddysfunction, restless leg syndrome

(RLS), or other cardiopulmonaryor neurologic disease

When should clinicians considerlaboratory testing in theevaluation of patients withinsomnia?Laboratory testing should not beused routinely in the evaluation ofinsomnia. However, judicious use

may be indicated in some patientswith clinical evidence of concomitantdisease that may be associated withinsomnia (10).

Polysomnography

The American Academy of SleepMedicine report recommends usingpolysomnography (overnight sleeptest) or a multiple sleep latency test(MSLT), or both, to evaluate pa-tients with sleep-disordered breath-

ing; specific sleep disorders, such asnarcolepsy and periodic limb move-ments; or insomnia resistant to ini-tial therapeutic measures (14).

Multiple Sleep Latency Test (MLST)

The MSLT is a standard nap testthat takes place in a sleep laborato-ry after an overnight sleep study.This test is a series of four 20-minutenaps designed to objectively measure

Things to Ask about When Taking

a Comprehensive Sleep History

Problems of sleep initiation, sleepmaintenance, early morning waking,or nonrestorative sleep

Ascertain if the patient has acute,short-term, or chronic insomnia

Stability or progression of symptomsthatis, if the insomnia is stable, worsening, orimproving

Precipitating causes of insomnia

Bedtime, wake time, length of sleep time

Caffeine and alcohol use

Any current or previous behavioral thera-pies used to treat insomnia

Previous over-the-counter or prescriptionsedative-hypnotic use

Shifting work and irregular sleep schedule

Potential acute stressors, such as:

Medical or psychiatric illness Medication use, both prescribed

and illicit

Acute stress at home or work Circadian rhythm stressors,

such as jet lag



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Table 1. Differential Diagnosis of Underlying Causes of Insomnia*

Disease Characteristics Notes

Extrinsic sleep disorders

Circadian rhythm sleep disorders

*ADHD = attention deficit hyperactivity disorder; CBC = complete blood count; COPD = chronic obstructive pulmonary disorder; OSAS = obstructive sleepapnea syndrome; PLMS = periodic leg movements in sleep; RLS = restless leg syndrome.

Psychophysiologic insomnia

RLS

Periodic limb movementdisorder

Sleep-state misperception

Idiopathic insomnia

Central sleep apneasyndrome

OSAS

Disturbed sleep from conditioned arousal,usually to the bedroom

An uncomfortable or restless feeling inlegs most prominent at night and at rest;alleviated by movement

Repetitive stereotypic leg movement

during sleep

Objectively normal sleep in the face of thepatient's complaint of insufficient sleep

Lifelong sleep problems with suspectedneurologic abnormality of sleep-wake system

Repetitive pauses in breathing duringsleep without upper airway occlusion

Upper airway obstruction duringinspiration in sleep

Look for a history of sleep improvement when away from thebedroom; patients may have an inordinate concern over sleep.

Look for a family history of RLS, history of caffeine abuse, irondeficiency, renal disease, pregnancy, ADHD, and, less likely, vitaminB12 or folate deficiency. RLS may also be present with colonadenocarcinoma. Approximately 80% of patients with RLS havePLMS on polysomnography. Occurs in 11% of general population.

Look for a history of repetitive leg movements during sleepthat leads to disturbed sleep. Polysomnography is necessary fordiagnosis.

Polysomnography will document normal sleep. The factor(s) thatgenerate the complaint are unclear. Patients have no obviouspsychopathology.

Look for lifelong persistent insomnia.

Look for associated history of congestive heart failure or centralnervous system disease. Polysomnography is necessary for diagnosis.

Look for a history of snoring, respiratory pauses, and daytimesleepiness. Polysomnography is needed for diagnosis. OSAS occursin about 2% of middle-aged females and 4% of middle-aged males.

Inadequate sleep hygiene

Environmental sleep disorder

Altitude insomnia

Hypnotic-dependent sleepdisorder

Stimulant-dependent sleepdisorder

Alcohol-dependent sleepdisorder

Toxin-induced sleep disorder

Disturbed sleep associated with caffeine,tobacco, alcohol use, or irregular sleephabits

Disturbed sleep associated withenvironmental elements

Disturbed sleep associated with altitude

Disturbed sleep associated with toleranceto or withdrawal from hypnotic drugs

Disturbed sleep associated with stimulantdrug use

Alcohol used to initiate sleep; sleep thatfollows is fragmented

Disturbed sleep associated with arsenic,copper, lead, or mercury ingestion

Comprehensive sleep history will facilitate the diagnosis. Believedto be a common factor in insomnia.

Comprehensive sleep history will facilitate the diagnosis.

Look for a history of ascent to high altitudes. Can begin as low as2000 m for persons from sea level and is common above 4000 m.Characterized by periodic breathing and central apnea events.

Ask for positive history of sustained hypnotic use with developmentof tolerance leading to increased dose.

Comprehensive sleep history will facilitate the diagnosis.

Ask for patient's history of alcohol use to facilitate sleep for at leastthe last 30 days. May be preceded by other sleep-disturbing factors.

The clinician must be alert to chronic or acute ingestion. Diagnosedwith tests for heavy metals, CBC, hepatic, and renal testing.

Shift-work sleep disorder

Delayed sleep-phasesyndrome

Advanced sleep-phasesyndrome

Time zone change syndrome(jet lag)

Sleep occurs at times that are counter tonormal circadian rhythm andenvironmental factors

A circadian rhythm disorder in which themajor sleep phase is delayed relative to

clock time

A circadian rhythm disorder in which themajor sleep phase is advanced relative toclock time

Travel leads to complaints of poor sleep,daytime sleepiness, or both. Physicialcomplaints may ensue (e.g., GI upset)

Look for a history of insomnia associated with shift work. Rememberthat shift work includes those patients working a permanent nightshift. Occurs in approximately 2% to 5% of population.

Look for a history of sleep-onset insomnia and difficulty awakeningat the desired time. Patients have no difficulty maintaining sleep

once asleep. Most common in adolescents.

Look for a history of inability to stay awake until desired bedtimeand early morning awakening. Occurs most commonly in theelderly.

Look for a history of recent travel across multiple time zones.



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15. Ancoli-Israel S, ColeR, Alessi C, et al. Therole of actigraphy inthe study of sleepand circadianrhythms. Sleep.2003;26:342-92.[PMID: 12749557]


daytime sleepiness and the onset ofREM sleep. A latency of less than 8minutes to stage 1 sleep suggestspathologic hypersomnolence.

Sleep Actigraphy

In this noninvasive test, the patient

wears a small, watch-like electronicdevice around the wrist of the non-dominant arm for an extended pe-riod of time. Although actigraphyprovides an accurate recording ofsleep patterns, it may underestimateseverity in patients with sleep-onsetinsomnia. Sleep actigraphs can pro-vide a reliable measurement of sleeppatterns and circadian rhythms (15)

and are most often used in researchsettings.

