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Evidence-Based Recommendations for the Assessment and
Management of Sleep Disorders in Older Persons
Harrison G. Bloom, M.D., AGSF1, Imran Ahmed, M.D.2, Cathy A. Alessi, M.D., AGSF3, Sonia
Ancoli-Israel, Ph.D.4, Daniel J. Buysse, M.D.5, Meir H. Kryger, M.D.6, Barbara A. Phillips, M.D.
7, Michael J. Thorpy, M.D.8, Michael V. Vitiello, Ph.D.9, and Phyllis C. Zee, M.D., Ph.D.10
1International Longevity Center-USA and Brookdale Department of Geriatrics and Adult
Development, Mount Sinai Medical School
2Albert Einstein College of Medicine
3UCLA David Geffen School of Medicine and GRECC, VA Greater Los Angeles Healthcare Systems
4University of California San Diego, School of Medicine and Veterans Affairs San Diego Healthcare
System
5Neuroscience Clinical and Translational Center, University of Pittsburgh School of Medicine
6Gaylord Sleep Center, Gaylord Hospital
7National Sleep Foundation and University of Kentucky College of Medicine
8Albert Einstein College of Medicine, Sleep-Wake Disorders Center-Montefiore Medical Center
9NW Geriatric Education Center, University of Washington
10Sleep Disorders Center, Northwestern University
Background and Significance
Sleep-related disorders are common in the general adult population, and as the population ages,
the prevalence of these disorders increases. A common misconception among clinicians and
the public is that this increased prevalence is a normal and expected phenomenon of aging.
However, this higher prevalence of sleep disruption is often the result of the increased presence
of medical, and psychosocial comorbidities in this population. The complicated multifactorial
interactions that generate sleep disorders in older individuals pose important challenges to
clinicians. Furthermore, many clinicians are unaware of the seriousness and potential morbidity
associated with sleep problems in older people, distinct from the morbidity of concurrent
disorders. As a result, these issues are often underinvestigated, or completely ignored.1
Because of the high prevalence, complexity, and health implications associated with sleep-
related disorders in older individuals, increasing attention is now being focused on this topic.
For example, a recent publication has recommended that sleep problems be approached as a
“multifactorial geriatric syndrome.”2
Of major clinical concern is the strong bidirectional relationship between sleep disorders and
serious medical problems in older persons. Individuals with sleep disorders are more likely to
Corresponding Author: Harrison G. Bloom, M.D., AGSF, International Longevity Center-USA, 60 East 86th Street New York, NY
10028, 212.517.1308, 212.288.5450, HarrisonB@ilcusa.org, Alternate Corresponding Author: Cathy A. Alessi, M.D., AGSF,
Cathy.Alessi@med.va.gov.
NIH Public Access
Author Manuscript
J Am Geriatr Soc. Author manuscript; available in PMC 2009 November 1.
Published in final edited form as:
J Am Geriatr Soc. 2009 May ; 57(5): 761–789.
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develop hypertension, depression, cardiovascular, and cerebrovascular disease. Conversely,
individuals with any of these diseases are at higher than normal risk of developing sleep
problems.3,4
Older individuals consider quality sleep to be an essential part of good health. A Gallup survey
of over 1000 Americans age 50 and older (43% of whom were age 65 or older) found that 80%
answered “a great deal” when asked whether sleep was important for healthy aging. In the
same survey, and contrary to the myth that older adults need less sleep, 45% believed they
required more sleep now than when they were younger and 25% believed they had a sleep
“problem.”5
The goal of this paper is not to present an exhaustive and comprehensive review of sleep and
sleep disorders in older persons. Rather, we present an overview of sleep disorders and suggest
appropriate evidence-based recommendations for assessing and treating sleep disorders in the
older adult population. These recommendations have been developed by professionals with
expertise in sleep disorders and in the clinical care of older people.
As in many areas of clinical research, older persons are often poorly represented (or specifically
excluded) in clinical sleep studies. Thus, there are less data available from randomized
controlled trials for this population compared to the general adult population. Nevertheless,
given the importance of the subject, and the opportunity for successful intervention, we believe
it is prudent and timely to propose recommendations based upon expert consensus of current
evidence. While there have been a number of publications aimed at clinicians concerning sleep
and sleep disorders in the adult and older adult populations, there are currently no
recommendations for systematically approaching the assessment, treatment and follow-up of
sleep disorders in the older adult population. 2,6-11
In developing these recommendations we are cognizant of a number of important themes: 1)
the tremendous heterogeneity of the older adult population, and thus the critical importance
for individualization of assessment and therapy; 2) the limited amount of time clinicians have
to spend with each patient, making lengthy assessments for sleep problems unrealistic; 3) the
body of knowledge regarding the approach to assessment and treatment of sleep disorders that
clinicians need to possess; 4) the role of sleep specialists in this process, and the importance
of recognizing when and where to refer; and 5) the frequent presence of comorbidities and
multiple medication usage in this population of patients, requiring a careful approach and
meticulous follow-up.
Sleep-related problems in the acute care hospital setting will not be addressed in this paper.
Such problems have received little attention in research studies compared to sleep problems
in outpatients, and the state of knowledge concerning these conditions is inadequate to make
recommendations with a reasonable level of confidence. In this paper, therefore, we focus on
chronic problems with sleep in older persons in the outpatient and long term care setting.
General Review of Sleep
Major physiologic changes occur in the context of aging. One such change that can be quite
problematic for many older adults is the often profound change of the daily sleep-wake cycle.
Sleep is composed of 2 very different physiologic states: rapid eye movement sleep (REM)
and non-rapid eye movement sleep (NREM). NREM is further divided into 4 stages. Stage 1
is the lightest stage of sleep. Stage 2 sleep has a higher arousal threshold and is the stage in
which most time sleeping is spent. Stages 3 and 4 are collectively referred to as “deep sleep,”
“delta sleep,” or “slow wave sleep,” (based upon their characteristic EEG profiles) and are
associated with a high arousal threshold. Recently, the American Academy of Sleep Medicine
(AASM) has revised this classification slightly, into 3 NREM stages (Stages N1, N2, and N3,
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where N3 represents the traditional stages 3 and 4 combined).12 Sleep typically occurs in
approximately 90-minute cycles of NREM/REM. However, more stage 3/4 sleep occurs in the
first half of the night, while more REM sleep takes place in the last half. This sleep pattern can
be interrupted by awakenings which may be extremely brief or of prolonged duration.
The sleep-wake pattern is regulated by a complex interaction between a time-awake-dependent
increase in homeostatic sleep drive and a circadian wakefulness drive which typically reaches
its maximum in the evening. Normally, homeostatic sleep drive and circadian wakefulness
drive are both high in the evening, but as homeostatic sleep drive continues to build and
circadian wakefulness drive declines sleep is initiated.
This normal sleep-wake process can be influenced by a wide variety of physiologic,
psychologic and environmental factors. The most striking change in sleep patterns in older
adults is the repeated and frequent interruption of sleep by long periods of wakefulness,
possibly the result of an age-dependent intrinsic change in the interaction of the sleep
homeostatic and circadian arousing processes that control sleep.13 Other age-dependent
changes in sleep include decreased total sleep time (TST), reduced sleep efficiency (time asleep
as a percentage of time in bed) and decreased slow wave and REM sleep, as well as increased
stages 1 and 2 sleep. These age-dependent changes in nocturnal sleep are accompanied by an
increased incidence of napping or falling asleep during the day.14-16 Aging is also associated
with a tendency to both fall asleep and awaken earlier and to be less tolerant of phase shifts in
the sleep-wake schedule such as those associated with jet lag and shiftwork.17 These changes
also suggest age-dependent alterations in regulation of the circadian sleep-wake cycle.
When the sleep of individuals who may be considered to be “optimally aging” is examined
and age-related medical and psychiatric comorbidities controlled for, it appears that most age-
dependent sleep changes occur in early and middle adulthood (years 19-60).13 Further age-
dependent sleep changes after age 60 are, at most, modest, assuming the individual is in good
health.13 The presence of medical and psychiatric illnesses, however, is associated with
exacerbations of age-dependent sleep disruption.13,18-20 Nevertheless, it is important to
recognize that such sleep disturbance in the presence of comorbidities is not necessarily simply
a symptom of the comorbid condition(s), but may represent an independent problem that may
benefit from treatment.21,22
In addition to the impact of age-dependent sleep changes and age-associated comorbidities,
the sleep of older adults can be further adversely impacted by common primary sleep disorders,
such as insomnia, obstructive sleep apnea (OSA) and restless leg syndrome (RLS).
Epidemiologic studies have consistently shown that the prevalence of sleep complaints and
sleep disorders grows steadily with advancing age.23 As many as 57% of older adults complain
of significant sleep disruption, 45% have periodic limb movements (PLMs) during sleep, 29%
suffer from insomnia, 24% have obstructive sleep apnea (OSA), 19% complain of early
morning awakening, and 12% have restless legs syndrome.24-28
Other factors such as prescription and over-the-counter medications, social drug use, and
psychosocial, behavioral, and environmental factors including poor sleep hygiene (the
behaviors and environmental factors that can improve or worsen sleep), can further contribute
to sleep problems.29,30 Indeed, the sleep of an older adult can be adversely impacted by any,
or several of these factors.30 In older adults, these sleep disturbances and increases in daytime
sleepiness can have a significant negative impact, not only on quality of life, but also on
morbidity and mortality.29,31,32
While sleep disturbances can have profound health implications, they may also be quite
situation-specific. For example, sleep disturbances in a community-dwelling older adult who
is aging optimally are likely to differ from those experienced by older adults in an acute hospital
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setting or in long term care, particularly in those with dementia who can neither describe their
symptoms nor engage as actively in treatment.
In 2006, the Institute of Medicine (IOM) released a report entitled, “Sleep Disorders and Sleep
Deprivation: An Unmet Public Health Problem” which recognized the wide range of
deleterious health and safety consequences of disturbed and inadequate sleep.33 The report
called for increased awareness among health care professionals about the physiology of healthy
sleep and sleep disorders across the lifespan, as well as for the development and implementation
of programs to promote the early diagnosis and treatment of sleep disorders.
The last 10 years have been marked by significant and rapid advances in our ability to diagnose
and treat sleep disorders in the general and the older adult population utilizing both behavioral
and pharmacologic approaches. The recommendations for the effective diagnosis and treatment
of sleep disorders in this population presented below are offered in the spirit of the IOM report
and the considerable recent progress made in the effective recognition and treatment of sleep
disorders in older adults.
Recommendations Development Process and Methods
Two 2-day conferences involving a multidisciplinary group of sleep experts and clinicians
representing major geriatric interest groups and societies, were held at the International
Longevity Center (ILC-USA, New York) in November, 2005 and December, 2006.
Participants in those conferences uniformly agreed that the time was appropriate to bring
together representatives form national sleep organizations, geriatric clinical organizations, and
other clinical organizations with an interest in geriatric care in order to develop and publish
evidence and expert consensus-based recommendations for the assessment and management
of sleep disorders in older persons. The development of such recommendations seemed
especially important given the recent increasing attention in the literature to sleep problems in
older adults and the absence of existing recommendations for this population.
A broad national group of 13 such organizations was assembled in 2007. In December of that
year, a third conference at the ILC brought together representatives from these organizations,
as well as other sleep experts and expert clinicians. Prior to the meeting, thought leaders in the
field were asked to prepare presentations on the major disorders related to sleep disturbances
in older adults, based upon their prevalence, potential morbidity and mortality, and possibility
for response to therapy. The attendees subsequently identified the sleep disorders to be included
and the authors were chosen because of their internationally recognized expertise in each
particular sleep disorder. They determined that the recommendations paper should be a multi-
authored document that would be submitted to a peer-review journal for publication and that
participating organizations would not be asked to provide review prior to recommendations
publication.
In addition to the references cited by the authors of the individual sections, a formal literature
search and review was performed for each of the sleep disorders, and for the section concerning
the specific sleep problems encountered in the long term care setting. The search focused on
randomized controlled trials (RCTs), metaanalyses, and systematic reviews. Non-randomized
clinical trials and controlled clinical trials were also included given the low volume of RCTs
in older adults with certain sleep disorders (eg, parasomnias, hypersomnias). More than 11,600
citations were identified from sources including PubMed, the Cochrane Database of Systematic
Reviews, the National Guideline Clearinghouse and Centre for Reviews and Dissemination/
Health Technology Assessment databases using key word searches for each condition and/or
intervention of interest. Approximately 1,700 abstracts for these citations were selected and
screened by panel members for evidence-based content. Selected full text, English language
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papers were summarized in evidence tables for review by all of the primary authors. The
number of evidence based studies on patients over age 65 is limited in some conditions and
consensus can vary on whether studies of younger subjects can be extrapolated to older
subjects.
The quality and strength of evidence for each recommendation was initially assigned by the
primary author proposing that specific recommendation (Table 1). All evidence designations
were then reviewed by the coalition panel and final designations were decided by consensus.
