Sleep-Wake Disturbances and Sleep Disorders in Patients With Dementia

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Sleep-wake disturbances and sleep disorders in patients

with dementia
Authors: Ariel B Neikrug, PhD, Sonia Ancoli-Israel, PhD
Section Editors: Cathy A Goldstein, MD, Ruth Benca, MD, PhD, Kristine Yaffe, MD
Deputy Editors: April F Eichler, MD, MPH, Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2022. | This topic last updated: Nov 12, 2021.
INTRODUCTION
Sleep disturbances are common complaints reported by patients with dementia and their
caregivers. Multiple factors contribute to sleep impairment in this population: age- and
dementia-related changes in sleep and circadian rhythms, primary sleep disorders, institutional
and environmental factors, and comorbid illnesses and medications. Sleep disturbances and
disorders are important to recognize and treat in patients with dementia, as they are a major
contributor to caregiver distress and are associated with an increased likelihood of
institutionalization [1]. Successful management can improve dementia symptoms as well as
quality of life more broadly.
This topic will review the clinical features, evaluation, and treatment of common sleep
disturbances and sleep disorders in patients with dementia. The evaluation and treatment of
other neuropsychiatric symptoms of dementia are reviewed separately. (See "Management of
neuropsychiatric symptoms of dementia".)
SLEEP CHANGES IN AGING AND DEMENTIA
Both the normal aging process and dementia-associated neurodegeneration can be associated
with major physiologic changes in sleep and circadian rhythms. Changes can be observed in
total sleep time, time spent awake after sleep onset, sleep architecture, and circadian rhythms.
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Sleep quality and duration
● Age-related changes – Total sleep time decreases by an average of approximately 30

minutes per decade starting in mid-life [2]. Subjective reports of worse sleep quality, which
increase with age [3], have been linked to cellular and other indices of aging [4].
There is also an age-dependent increase in the prevalence of sleep disorders that may
impact sleep quality and duration, including insomnia, obstructive sleep apnea (OSA),
restless legs syndrome (RLS), periodic limb movement disorder (PLMD), and rapid eye
movement (REM) sleep behavior disorder (RBD). (See "Risk factors, comorbidities, and
consequences of insomnia in adults", section on 'Epidemiology' and "Clinical features and
diagnosis of restless legs syndrome and periodic limb movement disorder in adults",
section on 'Epidemiology' and "Rapid eye movement sleep behavior disorder", section on
'Epidemiology'.)
Aging alone, however, is not responsible for all of the observed changes [5]. Population-
based studies suggest that chronic sleep disturbances and decreases in total sleep time
are often secondary to poor health and chronic disease rather than aging itself [5-7]. This
is further supported by observations that overall improvements in health correlate with
improvements in sleep in older adults [8], and that healthy older adults rarely exhibit
disordered sleep when assessed objectively with overnight polysomnography (PSG) [3].
● Dementia-related changes – Patients with neurodegenerative dementias report and

exhibit more disruptive sleep compared with age-matched controls [9-11]. There is a
bidirectional relationship between dementia and sleep. Poor sleep may be part of the
pathophysiologic process of dementia [12-14], but it is also a risk factor for cognitive
decline and dementia.
In observational studies, subjective reductions in total sleep time, increased nighttime

wakefulness, reduced sleep efficiency, poor subjective sleep quality, long (>9 hours) and
short (<7 hours) sleep times, and disturbed sleep have all been associated with an
increased risk for cognitive decline and/or incident dementia [15-18]. Sleep plays a critical
role in beta-amyloid regulation, the pathological process involved in Alzheimer disease
(AD), and sleep disturbances are linked to amyloid pathology even prior to onset of
cognitive impairment [19-22].
Changes in sleep quality and their timing also vary based on the underlying dementia
etiology. As an example, alpha-synucleinopathies (eg, Parkinson disease [PD], dementia
with Lewy bodies [DLB]) are characterized by nighttime sleep disturbances that tend to
occur early in the course of disease (even preclinically) and remain stable throughout the
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disease course [23-25]. By contrast, sleep disturbances in AD are usually more prominent
in later stages of the disease [23-25].
Sleep architecture
● Age-related changes – Sleep generally becomes lighter and more fragmented as

individuals age. There are more arousals and awakenings during the night as well as an
increased number of sleep stage shifts due to the arousals.
The percentage of time spent in REM sleep decreases with age, with a corresponding
increase in the time spent in lighter stages of sleep. Additionally, slow-wave sleep (also
called deep sleep) exhibits a linear and gradual decrease of roughly 2 percent per decade
of life starting in early to middle adulthood [3,26] and stabilizing by the seventh decade
[3].
While these age-related changes in sleep architecture are well documented, their
consequences are not well understood. Such changes in sleep architecture might reflect
age-related neural degeneration, or they may be a marker of increased risk for dementia
over time [27]. Decreases in the percentage of time spent in REM sleep have been
associated with poorer cognition in community-dwelling older men [28,29] and with an
increased risk of incident dementia in older adults without baseline cognitive impairment
[30].
● Dementia-related changes – Compared with healthy older adults, patients with dementia
have more severe changes in sleep architecture that are likely the result of the underlying
neurodegenerative process [31,32]. Patients with AD have more and longer awakenings,
with subsequent increases in stage 1 sleep and decreases in slow-wave sleep. Patients
with AD and PD exhibit a decreased percentage of REM sleep as well as reduced REM
episodes, latency, and density when compared with healthy older adults [29,30,33].
Additional electrophysiologic changes associated with specific types of dementia include a

decrease in the frequency and amplitude of K complexes in patients with AD [34-36] and
an increase in the prevalence of REM sleep without atonia in patients with alpha-
synucleinopathies [31]. (See "Rapid eye movement sleep behavior disorder", section on
'Video polysomnography'.)
Circadian rhythms — Virtually every tissue in the body demonstrates a circadian rhythm,

oscillating approximately every 24 hours. The sleep-wake cycle is the most apparent circadian
rhythm and is paralleled by the rhythms of core body temperature fluctuation and melatonin
secretion. Circadian rhythms are regulated by the hypothalamic suprachiasmatic nucleus (SCN),
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the endogenous clock of the brain. Zeitgebers are exogenous stimuli that entrain the circadian
rhythm, which is slightly longer than 24 hours, to the 24-hour day. The most important
zeitgeber is light; others include physical activity, meals, and social contact.
● Age-related changes – The most common circadian rhythm change of aging is phase
advancement. This manifests as getting sleepy earlier in the evening and waking up
earlier in the morning. Circadian rhythms also tend to weaken with age, becoming more
desynchronized and having reduced amplitude.
Endogenous section of melatonin and other pathophysiologic mechanisms involved in

robust circadian rhythms change with age [37-39]. It is hypothesized that deterioration of
the SCN leads to weakened functioning. These changes can result in more fragmented
sleep, decreased sleep efficiency, and increased daytime sleepiness.
In addition, the external cues that are necessary to entrain the circadian sleep-wake
rhythm may be weak or missing in older adults. Older adults tend to spend very little time
exposed to bright light; this is even more prominent among adults living in nursing
homes. Changes in circadian rhythms (eg, decreased rhythm amplitude and robustness,
delayed rhythms, increased rest-activity rhythm fragmentation) are evident in the
preclinical phase of AD and may themselves be risk factors for cognitive decline and
incident dementia in aging adults [40,41].
● Dementia-related changes – Circadian rhythm disturbances are more prominent and