Other Tests to Evaluate for Underlying

Comorbidity

Various other tests may be neededto check for underlying cardiac,

pulmonary, gastrointestinal, or neu-rologic disorders contributing to orcausing the insomnia.

Complete blood count and serumferritin levels can identify anemia,which is associated with RLS. Ablood urea nitrogen test and serumcreatinine test can check for renaldisease, which is also associatedwith RLS. Thyroid function tests

Table 2. Other Medical Disorders that Can Be Underlying Causes of Insomnia

Disease Characteristics Notes

Nocturnal leg cramps

Anxiety and depressivedisorders

Cerebral degenerative ortraumatic disorders

Dementia

Parkinsonism

Fatal familial insomnia

Sleep-related epilepsy

Sleep-related headaches

Asthma/COPD

Gastroesophageal refluxdisease

Fibromyalgia syndrome

Pain in calf or foot, resulting in sleepawakening

May trigger sleep initiation or sleep main-tenance problem

Insomnia associated with a cerebraldegenerative disorder

Insomnia associated with dementia;manifested by wandering, aggressivebehavior, verbalization, and delirium inearly evening hours

Insomnia is commonly associated withParkinson disease

Prion-related thalamic degeneration,resulting in progressive insomnia

Sleep-related epilepsy is defined as when75% of the events occur during sleep

A number of classes of headache areclosely tied to sleep, including migraine,cluster headache, and paroxysmalnocturnal hemicrania

Nighttime attacks of lower airwayobstruction may occur in asthma. Cough,sputum production, wheeze, or shortnessof breath may interrupt sleep in COPD

Symptoms or histologic changes in theesophagus due to the reflux of gastriccontents into the esophagus

Chronic generalized musculoskeletal pain,nonrefreshing sleep, fatigue associatedwith trigger points

Look for a history of painful cramps awakening the patient fromsleep. Predisposing factors include diabetes, exercise, pregnancy,and metabolic and endocrine abnormalities. May occur withParkinson disease and arthritis.

Look for a history of anxiety or depression. Most patients withanxiety and insomnia will present with anxiety first or concomitantwith insomnia. In contrast, depression tends to follow thecomplaint of insomnia

Look for the presence of abnormal body movements, reduced sleepefficiency, and increased awakenings. Objective testing (multiplesleep latency test or maintenance of wakefulness test) showsdaytime sleepiness. Insomnia complaints frequently complicatetraumatic brain injury.

Look for these symptoms in a patient with a progressive dementingillness. Note that other sleep disorders, such as sleep apnea, mayexacerbate this disorder.

Look for sleep-onset and maintenance problems. A number ofpotential causes to insomnia in Parkinson disease exist, includingdepression and anti-Parkinson drugs.

Look for a progressive problem initiating sleep associated with anumber of other symptoms, such as fever, excessive salivation, andsweating. Death occurs in 7 to 13 months.

This condition affects about 25% of patients with epilepsy. Seizure-related complaints include sudden awakenings, urinary incontinence,and unusual but stereotypic movements at night. Patients withnocturnal epilepsy do not commonly complain of insomnia.

Look for a history of headache arising during sleep or noted on firstawakening. Paroxysmal nocturnal hemicrania may respond toindomethacin.

Look for a history of nocturnal awakenings due to cough, wheeze,or shortness of breath. Note that asthma may present withsymptoms at night as an initial manifestation of suboptimal control.

Look for a history of sleep-related heartburn, nocturnal cough,and chest pain.

Look for muscle tenderness and trigger points. Laboratory testingfor inflammatory arthritis is normal.



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Diagnosis... Insomnia is most often due to underlying medical or psychologicalconditions, medications or other substances that interfere with sleep, or poor sleep

environment. A detailed history and physical evaluation is necessary in the evalua-

tion of insomnia. This might include the use of sleep diaries, sleep questionnaires,

and laboratory testing to evaluate for underlying conditions.


What is sleep hygiene and what is

its role in the treatment of


Sleep hygiene is the practice of fol-lowing simple guidelines (see Box)to promote sound sleep and day-time alertness.

Poor sleep hygiene can contributeto sleep fragmentation, circadianrhythm disturbance, discomfort, andoverstimulation. Clinicians shouldreview and correct poor sleep hy-giene in all patients complaining ofinsomnia, customizing the applica-tion of sleep hygiene rules to specificpatient needs, such as the need towork night shifts.

Stimulus control consists of advis-

ing patients to associate the bedand bedroom with sleepiness. It can

be an effective treatment for in-somnia when conditioned arousal

to the sleeping environment is aproblem and perhaps even in the ab-

sence of obvious evidence of condi-tioning. Patients should spend no

more than 20 minutes awake in bed

Treatment

Good sleep hygiene behaviors:

Maintain stable bed times andrising times

Spend no more than 8 hours in bed

Experience regular daytime lightexposure

Maintain a quiet, dark bedroom

Maintain adequate nutrition

Avoid sleep-fragmenting

substances, such as caffeine,nicotine, and alcohol

Avoid clock-watching

Maintain regular exercise

Avoid heavy exercise within 2 hoursof bedtime

Avoid bright light before bedtime

Maintain a 30-minute relaxationperiod before bedtime

Avoid using alcohol to initiate sleep

16. Morin CM, MimeaultV, Gagn A. Non-pharmacologicaltreatment of late-lifeinsomnia. J Psycho-som Res.1999;46:103-16.[PMID: 10098820]

17. McDowell JA, MionLC, Lydon TJ, InouyeSK. A nonpharmaco-

logic sleep protocolfor hospitalized old-er patients. J AmGeriatr Soc.1998;46:700-5.[PMID: 9625184]

18. Edinger JD, Wohlge-muth WK, RadtkeRA, et al. Does cog-nitive-behavioral in-somnia therapy alterdysfunctional beliefsabout sleep? Sleep.2001;24:591-9.[PMID: 11480656]

can reveal hypothyroidism or hyper-thyroidism, conditions that are as-sociated with sleep problems. Urinedrug screening may also be useful,because stimulant medication andbenzodiazepine hypnotic medica-tions may alter sleep.

Clinicians should consider electro-cardiography and echocardiography

if there is a concern about congestiveheart failure, which can interferewith sleep. A chest X-ray may be

used to identify heart failure or

chronic obstructive pulmonary dis-

ease. In patients with respiratory

symptoms, pulmonary function

testing may identify upper and low-

er airway obstruction. Barium swal-

low and 24-hour pH probe may be

helpful in the evaluation of patients

in whom symptoms suggest thatgastroesophageal reflux may be

contributing to insomnia.

and leave the bedroom to engage innonstimulating activity until tiredbefore returning to bed. Keeping setbedtimes and rising times is impor-tant, even if patients are awake dur-ing the night. Research has shownthat such practices can improvetime to onset of sleep and total

sleep time (16).