This assessment methodology has been widely used in previous guidelines.34
Detecting Sleep Disorders in an Ambulatory Setting: General Approach
The best method for detecting sleep-wake problems in ambulatory older people is simply to
inquire about sleep on a regular basis.
The clinician may do this initially during the patient visit. An alternative is to allow a staff
member to administer a brief sleep questionnaire before or during routine vital signs
assessments, perhaps prior to the first visit in all new patients and then at least semi-annually
in returning patients. The answers to these questions will then be immediately available to the
clinician to review and or expand upon if necessary. If a bed partner is with the patient, he or
she should assist with the answers.
The following 12 questions can serve as the initial assessment regarding sleep:
1. What time do you normally go to bed at night? What time do you normally wake up
in the morning?
2. Do you often have trouble falling asleep at night?
3. About how many times do you wake up at night?
4. If you do wake up during the night, do you usually have trouble falling back asleep?
5. Does your bed partner say (or are you aware) that you frequently snore, gasp for air
or stop breathing?
6. Does your bed partner say (or are you aware) you kick or thrash about while asleep?
7. Are you aware that you ever walk, eat, punch, kick, or scream during sleep?
8. Are you sleepy or tired during much of the day?
9. Do you usually take 1 or more naps during the day?
10. Do you usually doze off without planning to during the day?
11. How much sleep do you need to feel alert and function well?
12. Are you currently taking any type of medication or other preparation to help you
sleep?
If symptoms of a sleep complaint are suggested in this initial screening, further questions may
be appropriate to ask when taking a sleep history35:
1. Do you have the urge to move your legs or do you experience uncomfortable
sensations in your legs during rest or at night?
2. Do you have to get up often to urinate during the night?
3. If you nap during the day, how often and for how long?
4. How much physical activity or exercise do you get daily?
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5. Are you exposed to natural outdoor light most days?
6. What medications do you take, and at what time of day and night?
7. Do you suffer any uncomfortable side effects from your medications?
8. How much caffeine (eg, coffee, tea, cola) and alcohol do you consume each day/night?
9. Do you often feel sad or anxious?
10. Have you suffered any personal losses recently?
The patient's responses should indicate how to proceed with any further history, focused
physical examination or laboratory investigations. Specific questions, examinations,
laboratory tests, procedures, and possible referrals are discussed in more detail in the sections
concerning the particular sleep disorders. A flow diagram (Figure 1) may be helpful in
identifying and treating sleep complaints in older ambulatory individuals.
Insomnia
Definition
Insomnia is defined as a complaint of disturbed sleep in the presence of an adequate opportunity
and circumstance for sleep. The complaint may consist of difficulty initiating sleep, difficulty
maintaining sleep, waking up too early and/or nonrestorative or poor quality sleep. For the
diagnosis of an insomnia disorder to be made, the difficulty with sleep must have a negative
impact on daily function.36
Insomnia is classified as either primary or comorbid. Primary insomnia implies that no other
cause of sleep disturbance has been identified. Comorbid insomnia is more common and is
most often associated with psychiatric disorders (eg, depression, anxiety, or substance use
disorders), medical disorders (eg, cardiopulmonary disorders, neurologic disorders, or chronic
somatic complaints that result in sleep disruption), medications, and other primary sleep
disorders (eg, obstructive sleep apnea or restless legs).4,24 Comorbid insomnia does not suggest
that other condition(s) “cause” insomnia, but rather that insomnia and the other condition(s)
co-occur, and may each warrant clinical attention and treatment.
Prevalence
While the prevalence of insomnia in the general population has been estimated at 10-20%,
studies in older adults have found higher frequencies. In a study of more than 9000 adults over
the age of 65 years, 42% of participants had difficulty both falling asleep and staying asleep
with a higher prevalence found in those older adults with poor health and who were taking
medications for a variety of medical problems.24 Participants who were depressed were 2.5
times more likely to report insomnia, and those with respiratory symptoms were 40% more
likely to do so. The finding that a considerable proportion of sleep complaints among older
people may be associated with chronic disease and other health problems is corroborated in
other reports.19,20,37
Consequences of insomnia
Insomnia in the older adult is associated with significant morbidity and mortality. Compared
to controls, those with difficulty sleeping report decreased quality of life and increased
symptoms of depression and anxiety.38-41 Napping during the day and sleeping less than 7
hours a night have been associated with an increased risk of falls.42 Cognitive decline, difficulty
ambulating, difficulty with balance, and difficulty seeing are also associated with poor sleep,
even after controlling for medication use.43-47 The relative risk for increased mortality in the
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older adult has been associated with taking more than 30 minutes to fall asleep and with a sleep
efficiency (time asleep as a percentage of time in bed) of less than 80%.48
Comorbidities
As mentioned, much of the insomnia seen in older adults is likely to be comorbid with
psychiatric illness. It has long been known that depression and insomnia are associated, and
that the presence of depressed mood may predict insomnia. Many studies have suggested that
untreated insomnia is a risk factor for recurrent and a new onset of depression.49-53
Older adults with medical conditions are also more likely to complain of difficulty sleeping.
In the 2003 National Sleep Foundation survey of adults aged 65 years and over, more sleep
complaints and more dissatisfaction with sleep were reported by those with more medical
conditions, including cardiac and pulmonary disease.4 Pain associated with osteoarthritis,
cancer, or diabetes mellitus, shortness of breath due to chronic obstructive pulmonary disease
or congestive heart failure, nocturia due to an enlarged prostate, and neurologic deficits related
to cerebrovascular accidents or Parkinson's disease have all been associated with sleep
complaints and insomnia.54-59 Not only do older adults with medical and psychiatric problems
have more insomnia, but those with insomnia are also more likely to have medical problems,
including heart disease, cancer, high blood pressure, neurologic disease, breathing problems,
urinary problems, diabetes, chronic pain and gastrointestinal problems, even after controlling
for depression and anxiety.3
Medications
Many older adults regularly take multiple medications. Medications used to treat various
underlying chronic medical and psychiatric conditions also contribute to sleep disruptions,
including β-blockers, bronchodilators, corticosteroids, decongestants and diuretics, as well as
other cardiovascular, neurologic, psychiatric, and gastrointestinal medications. Medications
used to treat depression, such as selective serotonin reuptake inhibitors (SSRIs) and
serotonergic and noradrenergic reuptake inhibitors (SNRIs) may also cause or exacerbate
insomnia.60 In addition to prescription medications, older adults often take over the counter
preparations which can cause or exacerbate sleep disturbances. Examples include cough and
“cold” medications, especially those containing pseudoephedrine or phenylpropanolamine,
any caffeine containing drugs (e.g. acetaminophen/aspirin/caffeine combinations), and drugs
containing nicotine (e.g. nicotine gum or transdermal (patches).
Of course, cigarette smoking and coffee consumption themselves can impair sleep as well.
Assessment of insomnia
The diagnosis of insomnia in the older adult requires that the patient has difficulty falling asleep
or staying asleep for at least 1 month and that impairment in daytime functioning results from
difficulty sleeping. The differential diagnosis of chronic insomnia is broad, especially in older
adults with many medical and psychosocial comorbidities who are also taking multiple
medications. Therefore, a thorough clinical history is essential, especially with regard to
prescription and nonprescription drugs and remedies, as well as any comorbid conditions or
diseases. It is important to establish whether the individual's insomnia is primary or comorbid.
However, it is not uncommon for older people to have more than 1 etiologic contributing factor
responsible for the insomnia.
A focused physical examination, based upon the responses from the clinical history, is also
essential. Any laboratory evaluation should follow logically from the results of the history and
physical exam.
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Treatment of insomnia
Behavioral treatment—Behavioral treatments have been shown to be highly effective in
the treatment of insomnia in all age groups.36,61 Cognitive behavioral therapy for insomnia
(CBT-I) has been shown to be most effective. CBT-I combines different behavioral treatments,
including sleep hygiene instruction, stimulus control and/or sleep restriction, with cognitive
restructuring.62-64 In CBT-I trials in older adults, insomnia not only resolved, but the effect
was sustained for up to 2 years.62
A number of single-modality behavioral and other nonpharmacologic approaches have been
utilized to treat and manage insomnia in all age groups. These include relaxation therapy and
imagery, stimulus control, sleep restriction, sleep compression, improved sleep hygiene and
sleep education, and cognitive therapies. Exercise and physical activity, massage therapy,
chronotherapy and light therapy are also used. While any of these may be beneficial for an
older adult with insomnia, 2 approaches have met evidence-based criteria for efficacy: sleep
restriction-sleep compression therapy and multicomponent cognitive-behavioral therapy.65
Sleep hygiene and sleep education—Sleep hygiene and sleep education can be useful
when used together with other modalities, but are usually not adequate by themselves for the
treatment of severe, chronic insomnia. Addressing sleep hygiene entails examining sleep
habits, behaviors and environmental factors that can have an effect upon sleep. A practitioner
can educate patients about common habits or practices that may interfere with their sleep, and
implement strategies for avoiding them.66 Clinicians must be aware that, as often occurs in
this population, older adults may not voluntarily offer information about sleep practices unless
specifically asked about them.
Behaviors and habits that may impair sleep include66:
1. Frequent daytime napping
2. Spending too much time in bed
3. Insufficient daytime activities
4. Late evening exercises
5. Insufficient bright light exposure
6. Excess caffeine
7. Evening alcohol consumption
8. Smoking in the evening
9. Late heavy dinner
10. Watching television or engaging in other stimulating activities at night
11. Anxiety and anticipation of poor sleep
12. Clock watching
13. Environmental factors, such as the room being too warm, too noisy, or too bright. Pets
on the bed or in the bedroom, and/or active or noisy bed partners.
Sleep restriction- sleep compression
Sleep restriction therapy entails limiting time in bed to consolidate actual time sleeping. The
patient is counseled to reduce the amount of time in bed to correlate closely with actual time
sleeping. The recommended sleep times are based upon sleep logs kept for 2 weeks before
sleep restriction therapy is begun. Thus, an individual who reports spending 8.5 hours in bed,
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but sleeping only 5.5 of those hours, would be counseled to limit his or her time in bed to 5.5
to 6 hours. Time allowed in bed is gradually increased by 15-20 minute increments
(approximately once every 5 days if improvement is sustained) as sleep efficiency increases,
until the individual's optimal sleep time is obtained.64
In sleep compression, a variant of sleep restriction, patients are counseled to decrease their
time in bed gradually to match total sleep time rather than making an immediate substantial
change, as is the case in sleep restriction therapy.64 A number of studies support the efficacy
of sleep restriction-sleep compression therapy as a treatment for older patients with chronic
insomnia.67-69 These approaches can also be combined with other modalities.
Stimulus control
People suffering from chronic insomnia may adopt coping strategies that exacerbate the
problem. Watching television or reading in bed, worrying about falling asleep, or using the
bedroom for vigorous discussions or arguments are examples of behaviors that can impair sleep
by producing associations between the bed and bedroom and those activities; the bedroom
should be associated only with sleeping and sex. Stimulus control therapy attempts to eliminate
these behaviors in the bedroom and thereby strengthen the association between sleep and the
bed and bedroom.
The following are helpful instructions for utilizing stimulus control and practicing good sleep
hygiene.7,35,66
1. Develop a sleep ritual such as maintaining a 30-minute relaxation period before
bedtime or taking a hot bath 90 minutes before bedtime.
2. Make sure the bedroom is restful and comfortable.
3. Go to bed only if you feel sleepy.
4. Avoid heavy exercise within 2 hours of bedtime.
5. Avoid sleep-fragmenting substances, such as caffeine, nicotine, and alcohol.
6. Avoid activities in the bedroom that keep you awake. Use the bedroom only for sleep
and sex; do not watch television from bed, or work in bed.
7. Sleep only in your bedroom.
8. If you cannot fall asleep leave the bedroom and return only when sleepy.
9. Maintain stable bed times and rising times. Arise at the same time each morning,
regardless of the amount of sleep obtained that night.
10. Avoid daytime napping. If you do nap during the day, limit it to 30 minutes and do
not nap, if possible, after 2 pm.
Relaxation therapy
The goal of relaxation therapy is to guide individuals to a calm, steady state when they wish
to go to sleep. The methods used include progressive muscle relaxation (tensing and then
relaxing each muscle group), guided imagery, diaphragmatic breathing, meditation and
biofeedback.70
Cognitive behavioral therapy for insomnia (CBT-I)
This treatment combines multiple behavioral approaches, usually incorporating sleep
restriction, stimulus control and cognitive therapy, with or without relaxation therapy. Sleep
hygiene and sleep education are frequently included. Protocols for older adults may vary
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somewhat from those used for younger patients. All approaches, however, aim to correct the
common misperceptions regarding normal aging and sleep by providing information about
how much sleep is necessary to maintain health, and the physical and psychologic
consequences of sleep loss. Motivational strategies to increase compliance are also
emphasized.36 A number of studies have demonstrated the efficacy of multicomponent CBT
among older adults.71-73
Exercise and complementary and alternative treatment modalities
Some studies report that walking, Tai Chi, acupressure, and weight training improve sleep for
some individuals.74-77 However, how these approaches affect sleep is not well understood and
is likely to be complex.65 Also, difficulties inherent in these studies preclude their
recommendation as evidence-based. Nevertheless, there are many good reasons to encourage
regular physical activity in older individuals, given its positive effect on functional and
cognitive status.