more disabling in patients with dementia compared with healthy older adults [42,43].
Patients with dementia exhibit reduced rhythm amplitude as well as increased phase-
delay in activity rhythms and core body temperature [44,45]. As a result, it is very common
for patients with AD to have more activity during the night than during the day [44]. In
addition, the phenomenon of sundowning, where behavioral disturbances peak in the late
afternoon or evening, is closely related to circadian rhythm abnormalities. (See
"Management of neuropsychiatric symptoms of dementia", section on 'Symptom
assessment'.)
The deterioration of circadian rhythms in patients with dementia is likely a multifactorial

phenomenon, caused by the neurodegenerative process itself, pathologic changes in
retinal photoreceptors and the SCN, and environmental influences [46-49]. Dysregulation
of melatonin secretion, a natural hormone produced by the pineal gland and controlled by
the SCN, has also been noted in patients with dementia [50].
As in older adults, patients with dementia may have decreased exposure to environmental
zeitgebers or weakening of their impact [45,51]. Older adults average about 60 minutes of
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exposure to bright light per day, whereas patients with AD living at home average only 30
minutes; older adults in nursing homes may have no exposure to bright light per day [52,53].
SYMPTOM SPECTRUM
Difficulty falling or staying asleep — Difficulties with sleep initiation and sleep continuity are
extremely common in patients with neurodegenerative disorders. In a community-based study
of sleep disorders in patients with Parkinson disease (PD), 32 percent complained of difficulty
falling asleep, 39 percent reported frequent awakening during the night, and 23 percent
reported early morning awakenings [11]. Similarly, 19 to 44 percent of community-dwelling
patients with Alzheimer disease (AD) report such sleep difficulties [23,54].
Nocturnal sleep disturbances can be attributed to multiple factors, depending upon the type of
symptom. Difficulty falling asleep may be the result of an insomnia disorder, restless legs
syndrome (RLS), disturbed circadian rhythms, medications (eg, stimulants), or other substances
(eg, caffeine, nicotine). Difficulties staying asleep may be result of insomnia, obstructive sleep
apnea (OSA), periodic limb movement disorder (PLMD), circadian disturbances, or
environmental factors (eg, noise). (See 'Clinical assessment' below.)
● Insomnia disorder – A subset of adults with dementia meet formal criteria for insomnia
disorder, defined as complaints of difficulty falling asleep, difficulty staying asleep, or early
morning awakenings that are not attributable to other sleep disorders and that have a
significant impact on daytime function. Insomnia disorder affects 30 to 50 percent of older
adults [55,56] and an even higher proportion of adults with dementia compared with age-
matched controls.
Consequences of insomnia disorder may include mood disturbances, fatigue, worsening

of cognitive deficits, decreased quality of life, worse pain, and an increased risk of falls
[6,57].
● Irregular sleep-wake rhythm disorder – Some patients with dementia who present with
complaints of difficulty with sleep initiation and maintenance may have a primary
circadian rhythm disturbance called irregular sleep-wake rhythm disorder (ISWRD). ISWRD
is characterized by the lack of a clearly defined sleep-wake rhythm, with at least three
bouts of sleep that can last one to four hours throughout a 24-hour period ( figure 1
and table 1). Nonetheless, unlike insomnia, the overall sleep achieved during a 24-hour
period in ISWRD tends to be equivalent to that of normal aging.
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The etiology of ISWRD is not fully understood, but suprachiasmatic nucleus (SCN)
dysfunction likely plays a major role. Additionally, decrease or lack of environmental
zeitgebers such as light and social schedule may precipitate or further exacerbate the
disorder. The prevalence of ISWRD is not known, as most clinical studies do not include
ISWRD as a unique disorder [58,59].
Abnormal movements or behaviors during sleep
● Restless legs syndrome – RLS is a sleep-related movement disorder characterized by an

urge to move the legs, often unpleasant or uncomfortable, which occurs during periods of
inactivity, particularly in the evenings, and is transiently relieved by movement. (See
"Clinical features and diagnosis of restless legs syndrome and periodic limb movement
disorder in adults", section on 'Clinical features'.)
Patients with RLS may describe the uncomfortable sensations with terms such as "ants
crawling," "creepy-crawly," "crazy legs," or pain. In patients with dementia who are aphasic
or nonverbal, the following behavioral cues may be indicative of RLS when they occur in
the evenings:
• Restlessness
• Frequent limb movements
• Rubbing or kneading the limbs
• Wandering
• Difficulty falling asleep
RLS is increasingly common with age, affecting up to 25 percent of older adults [60-62].
The prevalence in adults with dementia is not well established but is likely at least as high
as the general older adult population. Medications known to cause or exacerbate RLS
symptoms, many of which are used for symptomatic management in patients with
dementia, include dopamine antagonists and serotonergic antidepressants [63,64]. (See
"Clinical features and diagnosis of restless legs syndrome and periodic limb movement
disorder in adults", section on 'Exacerbating factors'.)
● Periodic limb movement disorder – During sleep, patients with dementia may have
repetitive and periodic limb jerks, known as periodic limb movements of sleep (PLMS),
some of which are associated with arousals from sleep. Like RLS, PLMS and the related
disorder, PLMD, are increasingly common with age [45] and may increase risk for cognitive
impairment [65]. Patients with PLMD have PLMS that are thought to cause significant
sleep disturbance or impairment in mental, physical, social, occupational, educational, or
behavioral areas [66]. (See "Clinical features and diagnosis of restless legs syndrome and
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periodic limb movement disorder in adults", section on 'Periodic limb movements of

sleep'.)
● Rapid eye movement sleep behavior disorder – Rapid eye movement (REM) sleep
behavior disorder (RBD) is a parasomnia caused by loss of muscle atonia during REM
sleep, which results in patients "acting out" their dreams. RBD is highly prevalent in
patients with neurodegenerative dementias that are due to alpha-synuclein pathology (eg,
PD, dementia with Lewy bodies [DLB], multiple system atrophy), often emerging well
before overt signs and symptoms of dementia. (See "Rapid eye movement sleep behavior
disorder", section on 'Alpha-synuclein neurodegeneration'.)
RBD is important to recognize in patients with dementia, since dream enactment

behaviors can result in injuries to both patients and bed partners. Symptoms of RBD range
in severity from brief, nonforceful hand or arm gestures to violent thrashing, punching, or
kicking. Sleep-related vocalizations may be loud and laden with expletives. Symptoms
predominate during the second half of the sleep period, when REM sleep is most
prevalent. The diagnosis of RBD is based on clinical history of typical behaviors during
sleep and confirmatory findings on polysomnography (PSG). (See "Rapid eye movement
sleep behavior disorder", section on 'Diagnosis'.)
Abnormal breathing patterns during sleep — Sleep-related breathing disorders (SRBD)

become increasingly common with age and are particularly prevalent in older adults with
dementia residing in nursing homes [67]. SRBD includes obstructive sleep apnea (OSA), central
sleep apnea, and mixed types. The estimated prevalence of OSA ranges from 40 to 70 percent in
patients with AD [68-71] and 20 to 60 percent in patients with PD [72-75]. Central sleep apnea
also occurs with increased frequency in older adults and those with certain comorbidities, such
as stroke or congestive heart failure.
● Sleep apnea – Symptoms of OSA include snoring; witnessed periods of silence terminated
by loud snoring, nocturnal choking or gasping; daytime sleepiness; nocturia; and morning
headaches. In addition, and particularly relevant to patients with dementia, severe OSA
(apnea hypopnea index [AHI] ≥30) may lead to further impairments in neurocognitive
function, including deficits in attention, concentration, executive function, immediate and
delayed recall, planning and sequential thinking, and manual dexterity [76-81].
Because the symptoms of OSA and central sleep apnea are nonspecific, diagnosis requires
formal testing via in-laboratory polysomnography or home sleep apnea testing. (See
"Clinical presentation and diagnosis of obstructive sleep apnea in adults".)
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● Nocturnal stridor – Nocturnal stridor is a form of respiratory dysfunction commonly seen