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Is sleep restriction or other

behavioral therapy useful in

the treatment of patients

with insomnia?

Behavioral treatments may reduceinsomnia significantly in manypatients. In patients with chronicinsomnia, behavioral therapyshould be tried before instituting

drug treatment. Several studies sug-gest that nondrug therapies may bemore effective if not used in con-junction with drugs. However,behavioral therapy may also becombined with drug therapy toreduce the need for sleepingpills (17). A sleep disorders spe-cialist or knowledgeable therapistshould be consulted when consid-ering behavioral therapies forinsomnia.

Sleep Restriction

Sleep restriction is a behavioralintervention that limits, then slowlyincreases, the time for sleep. Patientskeep a sleep diary for 1 to 2 weeks,and then alter their sleep scheduleso that their time in bed is equal totheir average total sleep time,which is calculated based onthe sleep diary. Note, however, thatsleep restriction should be no less

than 5 hours in bed, and daily ris-ing time should be the same everyday. Using this method, patientsgradually increase the amount oftime they spend in bed. Patientsmake bedtime earlier by 15-minuteincrements as long as sleep efficiency(total sleep time divided by totaltime in bed) is 90% or better asdocumented by the sleep log.

Sleep restriction may be initiated in

patients with insomnia associatedwith no underlying medical or psy-chological disorder and in whomsleep hygiene maneuvers have beenunsuccessful. Clinicians should cau-tion patients that sleep restrictiontherapy may lead to excessive day-time sleepiness and that theyshould be careful performing

potentially dangerous activities,such as driving.

Cognitive Behavioral Therapy

Cognitive behavioral therapy(CBT) is used to correct miscon-ceptions about sleep. In CBT, thepractitioner reviews normal sleepneeds, specifically by reinforcingthe idea that patients require 7 to 8hours of sleep per night; discussingchanges in sleep with aging, such asincreased light sleep and decreaseddeep sleep; and alleviating exagger-ated patient concerns about the im-pact and consequences of insomnia.Studies have shown that CBT re-duces dysfunctional beliefs aboutsleep and alleviates insomnia, out-performing placebo and relaxationprocedures, and providing elementsnot found in other behavioral tech-

niques (18, 19).

A small, single-blind study found that onehalf of participants experienced a 50%

reduction in their time awake after sleep

onset using an abbreviated 2-session CBT

intervention (20).

Behavioral techniques were more effective

than drug therapy or placebo in the long-

term in a randomized, placebo-controlled

study of 78 older patients with chronic

insomnia (21).

A randomized, placebo-controlled trial of63 middle-aged and young adults found

that CBT was superior to drug therapy in

the treatment of insomnia characterized

by difficulty with sleep initiation (22).

Biofeedback and Progressive

Muscle Relaxation

Biofeedback and progressive musclerelaxation techniques also have po-tential usefulness in the manage-ment of insomnia. The literatureindicates that physiologic, muscu-lar, and cognitive arousal can inter-fere with sleep, and that relaxationcan help. However, any interventionthat increases the expectation offalling asleep more quickly, includ-ing placebo, might be equally effec-tive (23). In these interventions,patients practice ways to reduce highlevels of arousal by using specific

19. Edinger JD, Wohlge-muth WK, RadtkeRA, et al. Cognitivebehavioral therapy

for treatment ofchronic primary in-somnia: a random-ized controlled trial.JAMA.2001;285:1856-64.[PMID: 11308399]

20. Edinger JD, Samp-son WS. A primarycarefriendlycogni-tive behavioral in-somnia therapy.Sleep. 2003;26:177-82. [PMID: 12683477]

21. Morin CM, ColecchiC, Stone J, et al. Be-havioral and phar-macological thera-pies for late-lifeinsomnia: a random-

ized controlled trial.JAMA. 1999;281:991-9. [PMID: 10086433]

22. Jacobs GD, Pace-Schott EF, StickgoldR, Otto MW. Cogni-tive behavior thera-py and pharma-cotherapy forinsomnia: a random-ized controlled trialand direct compari-son. Arch InternMed. 2004;164:1888-96. [PMID: 15451764]




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23. Nicassio PM, BoylanMB, McCabe TG. Pro-gressive relaxation,EMG biofeedbackand biofeedback

placebo in the treat-ment of sleep-onsetinsomnia. Br J MedPsychol.1982;55:159-66.[PMID: 7104246]

24. Weiler JM, BloomfieldJR, Woodworth GG, etal. Effects of fexofena-dine, diphenhy-dramine, and alcoholon driving perform-ance: a randomized,placebo-controlledtrial in the Iowa Driv-ing Simulator. AnnIntern Med.2000;132:354-63.

25. Basu R, Dodge H,Stoehr GP, Ganguli

M. Sedative-hypnot-ic use of diphenhy-dramine in a rural,older adult, commu-nity-based cohort:effects on cognition.Am J Geriatr Psychia-try. 2003;11:205-13.[PMID: 12611750]

26. Balter MB, Uhlen-huth EH. The benefi-cial and adverse ef-fects of hypnotics. JClin Psychiatry.1991;52 Suppl:16-23.[PMID: 2071567]


techniques of tensing and relaxingdifferent muscle groups or usingvisual or auditory feedback thatfocuses on a specific physiologicmeasure. Although biofeedbackmay be effective, it requires specialequipment and training, and it mayonly be effective in subgroups ofpatients with insomnia. For in-stance, research indicates thatyounger patients respond better torelaxation techniques than olderpatients (16).

How should clinicians advisepatients about the use ofnonprescription agents in thetreatment of insomnia?Antihistamines

Products containing the antihista-mines diphenhydramine or doxy-lamine may induce sedation. Com-

binations of an antihistamine plus anonsteroidal anti-inflammatorydrug target minor pain-relatedinsomnia. Although over-the-counter products containing anti-histamines are marketed as sleepaids and are commonly used, theyare associated with adverse events,including strong anticholinergicside effects, daytime sedation, andcognitive impairment. Consequently,patients may not feel rested even if

insomnia is improved. Few datasupport a favorable risk-benefitratio for antihistamines in thetreatment of insomnia.

A cross-over study examined patient s au-tomobile driving performance when oper-ating a drivingsimulator after ingesting 50mg diphenhydramine,60 mg fexofenadine(a second-generation antihistamine), 50mg alcohol, or placebo. Driving perform-ance was poorest after participants tookdiphenhydramine, indicating that it nega-tively influenced driving performance

more than alcohol (24).

A study of more than 1600 subjects showedthat extended use of over-the-counterdiphenhydramine in an older rural popula-tion was associated with impairment onthe Mini Mental Status Examination (25).

In addition, a large telephone survey foundthat, althoughusersof prescription hypnoticsfelt favorably about themand reported few

adverse effects, those taking over-the-

counter sleep medications felt that they

were less effective and caused more side

effects (26).