Pharmacologic treatment
Ten drugs have been approved by the FDA for the treatment of insomnia, including
benzodiazepines, nonbenzodiazepines and a melatonin receptor agonist (Table 2). The
selection of any given drug should depend on matching the characteristics of the particular
drug with the patient's complaint. All should be started at the lowest available dose.
The benzodiazepines are psychoactive drugs with varying hypnotic, sedative, anxiolytic,
anticonvulsant, muscle relaxant and amnestic properties. Nonbenzodiazepines, also called
benzodiazepine receptor agonists, are comparatively new drugs whose actions are similar to
those of the benzodiazepines, although they are structurally unrelated. The one approved
melatonin receptor agonist, also comparatively new, has a different mechanism of action.
Melatonin receptors, acted upon by endogenous melatonin, are thought to be involved in the
maintenance of the circadian rhythm underlying the normal sleep-wake cycle.
The NIH State-of-Science Conference on Insomnia concluded that the benzodiazepine receptor
agonists are efficacious in the short-term management of insomnia and that the frequency and
severity of any adverse effects are lower than those found in the older benzodiazepines.36 The
NIH document was published prior to the availability of the melatonin agonist. However, while
the nonbenzodiazepines may have less of a tendency for dependence and abuse, adverse effects
can still become a problem with the newer drugs. To date, no significant effects indicative of
potential for abuse or motor and cognitive impairment have been demonstrated for the
melatonin receptor agonist.78
A metaanalysis that compared hypnotic use with placebo found that sleep quality improved,
total sleep time increased and number of nocturnal awakenings decreased.79 However, adverse
events were also more common with sedative-hypnotics than with placebo, although most
adverse events were reported to be reversible and not severe. Older people may be at greater
risk for adverse effects because of pharmacokinetic considerations, such as reduced clearance
of certain sedative-hypnotics. There is also some evidence of pharmacodynamic differences
such as increased sensitivity to peak drug effects. Impairment was shown to be dependent on
dose and time since dosing.
Other classes of medications have also been used to treat insomnia in the elderly. The 2005
NIH State-of-the-Science Conference on Insomnia concluded that there is no systematic
evidence for the effectiveness of many medications, including the antihistamines,
antidepressants, antipsychotics or anticonvulsants used off-label for the treatment of insomnia
and warned that the risks of use outweighed the benefits.36 Trazodone, a frequently prescribed
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antidepressant for insomnia in older persons, is very sedating, can cause orthostasis and has
no published evidence of sustained efficacy.11
Combination therapy
Combining both behavioral and pharmacologic therapy may provide for better outcomes than
use of either modality alone. Past studies in adults have shown that combination therapy has
been efficacious, with medications providing short-term onset relief and behavioral therapy
providing longer-term sustained benefit. Only 1 randomized, controlled clinical trial has
evaluated combination therapy in older adults.61 In this study, combination therapy was not
only more efficacious than placebo, it was more efficacious than either pharmacologic or
behavioral therapy alone. The study concluded that, while combination therapy was effective
for the short term management of insomnia in late life, sleep improvements were better
sustained over time with behavioral treatment. While results from the few controlled studies
that have been performed on combination therapy are encouraging, there is still enough of a
paucity of data to caution against overgeneralization.80
Summary
Insomnia in the older adult is most often comorbid with medical and psychiatric illness and
complicated by the polypharmacy conventionally associated with them. Treatment should
include behavioral therapy whenever possible. Successful management of sleep in the older
adult may result in significant improvement in quality of life and daytime functioning.
Future Research
1. Does improving insomnia in the older adult result in improvement in daytime
functioning (including decreased risk of falls, decreased daytime sleepiness,
improvement in memory and concentration, improved quality of life)?
2. Does improving insomnia in the older adult result in improvement in medical
comorbidities (including fewer doctor office visits)?
3. Does improving insomnia in the older adult result in improvement in psychiatric
comorbidities (particularly depression and anxiety)?
4. Will increasing slow wave sleep in the older adult result in improvements in overall
quality of sleep as well as improvement in daytime functioning?
Sleep Apnea
Definition
Sleep apnea is a condition in which people stop breathing while asleep.86 Apneas (complete
cessation of respiration) and hypopneas (partial decrease in respiration) both result in
hypoxemia and changes in autonomic nervous system activity, resulting in increases in
systemic and pulmonary arterial pressure and changes in cerebral blood flow.87,88 The episodes
are generally terminated by an arousal (brief awakening) which results in fragmented sleep.
These arousals are believed to be an important contributor to the symptoms of excessive
daytime sleepiness (EDS) and the neurocognitive impairment seen in sleep apnea.
Two types of sleep apnea are recognized. In obstructive sleep apnea (OSA), the primary
pathophysiologic event is obstruction of the upper airway, manifested by greatly diminished
or absent airflow in the presence of an effort to breathe. Central sleep apnea (CSA) is
characterized by recurrent episodes of apnea during sleep resulting from temporary loss of
ventilatory effort, due to central nervous system or cardiac dysfunction.89,90 This latter type
of apnea is commonly found in patients with congestive heart failure (CHF), particularly in
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those with Cheyne-Stokes respiration. In this guideline we will primarily focus on the much
more common OSA, defined as sleep apnea associated with EDS.
Prevalence
OSA has been described in all age groups. In the adult population OSA (defined as 10 or more
apneas and hypopneas per hour of sleep) occurs in about 15% of men and 5% of women.91 In
older adults, OSA occurs in up to 70% of men and 56% of women.27 The syndrome is much
more common in postmenopausal than premenopausal females, but the prevalence increases
in both genders with aging.92
Assessment
Signs and symptoms—EDS and a history of snoring are by far the most common
presenting symptoms in most patients with OSA. Other symptoms of OSA include observed
apnea, choking or gasping on awakening, morning headache, and nocturia.93 While most
younger OSA patients are obese, the elderly with OSA may not necessarily be obese.94
Risk factors—Risk factors for OSA include age, obesity, and anatomic abnormalities
affecting the upper airway. In the older population, OSA is also more common among Asians
compared to Caucasians.95 OSA has been associated with heart failure, atrial fibrillation and
stroke, conditions that are more common in the older population.96 In women, OSA is often
associated with a history of hypothyroidism.97
Morbidity and mortality
Studies show that older adults with OSA are excessively sleepy and that OSA likely contributes
to decreased quality of life, increased neurocognitive impairment, and greater risk of nocturia
and cardiovascular disease.98 Cardiovascular comorbidities particularly associated with OSA
include arterial hypertension, heart failure and stroke.87 Often, the hypertension is difficult to
control.99
Diabetes mellitus is also more common in this population, and there may be an association
between apnea and insulin resistance. Depression has also been found as a common
comorbidity in women with OSA.97 Although mortality is increased in untreated apnea patients
under age 50, the impact of OSA on mortality in the older population is unclear.100
Management of OSA
OSA is managed via a 4-step approach: a) confirming the diagnosis; b) determining optimal
treatment; c) general management measures; and d) ongoing, chronic follow-up.
a. Confirming the diagnosis
Taking the history: Because OSA is so common in older people, all older patients should be
questioned to determine if OSA symptoms are present.91,101,102 The history should be obtained
from the patient and a bed partner or caregiver, if possible, and should include questions
covering the cardinal symptoms of OSA, specifically EDS, snoring, and observed apnea.
Questions about nocturia and cognitive impairment, as well as any comorbidities should be
included as well. Physicians should consider OSA syndrome in individuals who are overweight
or have a history of heart disease, hypothyroidism, or stroke.
The Epworth Sleepiness Scale (ESS), although not validated for use in older persons, is useful
for documenting daytime drowsiness.103 Nocturia is a surprisingly common finding in OSA
patients. This symptom in males is commonly misinterpreted as being caused by prostatic
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hypertrophy.104 OSA should be suspected in all patients with hypertension, especially with
hypertension that is resistant to treatment.99
Physical examination: The physical should focus on the upper airway, including the nasal
and pharyngeal airways, to rule out anatomic obstruction. The skeletal structure of the face
must be assessed to exclude the possibility of jaw abnormalities (retrognathia or micrognathia)
which may cause OSA in the absence of obesity.105 Dental structures should be examined if
a mandibular advancement device is being considered. Obesity often involves the trunk and
neck, and documentation of neck collar size (>17 inches in men and >16 inches in women)
may be helpful, especially in males.
Differential diagnosis: OSA needs to be distinguished from sleep deprivation,
hypothyroidism, depression and the effects associated with using medications with sedating
effects. These can all elicit the main symptom: EDS. Prescribed medications and over-the-
counter products may also contribute to breathing difficulties during sleep or may produce
daytime sleepiness. Inquiring about alcohol use, and obtaining a detailed list of all medications
and other products, particularly sedative-hypnotics and opiate analgesics, are important.
106-110
Polysomnography (PSG): Patients suspected of having OSA based on historical features and
physical examination will almost always require objective documentation by PSG to confirm
the presence and severity of the apnea.111-114 The Center for Medicare Services (CMS) and
most insurance carriers require PSG for reimbursement of CPAP therapy. Comprehensive PSG
includes the measurement of variables to document sleep breathing disorders (oxygen
saturation in arterial blood, rib cage and abdominal movement, nasal and oral airflow, and
snoring sounds), data regarding sleep and stage of sleep (via electroencephalography,
electrooculography, and electromyography), and electrocardiogram and leg electromyogram
to document the presence of periodic leg movements. The PSG is usually followed by data
obtained during continuous positive airway pressure (CPAP) titration. Although PSG is usually
performed in a laboratory setting, home testing may be covered by CMS in selected patients.
111
Quantification of OSA: The apnea hypopnea index (AHI) is the most widely used metric for
characterizing the severity of the abnormalities of sleep respiration, and is based on the average
number of apneas plus hypopneas per hour of sleep in a single night's study. A value >5 is
considered diagnostic for OSA. CMS covers reimbursement for treatment when AHI is >15,
or if AHI exceeds 5 and comorbidities (such as sleepiness and/or cardiovascular disease) are
present.112,113
b. Determining optimal treatment
Determining treatment: When OSA in the older adult is associated with clinical symptoms,
particularly hypertension, cognitive dysfunction, nocturia, high levels of sleep disordered
breathing or cardiac disease, then it should be treated, regardless of the age of the patient. Most
patients with OSA will probably require referral to or management by sleep specialists,
including those with hypoventilation syndromes (eg, individuals suspected of having obesity-
hypoventilation, impaired ventilation secondary to neuromuscular diseases, or CSA), those
with significant respiratory disease (eg, chronic obstructive pulmonary disease [COPD], severe
asthma, or restrictive diseases), and those with significant cardiac disease such as CHF. Such
patients may require complex treatment.
Treatment: Currently there is no pharmacologic treatment for OSA. Continuous positive
airway pressure (CPAP) is the best approach and first-line of treatment for most patients. CPAP
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works by stenting open the airway, increasing functional residual capacity of the lungs, possibly
increasing pharyngeal dilator activity, and reducing afterload on the heart. Several studies have
confirmed that older adults tolerate nightly CPAP use.111,112
The choice of interface type of headgear (nasal mask, or oronasal mask) for securing the mask
to the head, and necessity for a chinstrap are determined objectively. Response to CPAP is
usually assessed as part of comprehensive PSG either during the latter part of the diagnostic
study night (split night study), or during an additional all night study. The CPAP titration is
performed in a split night study after the patient has been asleep for at least 2 hours and the
OSA diagnosis has been confirmed. This involves fitting the patient with an appropriate mask,
educating him or her about what is to transpire, and then applying increased levels of pressure
until OSA control is attained. Proper fit and education will help compliance and reduce
claustrophobia.
A split night study may not be appropriate if there is insufficient time during the night to make
a diagnosis and also determine optimal pressures. In addition, some patients may require a
more complex device than a standard fixed-pressure CPAP machine. Only after a review of
all diagnostic and therapeutic sleep studies can the optimal treatment approach be determined.
Patients without teeth can sometimes present a challenge for CPAP treatment because of bone
resorption in the upper and lower jaws. This situation presents difficulties for optimal mask
fitting and makes oral appliances unfeasible.
c. General management measures—Although the following general measures have not
been evaluated in rigorous randomized clinical trials, they are based on evidence from case
series and general physiologic findings.
Avoidance of alcohol, sedative-hypnotics and opiates: Alcohol or other agents (eg, opiates,
many anesthetic agents, and the sedative-hypnotics) can depress upper airway tone and may
worsen OSA syndrome.107,108,110 Older patients about to undergo surgery should be screened
for OSA, at least by history, since they might receive opiates during the perioperative period.