in patients with multiple system atrophy (MSA) [82]. Nocturnal stridor results from partial
obstruction of the larynx and is characterized by a high-pitched wheezing sound during
inspiration. It can occur throughout the day and is most common during sleep. Nocturnal
stridor can be life threatening and requires evaluation and treatment; CPAP has been used
effectively to avoid tracheotomy and improve sleep [83]. (See "Multiple system atrophy:
Clinical features and diagnosis", section on 'Sleep and breathing disorders'.)
Excessive daytime sleepiness — The inability to stay awake during the day (unintentional
naps), referred to as excessive daytime sleepiness (EDS), is common in patients with dementia
and may have a significant impact on quality of life and functioning.
The prevalence of EDS varies according to dementia etiology. EDS is significantly more common
in patients with DLB and PD than in those with Alzheimer disease (AD) [84]. EDS affects between
one-third and three-quarters of patients with PD [85-87]. (See "Clinical manifestations of
Parkinson disease", section on 'Excessive daytime sleepiness'.)
The etiology of EDS in patients with dementia is not well understood and is probably
multifactorial in most patients [88]. It may be a consequence of insufficient sleep, sedating
medications (eg, dopamine agonists), the underlying disease process, psychiatric comorbidities,
disturbed circadian rhythms, or major sleep disorders such as OSA.
EVALUATION
The best way to detect and diagnose sleep-wake disturbances in patients with dementia is to
routinely ask about them. As is the case with cognition and behavioral evaluation in patients
with dementia, caregiver or bed partner interview is crucial to supplement the history provided
by the patient.
Clinical assessment — The history should focus on three major areas of sleep complaints:
difficulty falling asleep or staying asleep, excessive daytime sleepiness (EDS), and unusual sleep-
related behaviors or movements. The following questions provide a framework for the initial
clinical interview [89]:
● What is the usual sleep time (going to sleep and waking up in the morning)?
● Does the patient experience trouble falling asleep at night? How long does it take to fall
asleep?
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● How often does the patient awaken during the night? How much time is spent awake after
sleep onset?
● Does the patient experience trouble falling back asleep if awakened during the night?
● Are there any unusual behaviors during the night or during sleep (eg, nighttime agitation
or confusion; kicking or thrashing about while asleep; walking, eating, punching, or
vocalizations during sleep)?
● Does the patient feel sleepy or tired during most of the day?
● How many naps are taken during the day? What is the duration?
● Are there any unintentional naps (dozing off without planning to) during the day?
● Does the patient use any medications (prescribed or over-the-counter) or behaviors to

help sleep?
Additional questions may be appropriate if the information elicited is suggestive of other sleep
disturbances. These questions can help identify specific disorders and direct further evaluation
and management:
● Restless legs syndrome (RLS) – Do you have the urge to move your legs or do you
experience uncomfortable sensations in your legs during rest or at night? If the patient
cannot engage in assessment, information about observed nighttime restlessness should
be elicited from the caregiver or bed partner [63].
● Periodic limb movement disorder (PLMD) – Is there any repetitive kicking while asleep?
● Obstructive sleep apnea (OSA) – Does the patient snore, gasp for air, or stop breathing
while sleeping?
● Parasomnias and rapid eye movement (REM) sleep behavior disorder (RBD) – Is there any
walking, eating, punching, kicking, or vocalization during sleep? Does the patient "act out"
dreams? RBD is particularly common among patients with Parkinson disease (PD),
dementia with Lewy bodies (DLB), and multiple system atrophy.
Habits, environment, and medications — Patients and caregivers should be questioned

about the sleep environment, behavioral factors, comorbid conditions, and medications that
may disrupt or alter sleep patterns. This includes inquiry about all of the following:
● Length/type of daily physical activity and timing of the activity
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● Length and timing of bright light exposure and amount of time spent outdoors
● Type of sleep environment (roommate-related disturbances, noise, staff interruptions)
● Type of medications, administration times, and side effects
● Caffeine use, quantity, and timing (eg, coffee, tea, cola, energy drinks)
● Alcohol and tobacco use (frequency, quantity, and timing)
● Symptoms of depression or anxiety
Formulating a diagnosis — Most sleep-wake disturbances are diagnosed by history alone or

with limited additional testing. Based on the initial assessment, complaints can usually be
categorized into one of three domains: difficulty falling asleep or staying asleep, EDS, and
unusual sleep-related behaviors or movements. In addition, sleep-related breathing disorders
such as OSA can present with a combination of fragmented sleep (due to apneas and arousals)
and EDS.
Based on this categorization, we suggest the following additional steps to arrive at a diagnosis.
This algorithmic approach was developed for older adults [89] and modified here for use in
patients with dementia:
● Difficulty falling asleep or staying asleep – When the initial assessment indicates
difficulty with sleep initiation and maintenance, the next step is to consider the timing of
sleep over the 24-hour cycle.
• If timing is unusual (eg, sleeping during the day more than night, going to sleep very
early or very late), a circadian rhythm disorder (eg, advanced sleep-wake phase
disorder, delayed sleep-wake phase disorder, or irregular sleep-wake rhythm disorder)
may be responsible. In such cases, a sleep diary and/or actigraphy are indicated to
better characterize the sleep-wake cycle and direct treatment. (See 'Additional testing'
below.)
• If the timing of sleep has not changed and seems appropriate, consider either RLS,
insomnia disorder, or other environmental, medical, psychiatric, or medication causes.
Addressing the environment and reviewing sleep hygiene are appropriate first steps.
(See 'Insomnia and other sleep-wake disturbances' below and 'Restless legs syndrome
and periodic limb movement disorder' below.)
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● Excessive daytime sleepiness – When the initial assessment indicates difficulty with
daytime functioning and sleepiness, both the timing of sleep and the quantity of sleep
should be further assessed.
• If sleep timing is unusual (eg, sleeping during the day more than night, going to sleep
very early or very late), consider a circadian rhythm disorder (eg, advanced sleep
phase, disturbed sleep-wake rhythms). (See 'Additional testing' below.)
• If timing is considered normal (eg, no change from the patient's lifetime average), the
next step is to assess whether there is adequate sleep duration and opportunity for
sleep. Insufficient sleep is a common cause of EDS. In such cases, increasing sleep
opportunity may be sufficient to resolve symptoms.
• When adequate opportunity for sleep exists and EDS is reported, consider testing for
OSA, especially when there are reports of snoring or breathing cessations. (See "Clinical
presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnostic
tests'.)
• Environmental, medical, psychiatric, and medication causes of EDS should also be

considered, especially when there is a temporal relationship between changes in any of
these factors and the onset of EDS ( table 2). (See "Approach to the patient with
excessive daytime sleepiness", section on 'Causes'.)
● Unusual sleep-related behaviors or movements – When the initial assessment indicates

unusual nighttime and sleep behaviors, additional history should be taken to further
characterize the behaviors.
• If behaviors are violent, aggressive, or involve vocalization and dream enactment,