Alternative Therapies

Other nonprescription agents in-clude natural remedies, such asmelatonin, valerian, kava, or St.Johns wort. The efficacy and safety

of these agents is not clear and hasnot been well-studied, and their useis generally discouraged. Melatoninmay be useful for short-term adap-tation to jet lag or other circadianrhythm sleep disorders. However,effectiveness for chronic insomniais less clear, and optimal dose andlong-term adverse effects also arenot known.

A small, randomized, cross-over study in 10

patients with primary insomnia did not

show that melatonin produced any sleepbenefit measured by sleep electroen-

cephalography, sleep duration, or subjec-

tive sleep quality (27).

When should clinicians considerprescription drug therapy for


When other approaches proveinadequate, prescription drug ther-apy tailored to the underlying causeof insomnia may be warranted. Al-

though drug therapy in the short-term is as effective as behavioralinterventions, concomitant use ofhypnotics and behavior therapymay mitigate the efficacy of thebehavioral measures.

Prescription treatment optionsinclude either benzodiazepines,such as clorazepate, diazepam,lorazepam, oxazepam, temazepam,and triazolam, or nonbenzodi-azepine hypnotics, such as zolpi-

dem, zaleplon, and eszopiclone(Table 3). The nonbenzodiazepinesare preferred because they do notalter sleep architecture and have amore favorable side-effect profile.

Benzodiazepines

Benzodiazepines exert their effectsthrough enhancement of thegamma-aminobutyric acid (GABA)

Things to Consider when Prescribing

Drugs to Treat Insomnia

Use a GABA agonist over othersedative-hypnotics for treatmentof acute or short-term insomnia.

Use the minimal effective dose.

Avoid long half-life medications,including long half-life metabolites.

Be aware of potential interactionsbetween drugs, including over-the-

counter drugs. Caution patients on these medica-

tions about interaction with alcohol.

Review potential side effectsinparticular, daytime sleepiness.

Look for rebound insomnia afterdiscontinuation.

Confer with the patient to deter-mine an appropriate period of use.

Consider intermittent or long-termuse of hypnotic medications, de-pending on the clinical situation.

Consider consultation with sleepspecialists before starting long-term therapy with hypnotic

medication. Recognize that concomitant use of

hypnotics and behavior therapymay mitigate the efficacy of thebehavioral measures.



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27. Almeida Montes LG,Ontiveros Uribe MP,Corts Sotres J,Heinze Martin G.Treatment of pri-mary insomnia withmelatonin: a double-blind, placebo-con-trolled, crossoverstudy. J PsychiatryNeurosci.2003;28:191-6.[PMID: 12790159]


Table 3. Drug Treatment for Insomnia*

Agent, Dosage Mechanism of Action Benefits Side Effects Notes

Benzodiazepines

Nonbenzodiazepine-sedative hypnotic agents

Dopaminergic agents

Antidepressants

Antihistamines

*GABA =-aminobutyric acid; REM = rapid eye movement; RLS = restless legs syndrome.

Estazolam, 12 mg

Flurazepam, 1530 mg

Quazepam, 7.530 mg

Temazepam, 7.530 mg

Triazolam, 0.1250.5 mg

GABA agonist Shorten sleep latencyand reduce unscheduledwaking

Daytime sedation,anterograde amnesia, falls,rebound insomnia

Temazepam is water-solubleinstead of lipid-soluble andhas a longer onset of action(about 1 hour). Flurazepamand quazepam have longhalf-life active metabolites.

Zolpidem, 510 mg

Zaleplon, 510 mg

GABA agonist Shorten sleep latencyand reduce unscheduledwaking

Daytime sedation,anterograde amnesia, falls,rebound insomnia

Zaleplon has the shortesthalf-life (about 1 hour).

Pramipexole,0.1251.5 mg in 23doses

Levodopa and carbidopa,up to 100200 mg individed doses

Ropinirole, 0.253 mg in23 divided doses

Pergolide, 0.0250.5 mgin 23 divided doses

Increased dopaminergicactivity via dopamineagonist activity(pramipexole, ropinirole,pergolide) or dopamineprecursor (levodopa)

Elimination of eveningand nighttime RLSsymptoms

Nausea/vomiting, nasalcongestion, swelling,bloating, and chest pain.

Evening/nighttime dose maypush RLS symptoms later intothe night and perhaps intothe day. Therefore, doseshould be taken 2 to 3 hoursbefore bedtime.

Tricyclic antidepressants

Amitriptyline, 1050 mg

Doxepin, 1050 mg

Trimipramine, 2550 mg

1

blockade Shorten sleep latencyand reduce unscheduledwaking

Daytime sedation,anterograde amnesia,rebound insomnia,anticholinergic side effects

Do not use in the absence ofunderlying depression.Trimipramine does not suppressREM sleep, as shown in aplacebo/lormetazepam-controlled study of 55 patients.

Mirtazapine, 15 mg

Trazodone, 50100 mg

Antagonizes 2

and5-HT

2receptors

1

blockade

Shorten sleep latencyand reduce unscheduledwaking

Shorten sleep latency

and reduce unscheduledwaking

Daytime sedation, flu-likesymptoms, tremor,abnormal dreams

Priapism, syncope

Do not use in the absence ofunderlying depression.Improves sleep and doesnot suppress REM sleep.

Do not use in the absence of

underlying depression.Evidence suggests thattrazodone may increase deepsleep.

Diphenhydramine,25 mg

Doxtlamine, 25mg

Ethanolamine H1

receptor antagonistsShorten sleep latencyand reduce unscheduledwaking

Anticholinergic activity,sedation, dizziness

Morning hangover effectsmay be greater than those ofGABA agonists.

benzodiazepine receptor complex.

GABA is an inhibitory neurotrans-mitter, which exerts its effect atGABA-A, -B, and -C receptorsubtypes, all of which are affectedby benzodiazepines. Benzodi-azepines are effective for increasingsleep duration; however, potentialtolerance and dependence limittheir use to short-term insomnia.

The therapy in the short-term is as

effective as behavioral interven-tions, but clinical efficacy tends todecline when patients take benzo-diazepines for longer than 30 days.

Adverse effects from benzodi-azepines include residual daytimecognitive impairment, hangover ef-fects, psychomotor impairment,and anterograde amnesia. At dis-



10/16

28. Krystal AD, Walsh JK,Laska E, et al. Sus-tained efficacy of es-zopiclone over 6months of nightlytreatment: results ofa randomized, dou-ble-blind, placebo-controlled study inadults with chronicinsomnia. Sleep.2003;26:793-9.[PMID: 14655910]

29. Maarek L, Cramer P,

Attali P, et al. Thesafety and efficacy ofzolpidem in insom-niac patients: a long-term open study ingeneral practice. JInt Med Res.1992;20:162-70.[PMID: 1521672]

30. Walsh JK, Roth T,Randazzo A, et al.Eight weeks of non-nightly use of zolpi-dem for primary in-somnia. Sleep.2000;23:1087-96.[PMID: 11145323]

31. The U.S. Food andDrug Administration.FDA Requests Label

Change for All SleepDisorder Drug Prod-ucts. Accessed atwww.fda.gov/bbs/topics/NEWS/2007/NEW01587.html on 9November 2007.