Weight loss: A great deal of evidence supports the strong positive correlation between weight
and OSA risk. Weight reduction plays an important role in the management of the obese OSA
patient.113-115 One study of older OSA patients monitored for 18 years found a reduction in
the severity of the apnea with which the weight loss was associated.115
Treatment of CHF: Patients with CHF are at risk of developing Cheyne-Stokes respiration,
a form of CSA. Cheyne-Stokes respiration can result in severe sleep onset and sleep
maintenance insomnia, as well as daytime sleepiness.116, 117 Older patients with CHF and
sleep apnea (particularly CSA) have a 2.7-fold greater risk of reduced survival than patients
with CHF or apnea alone.118
CHF treatment may improve breathing abnormalities in CSA, but results from a recent
randomized clinical trial indicate that CPAP may increase mortality in the first 2 years of
treatment. Therefore, CPAP is not currently recommended as a first-line treatment in CHF.
119 Small short-term clinical trials have suggested the effectiveness of oxygen and adaptive
servoventilation, a ventilatory support mode specifically designed for CHF breathing
abnormalities.120 No long term outcome studies are available.
General surgery in the OSA patient: Older people are more likely than younger people to
have general surgery, and to require general anesthesia. All older patients, especially those
with the risk factors for OSA, must be questioned about the possibility of OSA. If they are at
high risk, an objective assessment should be done. If OSA is confirmed during the preoperative
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assessment, nasal CPAP should be initiated prior to hospital admission, and the equipment
should be brought to the hospital at admission. The postsurgical period harbors significant risk
for such patients because anesthetic agents and opiates can worsen OSA in unprotected
individuals.110
Oral appliances: These devices, which move the lower jaw up and forward, can be effective,
especially in mild to moderate cases.113 Guidelines for their use are identical to those in younger
people. In older individuals, however, special attention must be paid to the examination of the
jaws and teeth since at least 8 healthy teeth in each of the upper and lower jaws are required
to anchor the appliances. At this time, patients without adequate dentition cannot be treated
with such appliances.
d. Ongoing, chronic follow-up—OSA is a chronic illness and as such requires long term
management. The main symptoms relate to neurocognitive function and daytime sleepiness.
The Epworth Sleep Scale (ESS), while not specifically validated in the older population, is the
most commonly utilized assessment instrument for daytime sleepiness. With CPAP treatment,
an improvement in the ESS score of 2 or more points is expected, as well as an overall
improvement in subjective sleepiness assessment. When CPAP is no longer effective or
sleepiness returns, the patient should be reevaluated.
Cognitively-impaired patients may have difficulty mastering the steps involved in putting on
their masks and cleaning their CPAP machines and headgear, although one study of patients
with mild to moderate Alzheimer's disease living at home showed that these patients were
compliant with CPAP treatment.121 Help either from a family member or caregiver is generally
necessary. Compliance can be monitored by some of the newer CPAP systems, but the clinical
utility of monitoring has not been rigorously determined.
Future research
1. What kind of alternatives to CPAP treatment in older people (who may have difficulty
due to lack of dexterity in using CPAP) can be developed?
2. Will the treatment of OSA in the older adult result in improvements in nocturia and
cognition?
3. What are the optimal diagnostic techniques for older people who are in skilled nursing
facilities or long term care?
Restless Legs Syndrome and Periodic Limb Movements of Sleep
Restless legs syndrome (RLS)
Definition—RLS is a sleep disorder characterized by unpleasant leg sensations that disrupt
sleep.90,126,127 The syndrome is classified as either primary or secondary. Primary, or
idiopathic RLS is likely to develop at an earlier age, has no known associated or predisposing
factors, and probably has a genetic basis. First and second degree relatives of patients with
idiopathic RLS have a significantly increased risk of developing RLS compared with relatives
of matched controls.128 Secondary RLS can result from a variety of medical conditions that
have iron deficiency in common. These include iron-deficiency anemia, end-stage renal
disease, and pregnancy.129
Prevalence—The prevalence of RLS symptoms is about 10% in most population-based
surveys.130-132 While the rate of RLS may be lower in Asian compared to European
populations, the prevalence is similar in African-Americans and Caucasians.133,134 Because
the diagnosis of RLS is based on symptom report, prevalence rates for frequency and severity
vary with different criteria. For example, in the Restless Legs Syndrome Prevalence and Impact
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(REST) study, RLS symptoms were reported by 7.2% of the survey population, but symptoms
occurring at least twice per week were noted by only 5%, and were moderately or severely
distressing in only 2.7%.132
The prevalence of RLS symptoms clearly increases with age for both men and women, at least
until the seventh or eighth decade. Higher rates of symptoms are consistently reported in
women compared to men.130-132 Some of the age-related increased risk is due to the fact that
although RLS can develop at any age, it rarely remits. Increasing prevalence of RLS with age
may also occur in association with the increasing presence of secondary causes in the aging
population, such as iron deficiency and renal failure.
Typical signs and symptoms—RLS sensations are usually described as a compelling urge
to move the lower extremities, but they may also be reported as a creepy-crawly, burning,
itching or even painful feeling. The resultant sleep disruption may lead to insomnia and daytime
sleepiness. Although symptoms most commonly involve the lower extremities, they have also
been described in the upper extremities and even the trunk. RLS has a circadian pattern, with
the intensity of the symptoms becoming worse at night and improving toward the morning.
Symptoms also tend to worsen when the individual is at rest. They improve with movement
such as walking, rubbing, or stretching. The diagnosis is made by history without the need for
polysomnography (PSG) in the majority of cases.90,127
Risk factors—A clear familial risk exists for the development of both RLS and periodic limb
movements of sleep (PLMS) (described in more detail below). In an Icelandic cohort of patients
with RLS and PLMS, a significant association was found with a common variant on
chromosome 6p21.2. The Icelandic investigators reported an association between the variant
and PLMS without RLS and no association for RLS without PLMS, suggesting that the variant
was a genetic determinant of PLMS.135
A variety of medications, including tricyclic antidepressants, SSRIs, lithium, and dopamine
antagonists (antipsychotics) have been reported to exacerbate RLS.131 In addition, several
social or lifestyle factors appear to contribute to RLS symptoms. These include increased body
mass index (BMI) and caffeine intake, sedentary lifestyle, tobacco use, and lower income.
131,136
Pathophysiology—The exact pathophysiology of RLS and PLMS remains unclear, but the
spinal cord, peripheral nerves, and central dopamine and narcotic receptors may be involved.
136,137 The impairment of dopamine transport in the substantia nigra due to reduced
intracellular iron appears to play a critical role in most patients with this disorder.137
Assessment
1. Is there an urge to move the legs, and is this urge accompanied or caused by
uncomfortable or unpleasant sensations in the legs?
2. Do the unpleasant sensations or the urge to move begin or worsen during periods of
rest or inactivity, such as sitting or lying down?
3. Are the unpleasant sensations or the urge to move partially or totally relieved by
movement, such as walking or stretching, for at least as long as the activity continues?
4. Do the unpleasant sensations or urge to move get worse or only occur in the evening
or night?
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The physical examination is usually unremarkable in primary RLS. Secondary causes such as
peripheral neuropathy or radiculopathy may be elicited during an examination, however.
Therefore a thorough neurologic exam is important.
There are no specific laboratory tests necessary to establish the diagnosis. However because
iron deficiency states are often associated with RLS from secondary causes, obtaining a serum
ferritin is recommended. Values less than 50 ng/mL are consistent with a diagnosis of RLS,
and suggest the need for iron supplementation.
The differential diagnosis for RLS includes peripheral neuropathies, vascular disease
(intermittent claudication), neuroleptic-induced akathesias, arthritides and venous varcosities.
A careful history is usually sufficient to distinguish RLS from each of these.138
Assessing RLS in the cognitively impaired: Cognitively impaired individuals may require a
broader approach when considering the diagnosis. The following are considered essential
criteria to make the diagnosis of RLS in these patients127:
1. Signs of leg discomfort, such as rubbing or kneading the legs and/or groaning while
holding the lower extremities
2. Excessive motor activity in the lower extremities, such as pacing, fidgeting, repetitive
kicking, tossing and turning in bed, slapping the legs on the mattress, cycling
movements of the lower limbs, repetitive foot tapping, rubbing the feet together, and
the inability to remain seated
3. Signs of leg discomfort exclusively present or worse during periods of inactivity
4. Signs of leg discomfort are diminished with activity
5. Criteria 1 and 2 occur only in the evening or at night, or are worse at those times than
during the day
Treatment
Pharmacologic approaches: The primary pharmacologic therapies are dopaminergic agents.
Opioids, benzodiazepines and anticonvulsants are considered second-line agents. If
pharmacologic therapy is required, evidence supports the use of dopaminergic agents as first-
line treatment, especially the newer dopamine receptor agonists such as ropinirole or
pramipexole (both FDA-approved for RLS).139 These agents are associated with less rebound
and symptom augmentation than dopamine precursors such as levodopa-carbidopa. Side
effects include nausea, orthostatic hypotension, sleepiness, headache, and compulsive
behaviors. In the older patient, particular consideration should be given to drug interactions
with other medications and the risk of orthostasis.
The beginning dose of ropinirole is 0.25 mg orally 1 to 3 hours before bedtime. The dose can
be increased after 2 to 3 days to 0.5 mg, and to 1 mg after 7 days. Titration upwards by weekly
0.5 mg increments to a maximum of 4 mg at week 7 if needed.59 Pramipexole 0.125 mg orally
should be administered 2 to 3 hours prior to bedtime. If needed, the dose can be doubled every
4 to 7 days to a maximum of 0.5 mg.140
Augmentation of RLS is characterized by worsening and earlier onset of symptoms in a patient
whose leg discomfort was initially controlled on medication. Typical presentations are
symptom onset earlier in the day, worsened intensity of symptoms, or spread of symptoms to
other parts of the body, such as from the calves to the thighs. The frequency of augmentation
with the newer FDA-approved dopamine agonists is unknown, but it is common in patients
who are treated with levodopa-carbidopa.141 There is no standard approach to the treatment of
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augmentation with the newer dopaminergic agents, but options include taking a dose earlier in
the day, splitting the existing doses into early evening and bedtime doses, or switching to a
different class of medication, such as an anticonvulsant.
Nonpharmacologic approaches: Nonpharmacologic approaches to the management of RLS
include modalities such as education, moderate exercise, smoking cessation, alcohol
avoidance, caffeine reduction or elimination, and discontinuation of offending medications if
appropriate.
Periodic limb movements of sleep (PLMS) and periodic limb movement disorder (PLMD)
Definition—This movement disorder of sleep, also sometimes called nocturnal myoclonus
or periodic leg movements, consists of repeated rhythmical extensions of the big toe and
dorsiflexions of the ankle with occasional flexions of the knee and hip. The movements may
cause brief awakenings or arousals from sleep, of which the individual may or may not be
aware.
Prevalence—As many as 90% of individuals with RLS have PLMS.142 PLMS associated
with arousals are linked to disturbed sleep in older women.143 PLMS are more common with
aging.25
Typical symptoms and signs—PLMS usually occur predominantly during the first part
of the night. Each movement lasts approximately 2 to 4 seconds with a frequency of about 1
every 20-40 seconds.90
Risk factors—PLMS are usually associated with other sleep disorders, including sleep
disordered breathing, but the most notable association occurs with RLS, suggesting a similar
pathophysiology. The rate of PLMS correlates with subjective RLS severity.140,144 PLMS are
also common in patients taking antidepressants.145 While the presence of PLMS supports the
diagnosis of RLS, limb movements are neither necessary nor sufficient to make the diagnosis
of RLS.
Assessment—The revised diagnostic criteria for PLMD (below) note that leg jerks occur
with many medical conditions and in the presence of many medications. These criteria also
“raise the bar” for the “abnormal” number of periodic limb movements in adults, from 5 to 15
as determined by the PLMS Index (the number of periodic limb movements per hour of total
sleep time as determined by PSG).
1. Polysomnography demonstrates repetitive, highly stereotyped, limb movements.
2. The PLMS Index exceeds 15 per hour in most adult cases.
3. There is clinical sleep disturbance or a complaint of daytime fatigue.
4. The PLMS are not better explained by another current sleep disorder, medical or
neurologic disorder, mental disorder, medication use, or a substance use disorder.
Note: If PLMS are present without clinical sleep disturbance, the PLMS can be reported as a
polysomnographic finding, but criteria are not met for a diagnosis of PLMD.
Treatment—There is very little evidence to support pharmacologic treatment to suppress
PLMS or PLMD, even in the face of insomnia or hypersomnia, particularly in older adults. No
agent has been FDA-approved to treat PLMS or PLMD.
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Future research
1. What medications are associated with an increased risk of RLS/PLMS in older
people?
2. Does treatment of RLS affect outcomes such as blood pressure, depression, sleep
measures, and health-related quality of life in older individuals?
3. What is the natural history of RLS in older individuals?
Circadian Rhythm Sleep Disorders (CRSD) in Aging
Definition
The hallmark of CRSD is the presence of relatively normal sleep that occurs at abnormal times.