consider the diagnosis of RBD and refer for diagnostic polysomnography (PSG). (See
"Rapid eye movement sleep behavior disorder", section on 'Diagnosis'.)
• If behaviors are not violent but rather involve leg kicks, consider the diagnosis of RLS
or PLMD. Of note, a diagnosis of RLS is made based on clinical history and does not
require PSG confirmation of the concurrent periodic limb movements of sleep (PLMS)
seen in a large proportion of RLS patients. (See 'Additional testing' below.)
Additional testing — Although many sleep-wake disorders are diagnosed by history alone,

some require further diagnostic tools or formal sleep testing. Examples include:
● Sleep diary and/or actigraphy for the evaluation of sleep-wake patterns and the
diagnosis of circadian sleep-wake rhythm disorders. Actigraphy is a noninvasive method
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for recording rest-activity cycles based on measurement of motor activity with a device
worn around the wrist. Actigraphy can be particularly useful in the evaluation of patients
with dementia because it provides longitudinal and objective data on sleep patterns,
activity, and light exposure (in some devices), independent of patient or caregiver recall (
figure 1). Actigraphy has also been extensively used and validated in patients with PD,
where motor symptoms can obscure the clinical assessment [90]. (See "Actigraphy in the
evaluation of sleep disorders".)
● Polysomnography for the diagnosis of RBD, OSA, or PLMD. For suspected RBD, the role of
PSG is twofold: to document characteristic REM sleep without atonia (RSWA), and to rule
out severe REM-related OSA, which can cause dream enactment by virtue of sleep
fragmentation. While in-laboratory PSG assessment may be necessary in certain cases (eg,
suspected RBD), such testing can be extremely challenging to complete in patients with
advanced dementia. If possible, ambulatory recording devices that require minimal
equipment and wires may be more pragmatic when there is a high suspicion for OSA or
PLMD. Different devices are required for each of these two conditions, however, and these
devices generally do not record sleep. (See "Home sleep apnea testing for obstructive
sleep apnea in adults".)
MANAGEMENT
Treatment goals should be well defined with the patient and their caregiver prior to initiating
therapy. Goals vary according to the primary symptom and may include reduced awakenings,
increased total sleep time, or improvement in daytime sleepiness.
A single intervention is rarely completely effective, and inclusion of multiple behavioral,

nonpharmacologic interventions is highly encouraged. However, the risks and burdens of
various interventions must be weighed against expected benefits. In general,
nonpharmacologic strategies should be fully explored and employed before considering
pharmacotherapy, with rare exceptions (eg, dopamine agonist for restless legs syndrome [RLS]
or periodic limb movement disorder [PLMD], melatonin or low-dose clonazepam for rapid eye
movement [REM] sleep behavior disorder [RBD] with potentially injurious behaviors).
Insomnia and other sleep-wake disturbances — Management of difficulties in sleep initiation

and maintenance (ie, insomnia) or irregular sleep-wake rhythm disorder (ISWRD) in patients
with dementia must be individualized according to patient needs, capabilities, and patient and
caregiver preferences. We approach insomnia and circadian sleep-wake rhythm disturbances
similarly. Behavioral, nonpharmacological treatments that focus on environmental changes and
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establishing consistent patterns are the mainstay of therapy, especially for patients who have
mild to moderate dementia and are able to follow behavioral planning with the help of a
caregiver.
In order to best gauge whether an intervention is working, we recommend regular outcome

assessments and routine use of sleep diaries ( table 3 and table 4) to be completed by
caregivers.
Environmental restructuring — Poor sleep is closely related to environmental disturbances,

particularly in the hospital and nursing home settings. Addressing these factors is important
across a range of sleep disturbances and etiologies in patients with dementia.
General recommendations for environmental restructuring include:
● Keep the environment dark during the night and bright during the day [91]
● Reduce noise at night
● Eliminate unnecessary nocturnal awakenings for vital signs and medication administration
● When possible, match roommates living in institutions based on their sleep-wake patterns
In institutional settings, noise and roommate disturbances can directly impact nocturnal sleep
quality. Multiple nighttime disturbances by clinicians and staff are common due to
requirements for vital signs checks, movement to avoid pressure sores, and medication
administration. In one study, nursing home staff was responsible for 50 percent of patients'
nighttime awakenings [92]. Many of these interruptions can be avoided or minimized by
scheduling them before and after regular sleep times.
Other environmental factors have an indirect impact on sleep through changes in circadian
rhythms, including changes in light exposure, exercise, and socialization. Institutionalized
adults have significantly lower exposure to diurnal light and higher exposure to nocturnal light
compared with community-dwelling older adults [51,52,93]. Strengthening these environmental
cues can help to entrain more normal circadian rhythms and thereby improve sleep quality.
Addressing polypharmacy — Polypharmacy is common among patients with dementia and is

often implicated in complaints of insomnia or other sleep-wake disturbances. In our
experience, sleep-related side effects of medications are commonly overlooked.
Medications for chronic medical and/or psychiatric conditions (eg, antipsychotic medications,
stimulants, respiratory medications, antihypertensives, and decongestants) may significantly
impact sleep and result in sleep disturbances ( table 2 and table 5). When possible, culprit
medications should be discontinued.
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For essential medications, the timing of medication administration should be considered, such
that stimulating medications and diuretics are taken earlier in the day and sedating
medications are administered prior to bedtime.
Multicomponent behavioral therapy — Behavioral therapy is best accomplished with a

multicomponent treatment program that involves both patient and caregiver, ideally over
multiple sessions. Support for this approach is drawn from a large body of literature on
cognitive behavioral therapy for insomnia (CBT-I) in the general population [94-96] and more
limited studies on the application and modification of these techniques for patients with
dementia [97-100]. The behavioral components of CBTI are most relevant in patients with
dementia, as opposed to the cognitive components (eg, restructuring maladaptive thoughts
about sleep).
Key aspects of a multicomponent approach include the following:
● Environmental restructuring (see 'Environmental restructuring' above)

● Management of polypharmacy (see 'Addressing polypharmacy' above)
● Sleep hygiene education ( table 6)
● Stabilization and maintenance of consistent sleep-wake schedules
● Stimulus control ( table 7)
Over multiple sessions, these components are modified based on patient response, the
environment, and other issues that arise during treatment. Depending upon symptoms and
response, treatment programs may include several components that focus on the environment
and also target circadian rhythm disturbances, such as light exposure and exercise.
● Sleep-wake scheduling – In our experience, stabilization and maintenance of a consistent

sleep-wake schedule are best achieved by setting a consistent wake-up time. If possible,
patients should also maintain a consistent bedtime; however, patients may find this
difficult for a variety of reasons (eg, napping during the day, exerting more energy on
some days). Even if a patient goes to sleep at different times, waking up at a consistent
time will help stabilize the rhythms.
● Light therapy – Bright light therapy can be achieved in several ways. Weather permitting,
spending time outdoors in the morning, paired with a physical activity such as walking, is
an optimal strategy that can be incorporated into the daily home or institutional routine.
Sunglasses should be avoided to maximize light reaching the eyes.
For patients who are more restricted, light boxes that emit appropriate light strength are
readily available for purchase. Light intensity is measured in lux (a measure of amount of
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light one receives at a specific distance from the source of the light). We suggest at least
30 minutes in front of the light box first thing in the morning using a 10,000 lux light box
or full spectrum light. Using a light box of lower intensity will require more exposure time
to achieve similar effect.
Supporting evidence for multicomponent behavioral sleep interventions in patients with