32. Balter MB, Uhlen-huth EH. New epi-demiologic findingsabout insomnia andits treatment. J ClinPsychiatry. 1992;53Suppl:34-9; discus-sion 40-2.[PMID: 1487478]


In March 2007, the Food and

Drug Administration (FDA)

required new, stronger

warnings for 13 sleep-

inducing pharmaceutical

products

continuation, tapering withdrawalmitigates rebound insomnia, irri-tability, and anxiety. The minimaleffective dose is advised to decreasethe likelihood of rebound insomnia.

Nonbenzodiazepine GABA Agonists

Nonbenzodiazepines are selectiveGABA agonists that result in fewerside effects than benzodiazepines

and other sedative-hypnotics. Ad-ditionally, half-lives of 1 to 5 hoursallow for more selective treatment.The 1-hour half-life of zaleplon,for example, makes it potentiallyhelpful for patients who have prob-lems with sleep induction. Studiesof intermittent nonbenzodiazepinedosing that examined patients self-regulating dosing and taking 3 to 5doses weekly report improved andsustained outcomes in some cases,

similar to daily dosing.One trial randomly assigned patients aged21 to 69 with primary insomnia to eszopi-clone 3 mg (n = 593) or placebo (n = 195)nightly for 6 months. Compared with

placebo, patients in the eszopiclone groupreported improvements in sleep latency,total sleep time, awakenings, wake time af-ter sleep onset, quality of sleep, and day-time alertness. Adverse effects includedheadache and unpleasant taste (28).

Following an open-label study of zolpidem

over 180 days in 96 patients, 49 patientscontinued zolpidem for another 180 daysand 47 discontinued the drug. Of the 47

patients who discontinued the drug, 21showed no rebound insomnia or with-drawal signs during follow-up, but datawere not reported for the other discontin-uers. About 90%of patients who continuedthe drug for a total of 360 days continuedto report improved sleep (29).

In a randomized trial, 163 adults with pri-mary insomnia received either placebo oras-needed zolpidem 10 mg 3 to 5 timesweekly for 8 weeks. Patients who took inter-mittent zolpidem reported better subjectivesleep outcomes compared with those whotook placebo. No evidence of reboundinsomnia was observed on nights that

zolpidem was not taken (30).

Adverse reactions associated withnonbenzodizepine hypnotic agentsinclude nausea, vertigo, general

malaise, residual sedation, disori-entation, nightmares, agitation,antagonistic morning mood, am-nesia, headache, and visual distor-tion. Clinicians should also warnpatients that zolpidem can lead tosleep driving, which is driving anautomobile while not fully awakeafter ingestion of a sedative-hyp-notic product with no recollectionof the event. Sleepwalking andsleep eating have been reported;however, these cases seem to occurwhen the drug is taken at a highdosage or mixed with alcohol orantidepressants.

In March 2007, the Food and DrugAdministration (FDA) requirednew, stronger warnings for 13sleep-inducing pharmaceuticalproducts: zolpidem (Ambien/

Ambien CR), butabarbital (Buti-sol), pentobarbital and carbromal(Carbrital), flurazepam (Dal-mane), quazepam (Doral), tria-zolam (Halcion), eszopiclone(Lunesta), ethchorvynol(Placidyl), estazolam (Prosom),temezepam (Restoril), ramelteon(Rozerem), secobarbital (Sec-onal), and Zaleplon (Sonata).These warnings describe potentialrisks, including severe allergic reac-tions, such as anaphylaxis and an-gioedema, and complex sleep-relat-ed behaviors, such as sleep driving.The agency also recommended thatmanufacturers develop patienthandouts and conduct clinical stud-ies to investigate the frequency ofadverse effects in association withindividual drugs (31).

Nonbenzodiazepine abuse canoccur, especially among patientswith comorbid substance abuse and

psychiatric illness. However, in gen-eral, GABA agonists are preferredover other sedating agents because oftheir safety profile. A number ofother sedative-hypnotic medica-tions may have lethal effects withoverdose. These include sedatingtricyclic antidepressants that affectcardiac conduction; barbituratesthat suppress respiration; and oth-



11/16

ers, such as chloral hydrate, thatalso suppress respiration.

Drug Therapy for Insomnia Secondary

to Restless Leg Syndrome

In the absence of increased caffeineintake or iron deficiency in patientswith RLS, a low bedtime dose of adopaminergic agonist agent, such aspramipexole or ropinirole, may behelpful. If dopaminergic agents areineffective, poorly tolerated, or con-traindicated, consider using a ben-zodiazepine, such as clonazepam;an opiate, such as propoxyphene,hydrocodone, or oxycodone; or anantiepileptic drug, such asgabapentin.

What is the appropriate duration

of prescription drug therapy for

insomnia?

Some literature, consensus opinion,and the FDA recommend that useshould be limited to 1 month, andmedications with a long half-life,including long half-life metabolites,should be avoided. Although mostsleep specialists do not recommendlong-term use of hypnotic agents,clinical practice suggests thatpatients who are using hypnoticslong-term to good effect andwithout side effects may continueto do so. One study estimated that10% to 15% of individuals whouse hypnotics do so for longerthan 1 year (32). Data supportinglong-term use are derived from asmall number of uncontrolledstudies (33).

Clinicians and patients should lookfor rebound insomnia after discon-tinuation. Tapering rather thanabrupt discontinuation may result

in less rebound insomnia; however,not all studies have found signifi-cant rebound.

One randomized, double-blind study com-

paring zolpidem, triazolam, and placebo

in 99 patients showed that zolpidem did

not manifest rebound insomnia, and tria-

zolam did so only on the first night of dis-

continuation (34).

An analysis of 75 sleep laboratory studies

of short-acting sedative-hypnotic agents

published from 1966 to 1997 showed ini-

tial efficacy for all 5 drugs studied. Toler-

ance with intermediate and long-term use

occurred with triazolam, was marginally

present with midazolam and zolpidem,and could not be estimated for brotizolam

or zopiclone because of insufficient data.

The studies suggested severe rebound in-

somnia on the first withdrawal night withtriazolam, mild rebound with zolpidem,

and data were insufficient for brotizolam,

midazolam, and zopiclone. The review

concluded that differences among therap-

idly eliminated hypnotics with respect to

tolerance and rebound insomnia suggest

that, in addition to short elimination half-

life, other pharmacologic properties con-

tribute to these side effects (35).