In the case of advanced sleep phase disorder (ASPD), sleep commences and ends at unusually
early times; in the case of irregular sleep-wake disorder (ISWD), sleep is dispersed across the
24-hour day in bouts of irregular length. The combination of age-related changes in sleep and
circadian rhythm regulation paired with decreased levels of light exposure and activity
contribute to the development of circadian rhythm-based sleep disorders in older people.
Pathophysiology
Optimal sleep quality is achieved when the desired sleep time coincides with the timing of the
endogenous circadian rhythm of sleep and wake propensity. CRSD arises from alterations of
the central circadian clock or a misalignment between endogenous circadian timing and the
external 24-hour social and physical environment. While the primary pathophysiology of
CRSD is a disruption of circadian timing, the actual clinical presentation of CRSD is often
influenced by a combination of physiologic, behavioral, and environmental factors. The
CRSDs which are most prevalent in older people are ASPD and ISWD.
Significant changes in both sleep and circadian regulation occur with aging. Common sleep
complaints among older adults include habitually earlier bedtimes and wake times, inability
to maintain sleep through the night, undesired early morning awakening and frequent daytime
sleepiness.26,147-149 These sleep disturbances may be caused in part by a change in the
circadian timing system of older people and/or in the interaction between the circadian and
homeostatic processes. Habitual wake time, the rise of hormone secretion and endogenous
temperature nadir of older subjects occurs at an earlier clock hour, suggesting that the earlier
wake time may be due to an advance of the circadian clock.150-153 There is also evidence that
the interaction of a reduction in the homeostatic drive for sleep with a reduction in the strength
of the circadian signal promoting sleep may be responsible for the impaired sleep of older
individuals in the early morning.154
Assessment
For a diagnosis of CRSD, an accurate clinical history, sleep diary and/or actigraphy (a small
motion sensor worn continuously, usually on the wrist) covering at least 7 days should be
obtained. Other physiologic markers of the circadian phase such as dim light melatonin onset
and nadir core body temperature are adjunctive tools to confirm the phase or amplitude of
circadian rhythms, but are not widely available clinically. Polysomnography (PSG) is not
routinely indicated. However, because of the age-related increase in the prevalence of other
sleep disorders, a careful assessment for conditions such as sleep apnea, restless legs and REM
sleep behavior disorder should be performed in all patients with CRSD.155 Furthermore,
psychiatric conditions, including depression and anxiety disorders, are frequent comorbidities
with CRSD and must be considered in the evaluation and differential diagnosis.
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Advanced sleep phase disorder (ASPD)
Clinical presentation—The defining characteristic of ASPD (also known as advanced sleep
phase syndrome or ASPS) is sleep-wake times that are earlier than desired or earlier than
conventional. Sleep onset times may be as early as 6:00 pm to 9:00 pm, even if the patient
attempts to delay sleep onset. These are coupled with wake times between 2:00 am to 5:00 am.
Excessive sleepiness during waking hours and sleep maintenance insomnia may occur in
conjunction with abnormal sleep timing. Sleep is otherwise normal when individuals are
permitted to sleep on their own particular sleep-wake schedule.
Diagnostic criteria require verification of the advanced sleep-wake phase through the use of at
least 1 week of actigraphy or sleep log. Other sleep disorders, medical or psychological
conditions (such as depression), medication factors or substance use disorders that may be
causing the symptoms need to be ruled out.155 As expected, an earlier onset of increased
melatonin levels and core body temperature minimum are seen and these can confirm the
diagnosis, but are not required in the routine assessment.156 Not all individuals with an
advanced sleep phase have ASPD, however. In fact, many older people are not particularly
bothered by their sleep phase and have no consequent functional impairment. Such individuals
can be considered “morning types” or “larks” rather than ASPD patients.
Prevalence—In middle- to older-aged adults, the prevalence of ASPD is estimated at 1%-7%.
157,158 ASPD is much less common in the general adult population, with only a few reported
cases of non-age-related ASPD.159-161
Pathophysiology—The pathogenesis of ASPD is thought to involve a combination of
behavioral and genetic factors. For example, early sleep times and ophthalmologic conditions
such as cataracts may decrease light exposure at a time that would delay the sleep phase (ie,
evening hours), thereby perpetuating the advanced sleep phase. Intrinsic factors, such as a
shortened endogenous circadian period (less than 24 hours) or alterations in the relationship
of circadian timing and sleep homeostatic regulation may play a role in the development of
ASPD.159,162 Furthermore, familial forms of ASPD have been reported in which the phenotype
segregates in an autosomal dominant inheritance pattern159,161,163 and mutations in the
circadian clock hPer2 and CK1 delta genes have been identified.164,165 Thus, decreased
exposure or weakened responses to entrainment agents such as light and physical activity,
together with intrinsic changes in circadian and sleep regulation and genetic predisposition
may all contribute to the development of ASPD in older individuals.166,167
Treatment—A combination of good sleep hygiene practices and methods to delay the timing
of sleep and wake times is often recommended for the treatment of ASPD. Chronotherapy has
been used successfully in ASPD. In this approach, sleep times are advanced every 2 days until
the desired sleep-wake time has been achieved. However, the need for rigorous compliance,
the length of the treatment, and the necessity for close follow-up limit its overall clinical
practicality. Therefore, use of evening light within the phase delay portion of the light phase
response curve (PRC) is one approach used to treat. In addition to light and good sleep hygiene,
other behavioral adjustments are also central to the effective treatment of the disorder.
Light: Successful phase delay with the use of evening light therapy has been reported in several
studies. Light therapy in these patients may additionally improve sleep efficiency and total
sleep time. 168,169 Bright light therapy used in the delay portion of the light PRC (that is, in
the evening between 7:00-9:00 pm) can help normalize or delay circadian rhythms in patients
with ASPD. Bright light therapy generally consists of broad spectrum light of 2500-10,000 lux
for 1-2 hrs duration. Unfortunately, light at lower intensities may not delay sleep phase
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effectively. In addition, older subjects appear to have reduced response to the generally superior
phase-shifting properties of short wavelength (blue) light compared to their younger
counterparts, raising the question of the usefulness of this spectrum of light in the treatment of
older subjects with ASPD.170, 171
Older adults may have difficulty tolerating bright light, however, and both compliance with
and efficacy of light therapy may decline over time. Close follow-up is advised. The clinician
should use the timing, intensity and duration of light exposure (7-9PM) as a general guideline
to initiate therapy. If the initial therapy fails, a referral to a specialist to adjust the timing or
duration of light therapy is recommended.
Side effects: Ultraviolet rays are filtered by light boxes. Therefore, they are considered to be
safe. However, side effects have been reported, including hypomania, mild headache, nausea
and vomiting, and self-limited visual problems.172 Patients with ophthalmologic disease should
be evaluated by a specialist before beginning light therapy, in order to determine if this
approach is appropriate. Additional caution is advised in subjects with preexisting mania,
retinal photosensitivity, and migraine.
Dosing and duration of treatment: Although the exact length of treatment and dosing levels
have yet to be clearly established, light therapy represents a potentially important instrument
in the manipulation of circadian phase. The American Academy of Sleep Medicine has
confirmed the potential usefulness of light therapy for CRSDs such as ASPD.173
Melatonin: Theoretically, melatonin delivered in the morning should result in a delay in sleep
phase based on the melatonin PRC.152 However, data supporting the efficacy of melatonin in
ASPD is lacking. Additionally, melatonin may produce soporific effects which may result in
residual morning sleepiness.
Irregular sleep-wake disorder (ISWD)
Clinical presentation—ISWD, also known as irregular sleep-wake rhythm (ISWR), is
characterized by the lack of a clearly identifiable circadian pattern of consolidated sleep and
wake times. Although the total amount of sleep obtained over a 24-hour period is within the
normal range, the time asleep is broken into at least 3 different periods of variable length.
Erratic napping typically takes place during the day, whereas nighttime sleep is severely
fragmented and shortened. Symptoms of chronic insomnia and/or daytime sleepiness may
appear as a consequence. To confirm the diagnosis, the exclusion of other disorders which may
better explain the patient's irregular sleep as well as at least 1 week of actigraphy or the use of
a sleep log demonstrating 3 or more sleep bouts within the 24-hour day is required.155
Prevalence—ISWD is most commonly encountered in patients with dementia, particularly
in those who are institutionalized. However, other disorders of the central nervous system (such
as traumatic brain injury and mental retardation) can lead to an irregular sleep-wake pattern.
153,174,175
Pathophysiology—The development and maintenance of an irregular sleep-wake rhythm
likely result from dysfunctional central processes responsible for circadian rhythm generation
as well as decreased exposure to external synchronizing agents such as light and social
activities.176 The pathogenesis of the disease may be related to a loss of neurons or other
deleterious changes within the suprachiasmatic nucleus (SCN).177 A few studies have
demonstrated a decrease in the number of neurons within the SCN in patients with Alzheimer's
disease.178,179 Also, residents of long term care facilities often lack exposure to adequate light
and do not participate in regular daytime activities. This may contribute further to a decrease
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in the amplitude of circadian rhythms. In fact, lower daytime light levels are associated with
an increase in nighttime awakenings, even after controlling for the degree of dementia.180
Treatment—The primary goal of treatment of ISWD is to consolidate the sleep-wake cycle.
To this end, measures aimed at restoring or enhancing exposure to the various zeitgebers
(“time-givers,” environmental cues that provide an estimate of time of day), are critical.
Patients should be exposed to bright light during the day, while avoiding it in the evening181,
182 Daytime physical and social activities should be strongly encouraged.177,183-185 A
multicomponent approach using a variety of behavioral treatment options is recommended.
Light: The overall approach to light therapy for the treatment of the irregular sleep-wake type
is to increase both the duration and intensity of light exposure throughout the daytime and
avoid exposure to bright light in the evening. Bright light exposure delivered for 2 hours in the
morning at 3,000 to 5,000 lux (a unit of light or illumination) over the course of 4 weeks has
been found to decrease daytime napping and increase nighttime sleep in demented subjects.
186 Light may further help consolidate nighttime sleep, decrease agitated behavior, and increase
the amplitude of circadian rhythms.181,182,186
Melatonin: Studies evaluating the use of melatonin in ISWD have yielded inconsistent results.
One trial involving patients with Alzheimer's disease found no statistically significant
differences in actigraphy-derived sleep measures between control subjects and individuals
taking 2.5 mg melatonin, although a trend towards improvement was seen with a 10 mg dose.
187 A review of current evidence has found inconclusive evidence for the efficacy of melatonin
treatment in circadian and sleep disorders.188,189 Melatonin may, however, be effective in
patients with known melatonin deficiency.190
Other therapeutic approaches: Structured physical and social activity may help provide the
temporal cues needed to increase the regularity of the sleep-wake schedule. A reduction in
nighttime light and noise and improvement in incontinence care can encourage a favorable
sleep environment that will minimize awakenings in nursing home residents.191 Furthermore,
elderly subjects with disrupted sleep-wake patterns consistent with ISWD slept less during the
day and increased participation in social and physical activities and social conversation when
they followed a routine of reduced time in bed during the day, structured bedtime routine at
night, 30 minutes or more of sunlight exposure a day and increased physical activity.192 A
multidimensional, nonpharmacologic approach that includes increased sunlight exposure and
social activity during the day, decreased time in bed during the day, and decreased nighttime
noise may be particularly effective.
Recommendations—Recommendations for evaluation of CRSD: see Table 6
Recommendations for management of ASPD see Table 7
Recommendations for the management of ISWD: see Table 8
Future research
1. Research is needed to define the timing, duration and optimal light wavelength of
bright light therapy for older adults with advanced sleep phase disorder.
2. Multicenter placebo-controlled randomized studies are necessary to determine the
efficacy, safety, and tolerability of long term therapy with bright light in older adults.
3. Placebo-controlled randomized clinical trials of the efficacy and safety of melatonin
receptor agonists are required in the treatment of ISWD in patients with dementia.
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4. Basic research to understand the pathophysiology of circadian rhythm sleep disorders,
including the role of genetics is also a priority.
Parasomnia: Rem Sleep Behavior Disorder
Definitions—Parasomnias are undesirable non-deliberate physical or emotional events that
occur during sleep. They most often appear during entry into sleep or during arousals and may
arise from specific sleep states, such as NREM or REM states. Parasomnias may include
abnormal movements, behaviors, emotions, perceptions, dream enactment and autonomic
activity that occur during sleep or are associated with arousal from sleep. Manifestations of
parasomnias include enuresis, sleepwalking, night terrors, dream anxiety attacks, nocturnal
complex seizures, and REM behavior disorder. The non-REM sleep parasomnias are more
common in children, whereas REM sleep behavior disorder (RBD) is more common in older
adults.