dementia includes the following studies:
● In two small randomized trials, community-dwelling patients with Alzheimer disease (AD)
and their caregivers were randomly assigned to a program involving sleep hygiene,
exercise, and light exposure or a control condition (general dementia education and
support) [98,99]. Over the course of six sessions, patients and their caregivers learned to
evaluate and identify sleep schedules, activities, and environmental factors that might
impact sleep as well as strategies to manipulate these factors in ways congruent with
improved sleep. Post-therapy, patients exhibited significant reductions in nighttime
awakenings, time spent awake during the night, and improved depression ratings.
● Another randomized trial evaluated the effectiveness of a similar multicomponent

treatment in nursing home residents who had major comorbidities and cognitive
impairment and demonstrated a decrease in daytime sleepiness, increase in social
participation and exercise, and decrease in nighttime awakenings [100].
When tested individually, bright light therapy, exercise, and environmental restructuring have
been shown to result in modest improvements in sleep and circadian rhythms in older adults
and patients with dementia [91,92,101-107].
Pharmacotherapy — Pharmacotherapy does not have a role in the routine management of

insomnia or other sleep-wake disturbances in patients with dementia. There are few controlled
trials of medications in this patient population, and older adults with cognitive impairment have
increased susceptibility to a variety of side effects (eg, drowsiness, confusion, gait instability,
nocturnal falls) [108,109].
Certain medications used for insomnia, such as nonbenzodiazepine benzodiazepine receptor

agonists (eg, zolpidem), are not recommended in dementia and are associated with risks that
are similar to or greater than those of benzodiazepines [110].
We strongly encourage a multicomponent, nonpharmacologic approach that should, over time,

obviate the need for pharmacologic sedation.
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A 2020 systematic review of placebo-controlled trials of insomnia medications in patients with

dementia found the following evidence [111]:
● Melatonin – The review found low-certainty evidence that melatonin doses of up to 10 mg

nightly have little to no effect on any major sleep outcome over 8 to 10 weeks (five trials, n
= 222).
● Trazodone – The review found low-certainty evidence that trazodone (50 mg nightly for
two weeks) may improve total sleep time in patients with moderate to severe AD (one trial,
n = 30). However, other outcomes, including number of awakenings and time awake
during the night, were similar between groups.
● Ramelteon – Ramelteon, an oral melatonin receptor agonist, showed no evidence of

benefit in a single trial in 74 patients with mild to moderate AD.
● Orexin receptor antagonists – The review identified moderate-certainty evidence that

orexin receptor antagonists (lemborexant and suvorexant) improve total sleep time and
decrease time awake during the night in patients with AD (two trials, n = 323). The
medications appeared to be well tolerated in short-term studies [112]. However, clinical
experience in this patient population is limited, and risks of sedation, confusion, and
imbalance must be weighed against potential benefits, as is the case for all other sedative
medications.
A National Institutes of Health expert panel concluded that there is no systematic evidence for
the effectiveness of antihistamines, antidepressants, anticonvulsants, or antipsychotics (eg,
quetiapine) for the treatment of insomnia, and that these drugs are associated with more risks
than benefits in the treatment of insomnia, particularly in older persons [109]. Patients who are
treated with medications should be frequently re-evaluated to assess response and determine
whether medication reduction or withdrawal is indicated [89].
Other disorders
Obstructive sleep apnea — Treatment options for obstructive sleep apnea (OSA) in patients
with dementia are similar to those in the general population. Continuous positive airway
pressure (CPAP) is the mainstay of therapy, along with efforts to modify risk factors such as
obesity. (See "Management of obstructive sleep apnea in adults".)
There is robust evidence from randomized trials in the general population that CPAP reduces or
eliminates apneas and hypopneas, and lower-quality evidence in older adults that CPAP
improves patient-important outcomes (eg, daytime sleepiness, motor speed, nonverbal
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learning, memory, nocturia) [113]. Studies in patients with dementia are more limited. In
addition, there are several unique barriers to CPAP use in patients with dementia. Patients with
significant memory deficits may require reminders from their caregiver; others may require
assistance in placing the CPAP due to impaired motor dexterity. (See "Causes of impaired sleep
including sleep apnea in older adults", section on 'Treatment'.)
Nonetheless, these potential difficulties should not deter clinicians from appropriate diagnosis
and treatment of OSA, particularly when OSA is associated with clinical symptoms such as
daytime sleepiness that are bothersome to the patient and family. Clinicians should be
prepared to help troubleshoot anticipated and unanticipated problems with CPAP application
and adherence. When CPAP therapy is initiated in patients with dementia, the caregiver should
be trained in how to use the mask and CPAP machine along with the patient. (See "Assessing
and managing nonadherence with continuous positive airway pressure (CPAP) for adults with
obstructive sleep apnea", section on 'First-line interventions'.)
The feasibility and efficacy of CPAP in patients with neurocognitive disorders has been
demonstrated in several small studies. In two separate randomized trials assessing the impact
of CPAP treatment on cognition, patients with AD and Parkinson disease (PD) used CPAP
effectively for an average of five hours per night [114,115]. Poor adherence in patients with AD
was associated with depression but not with dementia severity or age [115]. In both studies,
CPAP resulted in improved sleep, suggested by decreased arousals and deepening of sleep, and
reduced daytime sleepiness [114,115]. In patients with AD, CPAP treatment resulted in mildly
improved cognition; sustained use of CPAP in a small number of patients was associated with a
slower than expected deterioration in cognition and mood [116,117].
Rapid eye movement sleep behavior disorder — Patients with RBD may have violent dream
enactment. Establishing a safe sleeping environment is therefore the primary goal of
treatment. This can be achieved through modification of the sleep environment and
pharmacotherapy, if necessary.
Medications known to cause or exacerbate RBD, such as serotonin reuptake inhibitors,

serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants, should be
discontinued or avoided if possible. High-dose melatonin and low-dose clonazepam are
effective therapies in patients with frequent, disruptive or injurious behaviors. Clonazepam
should be used with caution in light of the risk of increased confusion and unsteadiness with
middle of the night awakenings. The diagnosis and treatment of RBD are discussed in detail
separately. (See "Rapid eye movement sleep behavior disorder", section on 'Management'.)
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Restless legs syndrome and periodic limb movement disorder — Treatment of restless legs
syndrome (RLS) and periodic limb movement disorder (PLMD) is similar in adults with and
without dementia. The goals of treatment are to ameliorate the symptoms and behavioral
disturbances (ie, less pacing or leg movements). Periodic leg movements themselves, outside
the context of RLS, should only be treated if they are associated with significant sleep
disturbance or daytime impairment that cannot be explained by other sleep disorders.
In addition to behavioral strategies such as exercise and leg massage, it is important to identify
potential aggravating factors such as decreased iron stores, sleep deprivation, and use of
certain medications (eg, antidepressants, dopamine-blocking antiemetics, sedating
antihistamines, antipsychotic drugs). (See "Management of restless legs syndrome and periodic
limb movement disorder in adults", section on 'Iron replacement' and "Management of restless
legs syndrome and periodic limb movement disorder in adults", section on 'Nonpharmacologic
therapy'.)
When nonpharmacologic strategies fail, treatment options for both RLS and PLMD include a
trial of a dopaminergic agonist or a gabapentinoid (eg, gabapentin, pregabalin). Of these, we
typically start with a dopamine agonist, as older adults with cognitive impairment may be more
prone to side effects from gabapentinoids. Clinicians should be aware of the possibility of
dopamine-induced psychosis in this population and begin with a low-dose trial (ie, ropinirole
0.25 mg nightly or pramipexole 0.125 mg nightly) [64]. (See "Management of restless legs
syndrome and periodic limb movement disorder in adults", section on 'Dopamine agonists'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Parasomnias,
hypersomnias, and circadian rhythm disorders" and "Society guideline links: Insomnia in adults"
and "Society guideline links: Cognitive impairment and dementia".)
SUMMARY AND RECOMMENDATIONS
● Both the normal aging process and dementia can be associated with major physiologic
changes in sleep and circadian rhythms. Changes can be observed in total sleep time, time
spent awake after sleep onset, sleep architecture, and circadian rhythms. (See 'Sleep
quality and duration' above and 'Sleep architecture' above and 'Circadian rhythms' above.)
6/20/22, 1:23 AM 97863
● Difficulties with sleep initiation and sleep continuity are probably the most common sleep-
wake disturbances in patients with dementia, affecting approximately one-third of
patients. Other common problems include excessive daytime sleepiness (EDS), increased
agitation in the evenings (sundown syndrome), and abnormal movements or behaviors
during sleep. (See 'Symptom spectrum' above.)
● The best way to detect and diagnose sleep-wake disturbances in patients with dementia is
to routinely ask about them. Caregiver or bed partner interview is crucial to supplement
the history provided by the patient. The history should focus on three major areas of sleep
complaints: difficulty falling asleep or staying asleep, EDS, and unusual sleep-related
behaviors or movements. (See 'Clinical assessment' above.)
● When the initial assessment indicates difficulty with sleep initiation and maintenance, the
next step is to consider the timing of sleep over the 24-hour cycle. Unusual sleep timing
(eg, sleeping during the day more than night, going to sleep very early or very late)
suggests a circadian rhythm disorder. If sleep timing is unchanged from the premorbid
state, the most likely causes are primary insomnia, restless legs syndrome (RLS), or effects
of medications or the environment. (See 'Formulating a diagnosis' above.)
● Many sleep-wake disorders in patients with dementia are diagnosed by history alone.
Others, such as obstructive sleep apnea (OSA) or periodic limb movement disorder
(PLMD), require further evaluation with polysomnography (PSG) or home sleep apnea
testing. (See 'Additional testing' above.)
● Poor sleep in adults with dementia is closely related to environmental disturbances,

particularly in hospital and nursing home settings. General strategies for environmental
restructuring include keeping the environment dark during the night and bright during
the day, reducing noise at night, eliminating unnecessary nocturnal awakenings, and
matching roommates based on sleep-wake patterns when possible. (See 'Environmental
restructuring' above.)
● For insomnia and circadian rhythm disturbances in patients with dementia, we suggest
behavioral, nonpharmacologic therapies that are individualized according to patient
needs, capabilities, and patient and caregiver preferences (Grade 2B).
• Patients with mild to moderate dementia who are able to follow behavioral planning
with the help of a caregiver are good candidates for multicomponent behavioral
therapy that focuses on environmental changes and establishing consistent sleep
patterns. (See 'Multicomponent behavioral therapy' above.)
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• For patients with advanced dementia, nonpharmacologic interventions consist

primarily of environmental restructuring and management of polypharmacy. (See
'Environmental restructuring' above and 'Addressing polypharmacy' above.)
• Pharmacotherapy for insomnia is poorly studied in patients with dementia and is

associated with a high risk of side effects. (See 'Pharmacotherapy' above.)
● Patients with mild to moderate dementia and comorbid OSA can tolerate and adhere to
continuous positive airway pressure (CPAP) treatment. CPAP has been shown to improve
sleep and have some positive impact on cognition in patients with dementia. (See
'Obstructive sleep apnea' above.)
● Rapid eye movement (REM) sleep behavior disorder (RBD) and RLS occur with increased
frequency in patients with dementia and are readily treatable with nonpharmacologic and
pharmacologic therapies. (See 'Rapid eye movement sleep behavior disorder' above and
'Restless legs syndrome and periodic limb movement disorder' above.)
Use of UpToDate is subject to the Terms of Use.
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101. Ancoli-Israel S, Gehrman P, Martin JL, et al. Increased light exposure consolidates sleep and
strengthens circadian rhythms in severe Alzheimer's disease patients. Behav Sleep Med
2003; 1:22.
102. Eggermont LH, Scherder EJ. Ambulatory but sedentary: impact on cognition and the rest-
activity rhythm in nursing home residents with dementia. J Gerontol B Psychol Sci Soc Sci
2008; 63:P279.
103. Eggermont LH, Blankevoort CG, Scherder EJ. Walking and night-time restlessness in mild-
to-moderate dementia: a randomized controlled trial. Age Ageing 2010; 39:746.
104. Van Someren EJ, Kessler A, Mirmiran M, Swaab DF. Indirect bright light improves circadian
rest-activity rhythm disturbances in demented patients. Biol Psychiatry 1997; 41:955.
105. King AC, Oman RF, Brassington GS, et al. Moderate-intensity exercise and self-rated quality
of sleep in older adults. A randomized controlled trial. JAMA 1997; 277:32.
106. Naylor E, Penev PD, Orbeta L, et al. Daily social and physical activity increases slow-wave
sleep and daytime neuropsychological performance in the elderly. Sleep 2000; 23:87.
107. Figueiro MG, Plitnick B, Roohan C, et al. Effects of a Tailored Lighting Intervention on Sleep
Quality, Rest-Activity, Mood, and Behavior in Older Adults With Alzheimer Disease and
Related Dementias: A Randomized Clinical Trial. J Clin Sleep Med 2019; 15:1757.
108. Yesavage JA, Friedman L, Ancoli-Israel S, et al. Development of diagnostic criteria for
defining sleep disturbance in Alzheimer's disease. J Geriatr Psychiatry Neurol 2003; 16:131.
109. National Institutes of Health. National Institutes of Health State of the Science Conference
statement on Manifestations and Management of Chronic Insomnia in Adults, June 13-15,
2005. Sleep 2005; 28:1049.
110. Richardson K, Loke YK, Fox C, et al. Adverse effects of Z-drugs for sleep disturbance in
people living with dementia: a population-based cohort study. BMC Med 2020; 18:351.
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111. McCleery J, Sharpley AL. Pharmacotherapies for sleep disturbances in dementia. Cochrane
Database Syst Rev 2020; 11:CD009178.
112. Herring WJ, Ceesay P, Snyder E, et al. Polysomnographic assessment of suvorexant in
patients with probable Alzheimer's disease dementia and insomnia: a randomized trial.
Alzheimers Dement 2020; 16:541.
113. Weaver TE, Chasens ER. Continuous positive airway pressure treatment for sleep apnea in
older adults. Sleep Med Rev 2007; 11:99.
114. Neikrug AB, Liu L, Avanzino JA, et al. Continuous positive airway pressure improves sleep
and daytime sleepiness in patients with Parkinson disease and sleep apnea. Sleep 2014;
37:177.
115. Ayalon L, Ancoli-Israel S, Stepnowsky C, et al. Adherence to continuous positive airway
pressure treatment in patients with Alzheimer's disease and obstructive sleep apnea. Am J
Geriatr Psychiatry 2006; 14:176.
116. Ancoli-Israel S, Palmer BW, Cooke JR, et al. Cognitive effects of treating obstructive sleep
apnea in Alzheimer's disease: a randomized controlled study. J Am Geriatr Soc 2008;
56:2076.
117. Cooke JR, Ayalon L, Palmer BW, et al. Sustained use of CPAP slows deterioration of
cognition, sleep, and mood in patients with Alzheimer's disease and obstructive sleep
apnea: a preliminary study. J Clin Sleep Med 2009; 5:305.
Topic 97863 Version 21.0
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GRAPHICS
Actigram from a patient with irregular sleep-wake rhythm disorder
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(A) 72-hour actigram in a patient with dementia showing a relatively well perceived sleep-wake
pattern. Although sleep is fragmented, there are distinct day-night differences.
(B) 72-hour actigram in another patient with dementia showing severe sleep fragmentation,
consistent with irregular sleep-wake rhythm disorder. There are no long intervals of consolidated
sleep or consolidated wake.
Note that these are double plots, so that the data from midnight-to-midnight at the end of day
one are repeated at the beginning of day two, etc. The activity data have been scored for wake
(thin line under the activity data) or sleep (thick line under the activity data).
Reproduced with permission from: Ancoli-Israel S, Jones DW, Hanger MA, et al. Sleep in the nursing home. In: Sleep and
Respiration in Aging Adults, Kuna ST, Suratt PM, Remmers JE (Eds), Elsevier, New York 1991. p.77. Copyright © 1991
Samuel T. Kuna, MD.
Graphic 103995 Version 2.0
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Diagnostic criteria for irregular sleep-wake rhythm disorder
Diagnostic criteria A-D must be met:
A The patient or caregiver reports a chronic or recurrent pattern of irregular sleep and wake
episodes throughout the 24-hour period, characterized by symptoms of insomnia during
the scheduled sleep period (usually at night), excessive sleepiness (napping) during the
day, or both.
B Symptoms are present for at least three months.
C Sleep log and, whenever possible, actigraphy monitoring for at least seven days, preferably
14 days, demonstrate no major sleep period and multiple irregular sleep bouts (at least
three) during a 24-hour period.
D The sleep disturbance is not better explained by another current sleep disorder, medical or
neurological disorder, mental disorder, medication use, or substance use disorder.
Reproduced with permission from: American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd
ed, American Academy of Sleep Medicine, Darien, IL 2014. Copyright © 2014 American Academy of Sleep Medicine.
6/20/22, 1:23 AM 97863
Differential diagnosis of excessive daytime sleepiness
Insufficient sleep
Sleep deprivation
Environmental intrusions
Sleep disorders
Obstructive sleep apnea
Central sleep apnea
Sleep-related hypoventilation or hypoxemia
Central disorders of hypersomnolence
Narcolepsy type 1 or 2
Kleine-Levin syndrome
Idiopathic hypersomnia
Circadian rhythm sleep-wake disorders
Delayed sleep-wake phase disorder
Advanced sleep-wake phase disorder
Irregular sleep-wake rhythm disorder
Non-24-hour sleep-wake rhythm disorder
Jet lag
Shift work
Restless legs syndrome
Periodic limb movement disorder
Other neurologic disorders