Agents aimed at the treatment ofinsomnia characterized by noctur-nal awakenings are under study, butnot yet approved by the FDA atthe time of this writing (36).

When should clinicians considerantidepressants in the treatment

of patients with insomnia?

Antidepressants are often used forinsomnia not specifically related todepression. However, expert con-sensus is that antidepressantsshould be reserved for treating un-derlying depression rather than for

treatment of insomnia itself (37).Compared with GABA agonists,the side-effect profile of antide-pressants, which includes cardiacdysrhythmia and orthostatic hy-potension, tends to be more severeand has limited evidence of greaterefficacy. Furthermore, some antide-pressants, such as fluoxetine, canexacerbate insomnia.

Limited data have documented the

ability of some antidepressants toincrease sleep time, sleep efficiency,and deep sleep. If sedating antide-pressants are required, considerusing trazodone, doxepin, trim-ipramine, or mirtazapine (Table 3).In persons with a history of drug oralcohol abuse, antidepressants mayhave less potential for abuse thanbenzodiazepines (38).

33. Kramer M. Hypnotic

medication in thetreatment of chronicinsomnia: non no-cere! Doesnt anyonecare? Sleep Med Rev.2000;4:529-541.[PMID: 12531035]

34. Ware JC, Walsh JK,Scharf MB, et al. Min-imal rebound in-somnia after treat-ment with 10-mgzolpidem. Clin Neu-ropharmacol.1997;20:116-25.[PMID: 9099463]

35. Soldatos CR, DikeosDG, Whitehead A.Tolerance and re-bound insomnia

with rapidly elimi-nated hypnotics: ameta-analysis ofsleep laboratorystudies. Int Clin Psy-chopharmacol.1999;14:287-303.[PMID: 10529072]

36. Roth T, Zammit GK,Scharf MB, et al. Effi-cacy and safety ofas-needed, postbedtime dosing withindiplon in insomniapatients with chron-ic difficulty maintain-ing sleep. Sleep.2007;30:1731-38.

37. Sharpley AL, CowenPJ. Effect of pharma-cologic treatmentson the sleep of de-pressed patients.Biol Psychiatry.1995;37:85-98.[PMID: 7718684]

38. Rush CR, Baker RW,Wright K. Acute be-havioral effects andabuse potential oftrazodone, zolpidemand triazolam in hu-mans. Psychophar-macology (Berl).1999;144:220-33.[PMID: 10435388]




12/16

What are the contraindications to

drug therapy in the treatment of


In general, H1-blocker antihista-

mines are not recommended forpatients with angina, heart disease,glaucoma, pulmonary disease, orproblems with urinating, as well aspatients taking some medications.Likewise, natural remedies, such asSt. Johns wort, may interact ad-versely with prescribed medications.

Patients taking sedative-hypnoticagents should restrict alcohol in-take, or avoid alcohol all together.They must use particular carewhen driving or using hazardousequipment.

Patients who are pregnant orbreastfeeding should avoid hyp-

notics. Patients with underlyingdisorders, such as OSAS, in whichhypnotic use can be counterproduc-tive should also avoid them.

Benzodiazepines are commonlyabused, and they should not beused by patients with a currentalcohol or drug abuse problem orby patients in recovery. Althoughintentional or accidental overdoseof benzodiazepines alone rarelyresults in death or serious illness,they are frequently taken witheither alcohol or other medications,which can be dangerous.

What is the evidence for thecomparative effectiveness ofbehavioral versus drug therapyand among the various drugtherapies for insomnia?Several studies suggest that non-drug therapies may be more effec-tive if not used in conjunction with

drugs, especially in long-term treat-ment. Behavioral interventions arecertainly also less likely than phar-macotherapy to cause side effects.Evidence comparing nonbenzodi-azepine sedative-hypnotics withone another is lacking.

Behavioral techniques were more effective

than drug therapy or placebo in the long-

term in a randomized, placebo-controlled

study of 78 older patients with chronic

insomnia (21).

In a randomized, placebo-controlled trialof 63 middle-aged and young adults, CBT

was found to be superior to drug therapyin the treatment of chronic sleep-onset

insomnia (22).

A meta-analysis of 21 studies including atotal of 470 patients showed that both

drug therapy and behavioral therapy hadsimilar magnitudes of effect (39).

One prospective open study of as-needed

zolpidem use in 2690 subjects noted thatbehavioral therapy on nights not using

zolpidem led to improved sleep with re-duced sleep latency and increased total

sleep time as well as a 30% reduction inuse of zolpidem (40).

A randomized, controlled trial of 26 sub-

jects with insomnia showed that behav-ioral therapy at 10 months wasmore effec-

tive than the combination of behavioraltherapy and hypnotics (41).

A randomized, controlled trial of both

medicated and nonmedicated patientswith insomnia (n = 41)showed that stimu-

lus control therapy was less effective in pa-tients taking hypnotics (42).

Clinical consequences of short half-life hypnotics may include earlymorning insomnia and tolerance orrebound with benzodiazepines.

Clinical consequences of long half-life hypnotics may include daytimesedation, motor incoordination, am-nesia, diminished responsiveness,and performance decrements andaccidents.

When should clinicians consider

specialty referral for patients with

insomnia?

Clinicians should consider referringpatients with insomnia to a sleep

specialist if diagnosis remainsunclear after evaluation, if daytimefunctioning is impaired, or if thepatient requests consultation. Con-sultation may also be helpful if 1 ofthe following conditions is suspect-ed: sleep apnea, parasomnias, RLS,narcolepsy, circadian rhythm distur-bances, and psychophysiologicinsomnia. Referral to a sleep

39. Smith MT, Perlis ML,Park A, et al. Com-parative meta-analy-sis of pharmacother-apy and behaviortherapy for persist-ent insomnia. Am JPsychiatry.2002;159:5-11.[PMID: 11772681]

40. Hajak G, BandelowB, Zulley J, Pittrow D.As neededpharma-cotherapy com-bined with stimuluscontrol treatment inchronic insomniaassessment of a nov-el intervention strat-egy in a primarycare setting. AnnClin Psychiatry.2002;14:1-7.[PMID: 12046635]

41. Hauri PJ. Can we mixbehavioral therapywith hypnoticswhen treating in-somniacs? Sleep.1997;20:1111-8.[PMID: 9493920]

42. Riedel B, Lichstein K,Peterson BA, et al. Acomparison of theefficacy of stimuluscontrol for medicat-ed and nonmedicat-ed insomniacs. Be-hav Modif.1998;22:3-28.[PMID: 9567734]




13/16


specialist offers an opportunity fora comprehensive assessment of themultiple causes of insomnia and,when necessary, performance ofpolysomnography.