REM sleep behavior disorder
Signs and symptoms—REM sleep behavior disorder is one of the most dramatic and
potentially injurious of the parasomnias. Patients report complex, often violent motor behaviors
associated with dream enactment. However, approximately 10% of patients do not have dream
recall.197 The potential for self- and bed-partner injury is high, especially during severe
episodes. The majority of cases occur with advancing age, typically manifesting in the sixth
or seventh decade.197
Pathophysiology—RBD is based on an underlying pathophysiology in which there is a lack
of the normal atonia associated with REM sleep due to a dysfunction of motor neuron
inhibition. The dream enactment is associated with loss of muscle atonia during REM sleep.
Polysomnography (PSG) demonstrates intermittent loss of REM sleep-associated muscle
atonia, with the patient manifesting complex, often violent motor activity associated with
dream mentation.198
Assessment—Diagnosis of RBD is made by the history and PSG evidence of increased
electromyographic activity during REM sleep (lack of atonia). The sleep study may also capture
the actual episodes of limb jerking and other complex, vigorous and violent behaviors. If there
is evidence of abnormal neurologic activity, a full neurologic workup, including a brain MRI,
may be needed.198-200
RBD has been seen in association with various brainstem abnormalities, extrapyramidal
neurologic disorders, and medical conditions (eg, Parkinson's disease, progressive
supranuclear palsy, Shy–Drager syndrome, multiple systems atrophy, brainstem stroke,
brainstem tumor, demyelinating disease, and medication toxicity or withdrawal). It may also
be idiopathic. The differential diagnosis of RBD includes non-REM parasomnia, sleep apnea,
periodic movements of sleep, nocturnal seizures, and nocturnal rhythmic movements.
Medications such as tricyclic antidepressants (TCAs), monoamine oxidase inhibitors
(MAOIs), and selective serotonin reuptake inhibitors (SSRIs) have been shown to induce or
exacerbate RBD and RBD has also been described during alcohol and barbiturate withdrawal
and with caffeine use.199-204
Treatment—Management of RBD involves pharmacologic treatment and interventions that
address environmental safety. The most effective drug therapy is clonazepam at a dosage of
0.5-1 mg at bedtime. Clonazepam may be taken earlier (1 to 2 hours before bedtime) by patients
who report sleep onset insomnia or morning drowsiness as a result of the medication.
Clonazepam is effective in 90% of cases. There is little evidence of abuse, and only infrequent
reports of tolerance in older patients. Beneficial effects are observed within the first week of
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clonazepam treatment, resulting in control of vigorous, violent sleep behaviors. However, mild
to moderate limb movement, sleep-talking, and other complex behaviors may persist.
Discontinuation of treatment usually results in recurrence of symptoms.198
Other medications that may be efficacious are levodopa, dopamine agonists and melatonin.
Although there are studies reporting the efficacy of melatonin, it is a nutritional supplement
that is not approved by the FDA, and in terms of pharmacologic preparation, is poorly regulated.
205-207 It should probably not be used in older patients.
Environmental safety is an important issue in RBD management. Patients should be advised
to remove potentially dangerous objects from the house, to pad hard and sharp surfaces around
the bed, to cover windows with heavy draperies, and even to place the mattress on the floor to
avoid falling out of bed, if necessary. The combination of drug therapy and implementation of
safety precautions offers safe and effective management of RBD.
Future research
1. Multicenter trials are needed of the safety and efficacy of pharmacologic therapies in
older adults with parasomnias, such as RBD. Trials should be conducted for
clonazepam, melatonin and dopamine agonists.
2. Research is necessary to elucidate the relationship between RBD and Parkinson's
disease.
Hypersomnias
Definition
The hypersomnias of central origin are a group of disorders characterized by a primary
complaint of excessive sleepiness that is not caused by disturbed nocturnal sleep or misaligned
rhythms. Excessive sleepiness is the inability to maintain wakefulness and alertness during the
major waking episode of the day. This may result in unintentional episodes of falling asleep
at inappropriate times or places, or in planned naps related to irresistible sleepiness. Patients
occasionally use the word “sleepy” to describe times when they are “fatigued” or “tired.”
However, the term “excessive sleepiness” is better reserved for cases characterized by an
increased sleep propensity and falling asleep at inappropriate times.
Disorders that cause disturbed nocturnal sleep with subsequent sleepiness during the waking
period may coexist with a hypersomnia. The nocturnal sleep disorder must be controlled prior
to assigning a diagnosis of hypersomnia. One example would be the patient with hypersomnia
and obstructive sleep apnea; the sleep apnea must be adequately treated before considering an
independent diagnosis of a hypersomnia.
A number of disorders are included under the category of hypersomnias. The more common
ones seen in older adults include narcolepsy with cataplexy, narcolepsy without cataplexy,
narcolepsy due to a medical condition (secondary narcolepsy), idiopathic hypersomnia with
long sleep time (sleep time longer than 10 hours), idiopathic hypersomnia without long sleep
time (total sleep time of 6-10 hours), hypersomnia due to a medical condition and hypersomnia
due to a drug or substance.
Prevalence
The prevalence and demographic characteristics for a number of the disorders in this category
are unknown. Narcolepsy with cataplexy has an overall prevalence of 0.05% with a slight
preponderance in males.90,209,210 Although all ages can be affected, the prevalence of
narcolepsy with cataplexy and the other hypersomnias specifically in older adults is unknown
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although the medical conditions, comorbidities and medication usage typically associated with
hypersomnia are very prevalent in this population.
Signs and symptoms
All the disorders in this category have several signs and symptoms in common. Each presents
with excessive sleepiness during waking hours. Other symptoms are more specific to individual
disorders.
Idiopathic hypersomnia
Idiopathic hypersomnia with long and short sleep times are defined by a 3 month history of
excessive daytime sleepiness with a sleep time longer than 10 hours or a total sleep time
between 6-10 hours, respectively.90,211-214 The daytime sleepiness may be shorter than 3
months in the case of hypersomnia due to a drug or substance.90 Some patients may experience
symptoms associated with excessive sleepiness such as memory lapses, concentration
problems, automatic behavior (an episode that occurs during a period of sleepiness and that is
not remembered subsequently by the individual), ptosis, and hallucinations.215-222
Narcolepsy (with or without cataplexy)
To establish a diagnosis of narcolepsy with cataplexy, excessive daytime sleepiness and a
definite history of cataplexy is required.90 Cataplexy is an episode of muscle weakness usually
manifesting as weakness in the legs or arms, buckling at the knees, and/or dropping items from
the hands in association with emotion (eg, laughter or anger). This symptom is absent in
narcolepsy without cataplexy.90 Other features of narcolepsy include automatic behaviors,
hypnagogic hallucinations, sleep paralysis, and disturbed nocturnal sleep. A hypnagogic
hallucination is a hallucination, most often visual, that occurs at sleep onset, and sleep paralysis
is an episode of immobility that occurs at sleep onset or upon awakening.
Hypersomnia associated with comorbidities
Patients with hypersomnia due to a medical condition have a complaint of excessive sleep
present almost daily for at least 3 months that is secondary to a significant medical or neurologic
condition90,223-225 Medical conditions include Parkinson's disease, post-traumatic brain
injury, Niemann-Pick disease type C, myotonic dystrophy, Prader-Willi syndrome,
Alzheimer's disease, stroke, multiple sclerosis, hypothyroidism, and hepatic encephalopathy.
223,226-234
Patients with hypersomnia due to a drug or substance have a complaint of sleepiness or
excessive sleep that is believed to be secondary to current use, recent discontinuation, or prior
prolonged use of drugs or prescribed medications.90,235 Because older individuals often
regularly take multiple medications, careful evaluation of an individual's drug regimen is an
essential part of the assessment of hypersomnia in an older adult.
Risk factors
Many hypersomnias have both genetic and non-genetic risk factors, but usually they are not
proven or definitively identified. For example, suggested precipitating factors for narcolepsy
with or without cataplexy have included head trauma, sustained sleep deprivation, or non-
specific viral illness.236
Morbidity and mortality
The morbidity and mortality associated with the hypersomnias of central origin are primarily
related to excessive daytime sleepiness (EDS). Cognitive impairment is a common feature
characterized by fatigue, tiredness, impaired memory, concentration, and coordination
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difficulties.237-240 Depression, problems at work (eg, loss of employment due to sleep-related
errors), or with social life (eg, withdrawal from family and social activities because of
sleepiness) are also common. Weight gain has also been linked to excessive sleep.241 There is
also an increased risk for traffic accidents or work-related injury due to sleepiness and
inattentiveness.242 Untreated narcolepsy with cataplexy can also be socially disabling, as the
cataplexy attacks can lead to social withdrawal in addition to the increased risk of accidents.
242,243
Assessment
Specific studies are lacking regarding the assessment or treatment of older patients with
hypersomnias of central origin. Therefore, the data collection tools used to assess patients are
not specifically validated for the older adult population. However, some extrapolations from
existing studies can be made.
Key issues and questions to be addressed in obtaining a history
1. If possible, obtain the history from the bed partner as well as the patient.
2. Questions should address excessive daytime sleepiness, cataplexy, symptom response
to napping (if any), presence of dreaming during naps, hypnagogic hallucinations,
sleep paralysis, and automatic behaviors.
3. Establish onset, frequency, and duration of the sleepiness as well as any episodes of
remission.
4. Include questions about the patient's medical, neurologic and psychiatric illnesses as
well as use or recent discontinuation of recreational drugs, prescription drugs, and/or
alcohol.
5. Questions about other comorbid sleep disorders such as obstructive sleep apnea
(OSA) or restless leg syndrome (RLS) are also relevant.208,224,235,244-246 A number
of subjective sleep questionnaires are available to assess sleep habits, sleep-wake
schedules, and sleepiness (eg, the Epworth Sleepiness Scale [ESS] and Karolinska
Sleep Scales [KSS]; sleep diaries are also useful assessment tools). The most
commonly used questionnaire is the ESS. Such questionnaires should be part of the
patient's evaluation.232,247
6. What is the duration of nighttime sleep?
Key areas to include in the physical exam
For patients suspected of having a hypersomnia of central origin, a thorough physical
examination, including a neurologic evaluation, is important. An assessment of cognition is
valuable and can be used to help make a diagnosis as well as to monitor treatment response.
Appropriate laboratory tests
For diagnosis, patients suspected of having hypersomnias of central origin usually require an
overnight polysomnography (PSG) followed by a multiple sleep latency test (MSLT).248-250
The MSLT is an electrophysiologic test of sleep tendency that involves 4 or 5 daytime naps at
2 hourly intervals with assessment of the latency to sleep onset and the type of sleep that occurs.
A mean sleep latency of 8 minutes or less and the presence of REM sleep on 2 or more naps
are indicative of narcolepsy. The MSLT is also required to support a diagnosis of one of the
other hypersomnias of central origin. Common medications used to treat chronic conditions in
older adults may complicate the interpretation of these studies, however.
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An MRI of the brain is useful to identify causes of hypersomnia or narcolepsy due to a
neurologic disease (eg, tumors, multiple sclerosis, intracranial bleeds, or strokes). Additionally,
blood work can help identify suspected medical conditions that may cause the patient's
excessive sleepiness (eg, thyroid stimulating hormone, liver function tests, complete blood
count, serum chemistry). Cerebrospinal fluid hypocretin levels can confirm a diagnosis of
narcolepsy with cataplexy in the absence of a MSLT.
Treatment options
Initial management of hypersomnias of central origin requires treatment optimization of any
underlying medical, neurologic or psychiatric disorder. Furthermore, careful withdrawal of
sedating medications or substances, if possible, is prudent. Ensuring an adequate opportunity
for nighttime sleep is important to exclude sleep deprivation as a cause of excessive sleepiness.
Excessive sleepiness is treated with one or more of the following: behavioral modification,
modafinil, or other stimulants.251-256 Cataplexy is controlled with behavioral modification,
antidepressants, or sodium oxybate.257
Behavioral
Some degree of behavioral modification is beneficial to most patients with excessive
sleepiness. Good sleep hygiene techniques should be adopted, and a regular sleep-wake
schedule allowing adequate time for nocturnal sleep should be maintained. Heavy meals
throughout the day and alcohol use should be avoided. Two short 15-20 minute naps, 1
scheduled around noon and the other around 4:00-5:00 pm, may alleviate some sleepiness.
The older patient who is still employed may benefit from occupation counseling. These
individuals should avoid shiftwork, on-call schedules, jobs that involve driving, or any other
job that demands continuous attention for long hours without breaks, especially under
monotonous conditions. Healthcare workers should assist the patient with occupational and
social accommodation for disabilities due to excessive sleepiness. Referral for support services
and to support groups such as the Narcolepsy Institute or the National Sleep Foundation is very
helpful to many patients.210,229,248,258
Pharmacologic
Traditionally, the stimulant medications (amphetamines, methamphetamines, D-
amphetamines and methylphenidate) are used to treat excessive daytime sleepiness.259
Recently, modafinil has gained favor for first-line use in the treatment of narcolepsy.259
Modafinil has also been increasingly used for the treatment of idiopathic hypersomnia as well
as hypersomnias due to a medical or neurologic condition. For elderly patients, a starting dose
of modafinil at 100 mg, once upon awakening in the morning, is recommended. This dose can
be increased at weekly intervals as necessary. Typical doses range from 200 to 400 mg per
day. The most common adverse reactions are nausea, headaches and nervousness.