Neurodegenerative disease
Parkinson disease
Dementia with Lewy bodies
Alzheimer disease
Multiple system atrophy
Myotonic dystrophy
Multiple sclerosis
Amyotrophic lateral sclerosis (via sleep-related breathing disorders)
Structural lesions affecting thalamus, hypothalamus, or brainstem
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Traumatic brain injury
Encephalitis lethargica
Cerebral trypanosomiasis
Medical and genetic disorders
Hypothyroidism
Obesity
End-stage renal disease
Adrenal insufficiency
Hepatic encephalopathy
Niemann-Pick type C
Prader-Willi syndrome
Psychiatric disorders
Depression
Anxiety
Substance abuse
Alcohol
Narcotics
Prescription opioid abuse
Stimulant withdrawal
Psychogenic sleepiness
Medications
Benzodiazepines
Nonbenzodiazepine sedatives
Antipsychotics
Opioid analgesics
Beta-blockers (lipophilic)
Barbiturates
Antihistamines
Antiseizure medications
Sedative antidepressants
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Consensus Sleep Diary
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Questions 1 through 10 are to be completed within one hour of getting out of bed in the morning. Question
15 are to be completed before bed.
Reproduced with permission from: Camey CE, Buysse DJ, Ancoli-Israel S, et al. The Consensus Sleep Diary: Standardizing prospective s
monitoring. Sleep 2012; 35:287. Copyright © 2012 American Academy of Sleep Medicine.
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Consensus Sleep Diary instructions
General instructions
What is a sleep diary?
A sleep diary is designed to gather information about your daily sleep pattern.
How often and when do I fill out the sleep diary?
It is necessary for you to complete your sleep diary every day. If possible, the sleep diary should be
completed within one hour of getting out of bed in the morning.
What should I do if I miss a day?
If you forget to fill in the diary or are unable to finish it, leave the diary blank for that day.
What if something unusual affects my sleep or how I feel in the daytime?
If your sleep or daytime functioning is affected by some unusual event (such as an illness or an
emergency), you may make brief notes on your diary.
What do the words "bed" and "day" mean on the diary?
This diary can be used for people who are awake or asleep at unusual times. In the sleep diary, the
word "day" is the time when you choose or are required to be awake. The term "bed" means the
place where you usually sleep.
Will answering these questions about my sleep keep me awake?
This is not usually a problem. You should not worry about giving exact times, and you should not
watch the clock. Just give your best estimate.
Sleep diary item instructions