Referral to a psychiatrist for diag-nostic evaluation can be helpfulwhen it is unclear whether a con-current psychiatric disorder, such asdepression, is present. Psychiatricconditions are prevalent in personswith chronic insomnia but mayprove difficult to identify (43). Anuntreated chronic psychiatric con-dition may lead to a worse out-come. Referral is also warrantedwhen the patient history elicitschronic use of moderate-to-largedoses of hypnotic medications withcontinuing complaint of insomnia,because there is no evidence to in-

dicate that moderate-to-large dosesof hypnotic medications are neces-sary to treat insomnia in theabsence of psychiatric conditions,such as stress and anxiety disorders.Psychiatric consultation may bewarranted for tapering patientsfrom long-term use of hypnotics.

Consider referral to other special-ists depending on the nature of theunderlying disorder. Consider

referral to a pulmonologist forpatients with sleep apnea syn-dromes. An otolaryngologist, oralsurgeon, or dentist may be con-sulted for surgical procedures onthe airway or mandibular position-ing or stabilization in patientswith sleep apnea. A neurologistmay be considered for manage-ment of complex neurologic dis-eases, such as Parkinson disease,cerebrovascular disease, or dementia.

How should clinicians manageinsomnia in hospitalized patients?

In hospitalized patients, the mostcommon causes of acute insomniaare the effects of illness, environ-mental sleep disruption, medica-tion, anxiety, and depression (44).Treatment should focus on correctingthe underlying medical disorders;reducing environmental sleep

disruptions; and lowering anxietywith psychological interventions,medication, and relaxation training.Special clinical problems includechronic pain, delirium, and insom-nia in the elderly.

Nondrug treatment can often beeffective in hospitalized patients.When sedative-hypnotic medica-

tions are needed, consideration ofpharmacokinetic profile is impor-tant, and long half-life hypnoticsshould be avoided. Intermediate-acting benzodiazepines, such aslorazepam or temazepam, are advised.Zaleplon and zolpidem are alsoattractive hypnotic agents;however, they are typically reservedfor second-line therapy because ofcost (45).

What type of follow-up careshould clinicians provide forpatients with insomnia?Treatment of insomnia is most of-ten long-term and always includessupportive follow-up. Cliniciansshould follow up patients withchronic insomnia until it is resolvedor alleviated. Follow-up visits areused to monitor response to thera-py, adjust therapy, provide educa-tion about sleep hygiene and be-havioral techniques, and to addressother potential underlying causes.One-month follow-up is needed inpatients on hypnotic therapy to as-sess side effects, efficacy, and theneed for continuing treatment. If aparticular hypnotic is ineffective,review the initial diagnosis andconsider alternative treatments,such as behavior therapy. Inpatients on dopaminergics for RLS,follow up at 1 month and at leastannually thereafter. Follow-up fre-

quency should be determined on acase-by-case basis in patients onantidepressants for mood disorderand insomnia to determine if theinsomnia and depression are resolv-ing. Frequent visits may be helpfulfor patients with psychophysiologicinsomnia in order to ensure thatthey understand and are carryingout behavioral recommendations.

43. Ford DE, KamerowDB. Epidemiologicstudy of sleep distur-bances and psychi-atric disorders. Anopportunity for pre-vention? JAMA.1989;262:1479-84.[PMID: 2769898]

44. Berlin RM. Manage-ment of insomnia inhospitalized pa-tients. Ann InternMed. 1984;100:398-404. [PMID: 6141753]

45. Lenhart SE, BuysseDJ. Treatment of in-somnia in hospital-ized patients. AnnPharmacother.2001;35:1449-57.[PMID: 11724098]



14/16


Practice

ImprovementAre there professional

organization guidelines for

insomnia?

Experts urge primary-care physi-cians to use American Academyof Sleep Medicine practice para-meters for the recognition ofinsomnia (10). This consensus-based document supports screen-ing for insomnia (because manypatients are unaware of the im-pact of insomnia on functioning),discusses the identification of

underlying causes of insomnia,

and considers the role of sleep

testing in the evaluation of

insomnia.

What is the role of patient

education in the management of

insomnia?

Patient education plays an impor-

tant role in insomnia management

(see Box) and clinicians should

provide patients with information

about insomnia and its treatment.

Important Components of Patient

Education About Insomnia

Insomnia has multiple causes.

Insomnia may precede or be a causeof depression or other mood disorders.

It is necessary to address allcontributing factors to insomnia.

Patients should actively engage inbehavioral treatments, includingmaking changes in sleep hygiene.

Behavioral treatments have longer-lasting benefit than drug therapyalone.

Progress often takes 1 to 2 months.

Behavioral recommendations must becontinued even after insomnia improves.

in

the

clinic

Tool Kitin the clinic

Insomnia

PIER Modules

PIER.acponline.org

Access the following PIER module: Insomnia. Provides updated information designed forrapid access at the point of care.

Patient Information

www.annals.org/intheclinic

Download a copy of the patient information page that appears on the following page forduplication and distribution to your patients.

www.acponline.org/atpro/timssnet/catalog/books/restful_sleep.htm

Order copies of the ACPs Guide to a Restful Sleep, a 30-minute patient education DVDand accompanying guidebook.

ACP Observer Article

www.acponline.org/journals/news/july06/special.pdf

View a copy of a July-August 2006 ACP Observer special focus article on insomnia.

Sleep Diary

pier.acponline.org/physicians/diseases/d166/figures/d166-figures.html

Web Sites

National Heart Lung and Blood Institute

www.nhlbi.nih.gov/health/dci/Diseases/inso/

American Academy of Sleep Medicine

www.aasmnet.org/

Treatment... Initial therapy for insomnia should address sleep hygiene and stimu-

lus control. Other behavioral interventions include sleep restriction, CBT, and

biofeedback, which require a clinician trained in these techniques. When behav-

ioral interventions are unsuccessful, therapy with GABA agonists (nonbenzodi-

azepines preferred) may be warranted, but side effects are common. Although

nonprescription antihistamines are often used to treat insomnia, they have

adverse effects and little evidence to support their effectiveness. Evidence is also

lacking for the effectiveness of herbal therapies. Antidepressants should be

reserved for patients with underlying depression. Some evidence, consensus opin-ion, and the FDA recommend limiting the use of sedative-hypnotics to 1 month.




15/16

THINGS PEOPLE SHOULD KNOWABOUT INSOMNIA

In the Clinic

Annals of Internal Medicine

P a t i e n t I n

f o r m a t i o n

People do not always know why they have insomnia, but some common causes are:

Stress

Caffeine

Alcohol

Depression (insomnia can cause depression, and depression can causeinsomnia)

Changes in work schedules

Pain or other symptoms from health conditions

If you have trouble sleeping, try these things:

People with insomnia have trouble falling asleep or staying asleep. People with insom-nia may feel sleepy during the day, depressed, moody, or have trouble concentrating.

Sometimes changing sleep habits is enough to make insomnia better. When other treat-ments are needed, behavioral treatments are usually better than taking medicines.Behavioral therapies may take 1 to 2 months to help insomnia and need to be kept up

even after the insomnia gets better.