Other medications used to treat excessive daytime sleepiness in patients with narcolepsy
include sodium oxybate, selegiline, and ritanserin253,257,260-263 Judicious use of caffeine may
also be beneficial. In patients with drug- or medication-induced sedation, the treatment is to
reduce or remove the drug or substance. This therapy should preferably be instituted under the
guidance of both a sleep specialist, who is familiar with these drugs, and the patient's primary
care physician, who knows the patient's medical problems and the medications he or she is
taking.
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Treatment of cataplexy and REM sleep intrusion into wakefulness
Sodium oxybate improves daytime sleepiness as well as cataplexy.260,261 In addition, sodium
oxybate may be used to treat the other symptoms of narcolepsy, including disrupted nocturnal
sleep, hypnagogic hallucinations, and sleep paralysis. Sodium oxybate is a liquid that is given
in 2 divided doses at night. The first dose is given at bedtime and the second 2.5- to 4 hours
later. Sodium oxybate can cause headaches, nausea, unexpected neuropsychiatric effects and
fluid retention. Selegiline, a MAOI rarely used in narcolepsy because of the potential for side
effects, not only improves daytime sleepiness, but can also treat cataplexy. Other REM sleep
suppressant medications, such as TCAs, SSRIs, venlafaxine and reboxetine, have all been used
to treat cataplexy, hypnagogic hallucinations, and sleep paralysis, although adequate scientific
evidence is lacking.
Follow-up
Most of the hypersomnias of central origin are long term or lifelong disorders and require
ongoing management.
Monitoring medications
As in most clinical scenarios, more frequent follow-up is usually necessary when starting a
medication or adjusting doses. For example, starting or adjusting the dose of a stimulant
requires monitoring for adverse effects, including hypertension, palpitations or arrhythmias,
irritability, or behavioral manifestations such as psychosis. Patients should be questioned about
excessive stimulatory effects or nocturnal sleep disturbances.
Monitoring symptoms
As medications such as modafinil generally only improve sleepiness and do not eliminate it,
frequent reassessment of impairments in functional ability due to residual sleepiness is
necessary. The ESS is a useful tool for monitoring subjective sleepiness and its response to
therapy at each patient visit. Once symptoms are stable, any future exacerbation of symptoms
(sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations or behavioral abnormalities)
needs to be evaluated formally by history, physical examination and/or repeat PSG. Healthcare
workers should continue to assist the patient with occupational and social accommodation for
disabilities due to excessive sleepiness.
Referral
Primary care physicians should refer a patient to a sleep specialist when narcolepsy or
idiopathic hypersomnia is suspected or the cause of the sleepiness is unknown. In addition,
complex patients who are unresponsive to initial or subsequent therapy may benefit from a
sleep specialist consultation.
Future research
1. The basic pathophysiologic mechanism(s) of excessive sleepiness due to idiopathic
hypersomnia, narcolepsy, and Alzheimer's disease needs to be further investigated.
2. There is a need for standardization and validation of MSLT studies in older adults.
3. The efficacy of treatment modalities, especially pharmacotherapy (eg, modafinil, lithium,
sodium oxybate) in older adults for hypersomnia of central origin requires further study.
4. There is a need for better understanding the comorbidities that may be associated with
hypersomnias of central origin in older adults (eg, cognitive deficits and obesity).
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5. There is a need for better understanding of how increasing age and comorbidities may modify
the symptoms and response to treatment in older adults.
Sleep Problems in Long Term Care Facilities
Background
Sleep disturbances are common among older people living in nursing homes, with many factors
specific to this setting and population contributing to sleep difficulties. Medical conditions
common to nursing home residents complicate these environmental factors. Frequently,
residents experience pain, paresthesias, nighttime cough and dyspnea, gastroesophageal reflux
and nocturia, all of which can interfere with sleep. Neurologic illnesses are also common in
this population, particularly neurodegenerative disorders such as dementia and Parkinson's
disease, which are also associated with sleep disturbance. Medications prescribed for nursing
home residents may also interfere with sleep, including diuretics, stimulating agents (eg,
sympathomimetics, bronchodilators, and stimulating antidepressants), anti-Parkinsonian
agents, antihypertensives, and cholinesterase inhibitors taken near bedtime, or sedating
medications (eg, antihistamines, anticholinergics, and sedating antidepressants) taken during
the day. The latter group may contribute to daytime drowsiness and further disrupt the sleep-
wake cycle.
Environmental factors may also play a role in sleep-wake problems in the nursing home. Many
residents have limited interaction with the community outside of the nursing home due to
physical and/or cognitive impairment. Most residents have very little, if any, bright light
exposure, which impedes the coordination of the internal circadian clock to the external
environment. Nursing home residents also spend extended periods in bed and are often
physically inactive during the day, factors that contribute to sleep-wake and circadian rhythm
abnormalities. Additionally, nighttime noise and light interruptions are also disruptive, and are
often caused by staff providing personal care to either the resident or a roommate.
Assessment
A variety of measures have been utilized to assess sleep in nursing home residents. Most studies
use wrist actigraphy for objective sleep measurement. Polysomnography (PSG) and portable
sleep recording is used less frequently. Subjective sleep measures generally involve
observations by research staff, resident questionnaires, nursing staff interviews or
questionnaires, or medical record review.
Prevalence
Probably because of the different methodologies used for measurement, prevalence data
regarding sleep problems in nursing homes vary. The lowest estimate, 6.3% of residents, was
estimated using Minimum Data Set (MDS) documentation from 34,000 nursing home residents
in the state of Michigan.43 However, given concerns about the accuracy of the MDS data for
insomnia, this is likely to be a significant underestimation.270
Residents have been reported to have significant sleep problems, including long sleep onset
latency (ie, time to fall asleep at night), long wake time after sleep onset (ie, amount of time
awake after initially falling asleep), low sleep efficiency (total sleep time as a percentage of
total time spent in bed), and a very high percentage of daytime napping.271
Structured daytime observations have shown in one study that nearly three-quarters of residents
sleep excessively during the day. Compared to residents without this pattern, those with
excessive daytime sleeping were observed more often in bed, were less likely to have any time
outdoors, had less social and physical activity, and required greater mean level of assistance
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for personal care activities. Excessive daytime sleeping was accompanied by significantly
reduced time asleep at night. Most residents also had evidence of nighttime sleep disturbance,
although this was very rarely documented in their charts.272
Factors associated with sleep disturbances among nursing home residents
Studies using actigraphy in demented nursing home residents suggest an association between
dementia and circadian rhythm disturbance, with more severely demented residents having
more disturbed circadian rest-activity rhythms.180,273 Older people on a rehabilitation ward or
nursing home have also described pain, discomfort and the need to go to the toilet as the most
common causes of sleep disturbance.274
Nocturia, noise and/or light disruption, and pain have been reported by cognitively intact
nursing home residents as the most common causes of subjective sleep disturbance. In addition,
greater comorbidity and more depressive symptoms were both significant independent
predictors of worse Pittsburgh Sleep Quality Index scores.275
Mild-to-moderate sleep apnea has been reported in one study in 32% of residents, with another
38% having evidence of severe sleep apnea. There was a strong relationship between sleep
apnea and dementia in this sample.276 A later study in nursing home residents with dementia
found that over 50% had evidence of severe sleep apnea.277
The evidence for a relationship between sleep and psychotropic medications in nursing home
residents has been mixed. For example, one study found that sleep fragmentation (estimated
by actigraphy) was not associated with sedative-hypnotic use while another found that residents
on psychoactive medications had a dampening of the normal day/night variation in sleep and
waking over 24-hours.278,279 Another study showed that use of psychotropic medications (eg,
antipsychotics, sedative-hypnotics and/or antidepressant medications) was not associated with
measures of daytime or nighttime sleep. However, residents on psychotropic medications did
have less in-bed body movement at night, which may increase risk of skin breakdown.280
Institutional factors contribute to sleep disturbance in the nursing home setting. One study that
used a bedside monitor in residents' rooms to measure noise and light levels found that half of
nighttime awakenings were associated with noise and/or light.281
Many residents also have limited exposure to bright light, which is a key zeitgeber (“time-
giver”) to time intrinsic biological rhythms to the external clock. Studies have shown that
residents do not get much, if any, exposure to bright light, with nearly half of residents having
no bright light exposure at all.170,273 Residents with higher light levels had fewer nighttime
awakenings and a later rest-activity acrophase, a measure of circadian rhythm.170
Sleep disturbances in nursing home residents are associated with significant negative
consequences. Sleep disturbance has been identified as a significant predictor of increased
mortality among nursing home residents.282 Excessive daytime sleeping has also been
associated with worse quality of life (less participation in social and physical activities, less
social conversation) and more functional impairment (more nursing assistance for eating,
drinking, bathing, dressing, grooming, and toileting).271
Although little evidence of a relationship between psychoactive medications and sleep has been
found among nursing home residents, there is clinical concern for a potential relationship
between sedating medications and the risk of falls. One study found that use of benzodiazepines
was associated with increased risk of daytime and nighttime falls.283 Risk of daytime and
nighttime falls was the same regardless of use of benzodiazepines with intermediate or long
half-lives, although use of benzodiazepines with short half-lives were only predictive of falls
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during the night. Another large study suggested that it was insomnia, rather than the use of
hypnotics, that was associated with greater risk of falls although the findings from this study
remain controversial. 43,271
Interventional studies
Studies on sleep in nursing home residents have included interventions involving bright light
therapy, exercise or physical activity, multicomponent nonpharmacologic programs, changes
to nighttime nursing care, social and individualized activities, client-centered nursing care,
medications, and discontinuation of antipsychotic medication.
Beneficial effects of morning bright light therapy have been reported.182,284-286 Demented
nursing home residents receiving bright overhead lighting in the morning or all day long have
been shown to have increased total sleep time at night, with the effect most pronounced in
participants with severe dementia.287 Importantly, the most relevant dimensions of light
therapy may be the timing, duration and intensity of the intervention.
The beneficial effects exercise and physical activity on sleep in nursing home residents has
been demonstrated in a number of studies.280,288,289 Positive sleep effects have also been
reported with use of a stationary bicycle and Tai Chi.290,291 The combination of daily social
and physical activity among residents of a continuing care facility has also been shown to be
associated with increased slow wave sleep (as assessed by PSG) and improvement in memory-
oriented tasks.167
Efforts to improve the nighttime nursing home environment to make it more conducive to sleep
have been difficult to implement. A nursing intervention that decreased nighttime noise and
light disruption was shown to be associated with reduced nighttime arousals.191
Multicomponent nonpharmacologic interventions have also had mixed results. A study which
combined efforts to increase daytime physical activity and sunlight exposure, decrease time in
bed during the day, provide a bedtime routine and decrease nighttime noise and light levels
found a decrease in duration of nighttime awakenings and daytime sleeping, and an increased
participation in social activities, conversation, and physical activity during the day.192 A similar
multicomponent nonpharmacologic intervention found no significant effects on nighttime
sleep, but did show a modest but significant decrease in daytime sleeping.292
Few studies have tested sleep medications specifically in the nursing home setting. A
randomized trial of temazepam, diphenhydramine or placebo in residents with sleep problems
found that those who received diphenhydramine reported a shorter sleep latency than those
given placebo, with some report of a longer duration of sleep compared with temazepam
treatment, but those on medication performed more poorly on tests of neurologic function, and
exhibited more daytime hypersomnolence.293 Another study in patients with Alzheimer's
disease (including some participants in long term care facilities) comparing melatonin with
placebo found no significant differences between groups in objective sleep measures (wrist
actigraphy), and only an isolated finding of improved sleep quality with melatonin based on a
caregiver rating.187
The American Medical Directors Association (AMDA) has developed a clinical practice
guideline which offers a 16-step approach to managing sleep problems among nursing home
residents. They divide their approach into 4 different categories: recognition, assessment,
treatment and follow-up.294
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Recommendations for future research
1. Future research should clarify the consequences of sleep disturbance among nursing
home residents, particularly in terms of effects on quality of life.
2. The effectiveness of pharmacologic interventions to improve sleep among nursing
home residents should be tested, with careful attention to the balance of potential risks
and benefits in this vulnerable population.
3. More effective behavioral and other nonpharmacologic interventions must be
identified that will help to improve disturbed sleep patterns among nursing home
residents.
4. The relationship between insomnia, sedative-hypnotic medications and adverse
events, including falls, among nursing home residents must be clarified.
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Figure 1. Diagnostic algorithm for sleep disorders in older persons
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Table 1
Quality of Evidence
Level I Evidence from at least 1 properly designed randomized, controlled trial
Level II Evidence from at least 1 well-designed clinical trial without randomization, from cohort or case-controlled analytic studies, from multiple time-
series studies, or from dramatic results in uncontrolled experiments
Level III Evidence from respected authorities, based on clinical experience, descriptive studies, or reports of expert committee
Strength of Evidence
A Good evidence to support the use of a recommendation; clinicians should do this all the time
B Moderate evidence to support the use of a recommendation; clinicians should do this most of the time
C Poor evidence to support or reject the use of a recommendation; clinicians may or may not follow the recommendation
D Moderate evidence against the use of a recommendation; clinicians should not do this
E Good evidence against the use of a recommendation; clinicians should not do this
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Table 2
FDA-Approved Hypnotics for Insomnia1
Generic Name Trade Name Indication Geriatric Dose Half life in older persons (hours) Comments
Benzodiazepines2
flurazepam Dalmane®
Short term treatment of insomnia
15 mg 126-158 Should not be used in older adults because of very long half-life
quazepam Doral®7.5 mg 78 Should not be used in older adults because of very long half-life
estazolam ProSom™ 0.5-1 mg 10-24 Due to long half-life, residual CNS effects are likely.
temazepam Restoril®7.5-15 mg 3.5-18.4
triazolam Halcion®0.0625-0.25 mg 1.7-5 Poor choice due to very short half life and high incidence of CNS
adverse reactions
Nonbenzodiazepines3
eszopiclone Lunesta®
No short-term limitation for use; sleep onset and
sleep maintenance insomnia
1-2 mg 9 AEs>10%: headache, unpleasant taste
zolpidem ER Ambien CR®6.25 mg 1.9-7.3 AEs>10%: dizziness, headache, somnolence
zolpidem Ambien®5 mg 2.9-3.7 AEs>10%: dizziness, headache, somnolence
zaleplon Sonata®5 mg 1 AEs: nausea (7%), myalgias (7%)
Melatonin receptor agonist
ramelteon Rozerem™ No short-term limitation for use; sleep onset
insomnia 8 mg 1-2.6
AEs: Headache (7%)
Somnolence (5%)
Dizziness (5%)
Not a Class C-IV scheduled drug
1New interpretive guidelines (F329) from CMS also mandate quarterly review of sedative-hypnotic compounds for residents of long-term care facilities to assess continued need, dose and possible side-
effects including possible decline in functional status or increased incidence of falls.
2All are Class C-IV scheduled drugs, and may also be associated with amnesia and complex sleep-related behaviors such as sleepwalking or sleep-eating.
3The nonbenzodiazepines have a fast onset of action (30-45 minutes).
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Table 3
Insomnia
Recommendations Quality of Evidence (with references) Strength of Evidence
1. The healthcare practitioner should periodically screen patients for symptoms of insomnia
during health examinations. III 81 A
2. An in-depth sleep history is essential in identifying the cause(s) and consequences of
insomnia. Additionally, a physical examination is an important element in the evaluation of
insomnia patients with medical symptoms. III 81 A
3. CBT-I is an effective treatment for insomnia in the older adult. I 36 A
4. Nonbenzodiazepines
And
melatonin receptor agonists are the safest and most efficacious hypnotic drugs currently
available.
II 36, 82
I 83 B
B
5. All FDA approved drugs for the treatment of insomnia can be associated with clinically
significant adverse events. III 79 A
6. Combining CBT-I and pharmacologic therapy can be helpful in some patients. III 61,80 A
7. Antihistamines
And
antidepressants, anticonvulsants, and antipsychotics are associated with more risks than
benefits in the treatment of insomnia, particularly in older persons.
II 36,84
III 36,85 B
B
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Table 4
Sleep Apnea
Recommendations Quality of Evidence (with references) Strength of Evidence
1. OSA is very common in older people. All older people should be screened for the
possibility of OSA by asking whether the 3 key features are present: daytime sleepiness,
snoring, and observed apnea. II 27,91,98,101,102,122,123 A
2. All older patients who are found to be at high risk of OSA should be assessed to document
whether the condition is present. This will consist of either a referral to a sleep specialist, or
by obtaining a PSG. III 116 A
3. Older patients whose sleep apnea is associated with CHF or respiratory disease should be
referred to a sleep specialist. III A
4. CPAP is the most reliable treatment at this time for OSA (but not for CSA). Oral appliances
may be appropriate for some patients with adequate dentition I 111,112,118-120,124 A
5. All older patients prescribed CPAP should receive education on the rationale, methods of
application, expectations, and follow-up. Bed partners should also be educated. This
information improves adherence to treatment. II 112,113,125 B
6. Since obstructive apnea is a chronic disease with associated chronic comorbidities, older
patients should be followed up frequently, especially during the first 6 months following
onset of treatment to assess response to treatment, and to monitor compliance. III 113 A
7. Patients with OSA should take their CPAP equipment with them on trips, and to the
hospital, particularly if they are expecting to undergo a surgical procedure. III 110 A
8. A weight loss program should be part of the treatment plan in overweight patients with
OSA. II 114,115 A
9. The older sedative-hypnotics should not be prescribed for patients with confirmed OSA,
and patients should be advised to avoid drinking alcohol within 2 hours of bedtime. III 107,108,110 A
10. Patients with OSA require follow-up for their comorbidities, particularly patients with
hypertension. Patients treated with CPAP may have a change in their requirements for
antihypertensive medications. III 99 A
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Table 5
Restless Legs Syndrome and Periodic Limb Movement of sleep (RLS/PLMS)
Recommendations Quality of Evidence (with references) Strength of Evidence
1. Patients with sleep onset insomnia should be asked about uncomfortable leg sensations. III 90,127,132 A
2. Patients with RLS should have a serum ferritin level checked. III 137 B
3. Dopaminergic agents are the first-line treatment for RLS. II 139 B
4. Patients who are treated with dopaminergic agents should be warned about the possibility
of augmentation. III 90,132 A
5. Periodic limb movements rarely need to be treated with medication in the absence of RLS
symptoms. III 144,146 B
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Table 6
Circadian Rhythm Sleep Disorders (CRSD)
Recommendations for evaluation of CRSD Quality of Evidence (with references) Strength of Evidence
1. All older people with symptoms of insomnia and excessive daytime sleepiness (EDS)
should be screened for the possibility of a circadian rhythm sleep disorder. III 90 A
2. Diagnosis is made primarily by history. In addition, a sleep diary or actigraphy should be
performed for at least 7 consecutive days to confirm the circadian sleep and wake pattern. III 90 A
3. Circadian phase markers (eg, core body temperature, melatonin) are useful to confirm the
diagnosis, but there is insufficient evidence to recommend their routine use in diagnosis and
they are not available clinically. III 90 C
4. PSG is indicated if other primary sleep disorders are suspected, but is not indicated for
diagnosis. III 90 B
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Table 7
Advanced Sleep Phase Disorder (ASPD)
Recommendations for management of ASPD Quality of Evidence (with references) Strength of Evidence
1. Chronotherapy (sleep-wake scheduling) is achieved by advancing sleep and wake times
until the desired sleep and wake times are achieved. This approach, although possibly useful,
is often clinically impractical. III 160 C
2. Scheduled bright light in the evening delays circadian rhythms and improves sleep in
patients with ASPD. II 168,193 B
3. Melatonin should not be used in older persons with ASPD. III 193 B
4. Overall, there is little scientific evidence to support the efficacy of behavioral
interventions. However, because of the lack of alternative approaches and since the risks and
relative costs are low, behavioral interventions are recommended. III B
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Table 8
Irregular Sleep-Wake Disorder (ISWD)
Recommendations for the management of ISWD Quality of Evidence (with
references) Strength of Evidence
1. For institutionalized ISWD patients in whom dementia is common, increasing exposure to bright
light during the day can improve sleep-wake consolidation and circadian rest/activity rhythm. II 193,194 A
2. Melatonin is not indicated for the treatment of ISWD in older adults with dementia. I 187 B
3. Multimodal approaches that combine bright light exposure during the day, decreasing light exposure
at night, physical activity, social activity
And
structured bedtimes and wake times and noise reduction can decrease nighttime awakenings, total wake
time and daytime sleepiness.
I 182
II 195,196 A
A
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Table 9
Parasomnias
Recommendations Quality of Evidence (with references) Strength of Evidence
1. All older adults with a history of vigorous motor behaviors during sleep should be queried
about prior episodes or the potential for injurious behavior associated with dream mentation. III 90,198-200 A
2. PSG is indicated for the diagnosis of RBD. III 90,198-200 A
3. In a patient with RBD and an abnormal physical examination, further neurologic
evaluation is recommended. III 201-204 B
4. Clonazepam has demonstrated efficacy and is indicated for the treatment of RBD. III 198,208 B
5. Other medications, such as dopamine agonists may be indicated for the treatment of RBD. II 207 B
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Table 10
Hypersomnias
Recommendations Quality of Evidence (with references) Strength of Evidence
1. A complaint of excessive sleepiness should be thoroughly evaluated by means of
a detailed history and the appropriate use of subjective questionnaires. III 16,221-224,230,231,244,245,247,264-267 A
2. An accurate diagnosis should be established in older patients with hypersomnia
by means of a PSG and MSLT. II 210,248-250 B
3. In patients with hypersomnia, management of any medical, neurologic, and
psychiatric disorders should be optimized. III 16,208 A
4. In patients with hypersomnia, medications or substances with sedating properties
should be withdrawn when possible or the timing of the medications should be
changed to minimize sedation during waking hours. III 208,235,246 A
5. Behavioral modification of sleep-wake behavior is an effective treatment strategy
that is useful for many patients with excessive sleepiness and should be advised. II 208,229,246,259 A
6. Scheduled naps can be beneficial to relieve sleepiness with or without the use of
pharmacologic agents. II 259,268 B
7. Pharmacologic management should be considered for all patients who have a
diagnosis of hypersomnia of central origin. III 208,210,269 A
8. There is little evidence that sleepiness due to medications is improved with other
medications that are used to counteract sleepiness. If possible, discontinue the
offending medication or change the timing and/or dose. III A
9. The following medications are effective treatments for narcolepsy with or without
cataplexy: Modafinil: effective for excessive sleepiness due to narcolepsy.
Sodium oxybate: may be effective for EDS due to narcolepsy in the older adult
population
And
may be effective for cataplexy in the older adult.
Methylphenidate and amphetamine derivatives: may be effective for excessive
sleepiness due to narcolepsy in the older adult.
Antidepressant medications: may be an effective treatment for cataplexy.
I 210,251-253,269
I 257,261,269
I 257,260,261,269
II 208
II 208,210,262,263,269
B
C
B
C
B
10. Modafinil, methylphenidate and amphetamine derivatives may be effective for
the treatment of excessive sleepiness due to idiopathic hypersomnia or recurrent
hypersomnia, as well as hypersomnia due to a medical condition. II 208,229,253-256 C
11. Regular follow-up of patients with excessive sleepiness is necessary to monitor
and ensure effective treatment. III 210,230 A
12. Referral to a sleep specialist should be undertaken when narcolepsy or idiopathic
hypersomnia is suspected or if the cause of the sleepiness is unknown III A
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Table 11
Long-term Care (LTC)
Recommendations Quality of Evidence (with references) Strength of Evidence
1. Given the high prevalence of sleep problems among nursing home residents, the clinician
should consider sleep disturbance as a potential issue in every nursing home resident. II 271,272 A
2. Excessive daytime sleeping is common among nursing home residents, and should be
addressed. II 272 B
3. Wrist actigraphy for the identification of sleeping problems in nursing home residents
should be used if possible. Trained staff observations, resident self-report, or nursing staff
report should be used if actigraphy is not available. II 180,271-273,275,295 B
4. Clinicians should have a high index of suspicion for sleep disordered breathing among
nursing home residents, particularly those with dementia. II 275 B
5. Careful review of medical conditions and medications that may be causing or contributing
to sleep disturbance is warranted in every nursing home resident with evidence of a sleep
problem. III A
6. Clinicians should encourage nursing home facilities to address nighttime environmental
conditions and nursing care practices contributing to a nighttime environment that is not
conducive to sleep. II 281 B
7. Clinicians should encourage nursing home facilities to implement measures to decrease
amount of time residents spend in bed during the daytime and increase daytime physical
activity. III 28 B
8. There is good evidence that daytime bright light exposure improves sleep-wake patterns
among nursing home residents. Clinicians should encourage facilities to implement measures
that increase bright light exposure via either commercially available light boxes or sunlight
exposure.
I 182,285-288 A
9. There is essentially no evidence regarding the effectiveness of sedative-hypnotic
medications in the nursing home population. Careful review of potential risks and benefits
of these medications in nursing home residents is warranted, particularly concerns about
risks of daytime sedation and falls.
III 284 B
10. Use of medications not FDA-approved for the treatment of insomnia (eg, sedating
antidepressants and sedating antipsychotics) should not be used in nursing home residents,
except in those for whom other indications for use of these agents are present (eg, depression,
psychotic symptoms, agitation).
III B
11. There is essentially no evidence to support the use of melatonin for sleep disturbance
among nursing home residents with dementia. I 187 B
12. Any medication treatment for sleep disturbance among nursing home residents should
be reviewed for effectiveness and adverse consequences, with frequent reevaluation to assess
whether medication reduction or withdrawal is indicated. III A
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