Your doctor may want you to fill out a sleep diary. The diary will help you keep track ofwhen you go to bed, how long you lie in bed before falling asleep, how often you wakeduring the night, when you get up in the morning, and how well you sleep.

Sleeping pills may only help for a short time, have side effects, and can be unsafe insome people. Sleeping pills should not be used for longer than a few days. Using themregularly can make insomnia worse.

If you have insomnia, see your doctor for help.

Web Sites with Good Information about Insomnia

National Heart Lung and Blood Institutewww.nhlbi.nih.gov/health/dci/Diseases/inso/

American Academy of Sleep Medicinewww.sleepeducation.com

Consumer Reports Best Buy Drugswww.crbestbuydrugs.org/drugreport_DR_sleepingpills.shtml

Do not use caffeine, alcohol, and stimulant medications (includingsome cold and allergy medicines)

Try to go to sleep around the same time each night and wake uparound the same time each morning

Follow a bedtime routine that helps you relax before bed (reading,listening to music, or taking a bath)

Do not exercise or eat big meals shortly before bedtime

Make your bedroom comfortable, quiet, dark, and do not turn on

the television or computer



16/16

CME Questions

Questions are largely from the ACPs Medical Knowledge Self-Assessment Program (MKSAP). Go to www.annals.org/intheclinic/

to obtain up to 1.5 CME credits, to view explanations for correct answers, or to purchase the complete MKSAP program.

A 38-year-old woman is evaluated for a 4-week history of awakening in the middle ofthe night, although she falls asleep with-out difficulty. During the day, she notes afeeling of hyperarousal and irritability,which is interfering with her effectivenessat work. She is in excellent health and runscompetitively. She does not smoke or drinkalcohol. She has used over-the-counterantihistamines to help her sleep, but theyare no longer effective.

Pulse rate is 60/min, and blood pressureis 120/75 mm Hg. The BMI is 20. Theremainder of the examination is normal.Acute insomnia is diagnosed, and thepatient is advised to avoid strenuousexercise or alcohol within a few hours ofbedtime, develop a relaxing evening rou-tine, and avoid afternoon caffeine. The

patient follows this advice but continuesto have difficulty sleeping.

Which of the following is the mostappropriate treatment for this patient?

A. KavaB. Zolpidem

C. Selective serotonin reuptake inhibitorD. DiphenhydramineE. Triazolam

A 73-year-old woman who lives in anursing home is evaluated for a 6-monthhistory of frequent awakening during the

night, although she falls asleep withoutdifficulty. The patient is fatiguedthroughout the day. Her medical historyis significant for dementia secondary tocerebral vascular disease and hyperten-sion. She does not have urinary inconti-nence. A diagnosis of primary insomnia isestablished, and a recommendation isgiven to the patient to avoid drinkingcaffeinated beverages and eating beforebedtime, as well as to minimize nighttimedisturbances. When nighttime awakeningpersists, the patient begins taking triazo-lam before bedtime. After a few days oftreatment, the patient is noted to beconfused.

She is afebrile. The pulse rate is 63/min,respiration rate is 12/min, and bloodpressure is 120/72 mm Hg. The neuro-logic examination indicates no new focalfindings. She is oriented to person but

not to place or time. Laboratory studies,including complete blood count, serumchemistries, and urinalysis, are normal.

Which of the following is the mostappropriate next step in management?

A. Discontinue triazolamB. Decrease triazolam doseC. Perform CT of the head and blood

and urine culturesD. Substitute diphenhydramine for

triazolam

E. Initiate cognitive behavioraltherapy

A 47-year-old man is evaluated for diffi-culty falling asleep and resulting daytimefatigue occurring at least 3 to 4 timesper week for the past several months. He

denies snoring or sleepwalking, shortnessof breath, and chest pain. He recentlywent through a divorce, which hascaused some personal and financial stressin his life. He smokes one-half pack perday of cigarettes. Pulse rate is 72/min,and blood pressure is 138/85 mm Hg. TheBMI is 26. The remainder of the examina-tion is normal. Laboratory studies includea hematocrit of 42%, a leukocyte countof 4200/L (4.2 x 109/L), a fasting plasmaglucose of 100 mg/dL (5.55 mmol/L), anda serum thyroid-stimulating hormonelevel of 2.5 U/mL (2.5 mU/L). Results of a

chest radiograph and electrocardiogramare normal.

Which of the following is the mostappropriate next diagnostic step?

A. PolysomnographyB. Spirometry

C. Cardiac stress testingD. Depression screening

A 68-year-old woman describes a 2-yearhistory of insomnia, which she attributesto an inability to get comfortable in bedbecause of a creepy-crawly sensation in

her lower limbs. The sensation is absentduring the day, but it has begun to both-er her in the evening and is especiallytroublesome in bed. Walking relieves thesensation. Physical examination, includ-ing neurologic examination, is normal.

Which of the following studies should bedone next?

A. Serum ceruloplasmin level

B. Serum ferritin levelC. Urine porphyrin level

D. Nerve conduction studyE. Magnetic resonance imaging of the

brain

A 50-year-old woman has a 1-yearhistory of difficulty falling and stayingasleep, not feeling refreshed on awaken-ing in the morning, and inability to nap.Her husband has noted striking personalitychanges. The patient also has loss oflibido, occasional low-grade fevers in theevening, and periods of sweating or tear-ing. She has mild hypertension treatedwith hydrochlorothiazide and captopril.

Family history is unremarkable.

The patient is alert and oriented butanswers questions in monosyllables afterlong delays. Temperature is 37.3C(99.1F), pulse rate is 88/min, respirationrate is 18/min, and blood pressure is164/98 mm Hg. Cardiopulmonary andabdominal examinations are normal. Thegait is normal. There is slight horizontalnystagmus on lateral gaze and a hyperac-tive gag reflex. Cranial nerves are other-wise normal. Muscle strength is goodsymmetrically. Myoclonic jerks are noted.

Unsustained clonus with biceps, patellar,and ankle jerks is also present. There areno fasciculations. Deep tendon reflexesare hyperactive bilaterally. Hemoglobin12 g/dL (120 g/L), hematocrit 36%,leukocyte count 6700/L (6.7 x 109/L),platelet count 222,000/L (222 x 109/L),blood urea nitrogen 21 mg/dL (7.5mmol/L), serum creatinine 0.9 mg/dL(79.58 mol/L), urinalysis; Cerebrospinalfluid examination is normal. MRI of thehead shows mild cerebral atrophy, anddiffusion-weighted imaging reveals slighthyperintensity of the cerebral cortex and

basal ganglia.

Which of the following is the mostlikely diagnosis?

A. Herpes simplex virus encephalitisB. West Nile virus infectionC. DepressionD. Fatal familial insomnia

1.

2.

4.

3.

5.

annals insomnia

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