Use the guide below to clarify what is being asked for each item of the sleep diary.
Date: Write the date of the morning you are filling out the diary.
1. What time did you get into bed?
Write the time that you got into bed. This may not be the time you began "trying" to fall asleep.
2. What time did you try to go to sleep?
Record the time that you began "trying" to fall asleep.
3. How long did it take you to fall asleep?
Beginning at the time you wrote in question 2, how long did it take you to fall asleep?
4. How many times did you wake up, not counting your final awakening?
How many times did you wake up between the time you first fell asleep and your final awakening?
5. In total, how long did these awakenings last?
What was the total time you were awake between the time you first fell asleep and your final
awakening? For example, if you woke 3 times for 20 minutes, 35 minutes, and 15 minutes, add
them all up (20 + 35 + 15 = 70 minutes or 1 hour and 10 minutes).
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6a. What time was your final awakening?
Record the last time you woke up in the morning.
6b. After your final awakening, how long did you spend in bed trying to sleep?
After the last time you woke up (item #6a), how many minutes did you spend in bed trying to
sleep? For example, if you woke up at 8:00 AM but continued to try and sleep until 9:00 AM, record
1 hour.
6c. Did you wake up earlier than you planned?
If you woke up or were awakened earlier than you planned, check yes. If you woke up at your
planned time, check no.
6d. If yes, how much earlier?
If you answered "yes" to question 6c, write the number of minutes you woke up earlier than you
had planned on waking up. For example, if you woke up 15 minutes before the alarm went off,
record 15 minutes here.
7. What time did you get out of bed for the day?
What time did you get out of bed with no further attempt at sleeping? This may be different from
your final awakening time (eg, you may have woken up at 6:35 AM but did not get out of bed to
start your day until 7:20 AM).
8. In total, how long did you sleep?
This should just be your best estimate, based on when you went to bed and woke up, how long it
took you to fall asleep, and how long you were awake. You do not need to calculate this by adding
and subtracting; just give your best estimate.
9. How would you rate the quality of your sleep?
"Sleep quality" is your sense of whether your sleep was good or poor.
10. How restful or refreshed did you feel when you woke up for the day?
This refers to how you felt after you were done sleeping for the night, during the first few minutes
that you were awake.
11a. How many times did you nap or doze?
A nap is a time you decided to sleep during the day, whether in bed or not in bed. "Dozing" is a
time you may have nodded off for a few minutes, without meaning to, such as while watching TV.
Count all the times you napped or dozed at any time from when you first got out of bed in the
morning until you got into bed again at night.
11b. In total, how long did you nap or doze?
Estimate the total amount of time you spent napping or dozing, in hours and minutes. For
instance, if you napped twice, once for 30 minutes and once for 60 minutes, and dozed for 10
minutes, you would answer "1 hour 40 minutes." If you did not nap or doze, write "N/A" (not
applicable).
12a. How many drinks containing alcohol did you have?
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Enter the number of alcoholic drinks you had where 1 drink is defined as one 12 oz beer (can), 5 oz
wine, or 1.5 oz liquor (one shot).
12b. What time was your last drink?
If you had an alcoholic drink yesterday, enter the time of day in hours and minutes of your last
drink. If you did not have a drink, write "N/A" (not applicable).
13a. How many caffeinated drinks (coffee, tea, soda, energy drinks) did you have?
Enter the number of caffeinated drinks (coffee, tea, soda, energy drinks) you had where for coffee
and tea, one drink = 6 to 8 oz, while for caffeinated soda one drink = 12 oz.
13b. What time was your last caffeinated drink?
If you had a caffeinated drink, enter the time of day in hours and minutes of your last drink. If you
did not have a caffeinated drink, write "N/A" (not applicable).
14. Did you take any over-the-counter or prescription medication(s) to help you sleep?
If so, list medication(s), dose, and time taken: List the medication name, how much and when you
took EACH different medication you took tonight to help you sleep. Include medication available
over the counter, prescription medications, and herbals (example: "Sleepwell 50 mg 11:00 PM"). If
every night is the same, write "same" after the first day.
15. Comments:
If you have anything that you would like to say that is relevant to your sleep, feel free to write it
here.
Reproduced with permission from: Camey CE, Buysse DJ, Ancoli-Israel S, et al. The Consensus Sleep Diary: Standardizing
prospective sleep self-monitoring. Sleep 2012; 35:287. Copyright © 2012 American Academy of Sleep Medicine.
6/20/22, 1:23 AM 97863
Risk factors and comorbidities of chronic insomnia in adults
Psychiatric conditions Neurological conditions

Depression Neurodegenerative diseases (eg, Alzheimer
dementia, Parkinson disease)
Anxiety
Neuromuscular disorders including painful
Substance use disorders
peripheral neuropathies
Posttraumatic stress disorder
Cerebral hemispheric and brainstem strokes
Medical conditions
Brain tumors
Pulmonary
Traumatic brain injury
Chronic obstructive pulmonary disease
Headache syndromes (eg, migraine, cluster,
Asthma hypnic headache, and exploding head
syndromes)
Rheumatologic
Fatal familial insomnia
Arthritis
Fibromyalgia
Medications and substances
Chronic pain Central nervous system stimulants
Cardiovascular Central nervous system depressants
Heart failure Bronchodilators
Ischemic heart disease Antidepressants
Nocturnal angina Beta antagonists
Hypertension Diuretics
Endocrinologic Glucocorticoids
Hyperthyroidism Caffeine
Urinary Alcohol
Nocturia Other sleep disorders
Gastrointestinal Restless legs syndrome
Gastroesophageal reflux Periodic limb movement disorder
Diabetes Sleep apnea
Cancer Circadian sleep-wake rhythm disorders
Pregnancy Delayed sleep-wake phase disorder
Menopause Advanced sleep-wake phase disorder
Lyme disease Irregular sleep-wake rhythm disorder
Human immunodeficiency virus (HIV) infection Non-24-hour sleep-wake rhythm disorder
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Chronic fatigue syndrome Shift work disorder
Dermatologic (eg, pruritus) Jet lag
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Sleep hygiene guidelines
Recommendation Details
Regular bedtime and rise Having a consistent bedtime and rise time leads to more regular sleep
time schedules and avoids periods of sleep deprivation or periods of
extended wakefulness during the night.
Avoid napping Avoid napping, especially naps lasting longer than 1 hour and naps
late in the day.
Limit caffeine Avoid caffeine after lunch. The time between lunch and
bedtime represents approximately 2 half-lives for caffeine, and this
time window allows for most caffeine to be metabolized before
bedtime.
Limit alcohol Recommendations are typically focused on avoiding alcohol near

bedtime. Alcohol is initially sedating, but activating as it is
metabolized. Alcohol also negatively impacts sleep architecture.
Avoid nicotine Nicotine is a stimulant and should be avoided near bedtime and at
night.
Exercise Daytime physical activity is encouraged, in particular, 4 to 6 hours

before bedtime, as this may facilitate sleep onset. Rigorous exercise
within 2 hours of bedtime is discouraged.
Keep the sleep environment Noise and light exposure during the night can disrupt sleep. White
quiet and dark noise or ear plugs are often recommended to reduce noise. Using
blackout shades or an eye mask is commonly recommended to
reduce light.
This may also include avoiding exposure to television or technology

near bedtime, as this can have an impact on circadian rhythms by
shifting sleep timing later.
Bedroom clock Avoid checking the time at night. This includes alarm clocks and other
time pieces (eg, watches and smart phones). Checking the time
increases cognitive arousal and prolongs wakefulness.
Evening eating Avoid a large meal near bedtime, but don't go to bed hungry. Eat a
healthy and filling meal in the evening and avoid late-night snacks.
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Stimulus control therapy rules
1. Go to bed only when sleepy.
2. Do not watch television, read, eat, or worry while in bed. Use bed only for sleep and sex.
3. Get out of bed if unable to fall asleep within 20 minutes and go to another room. Return to bed
only when sleepy. Repeat this step as many times as necessary throughout the night.
4. Set an alarm clock to wake up at a fixed time each morning, including weekends.
5. Do not take a nap during the day.
Data from: Bootzin RR, Perlis ML. Nonpharmacologic treatments of insomnia. J Clin Psychiatry 1992; 53:37.
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Contributor Disclosures
Ariel B Neikrug, PhD No relevant financial relationship(s) with ineligible companies to disclose. Sonia
Ancoli-Israel, PhD Consultant/Advisory Boards: Merck [Insomnia]; Eisai [Insomnia]; Biogen [Sleep/PD]. All
of the relevant financial relationships listed have been mitigated. Cathy A Goldstein,
MD Consultant/Advisory Boards: Huxley Medical[Sleep apnea].
Other Financial Interest: Arcascope, LLC
[Sleep and circadian rhythm].
All of the relevant financial relationships listed have been mitigated. Ruth
Benca, MD, PhD Grant/Research/Clinical Trial Support: Eisai [Insomnia].
Consultant/Advisory Boards: Eisai
[Insomnia];Genomind [Genetic testing for personalized medicine];Idorsia [Insomnia];Jazz Pharmaceuticals
[Hypersomnia];Merck [Insomnia];Sage [Depression].
All of the relevant financial relationships listed have
been mitigated. Kristine Yaffe, MD Consultant/Advisory Boards: Alector [Dementia];Eli Lilly.
All of the
relevant financial relationships listed have been mitigated. April F Eichler, MD, MPH No relevant financial
relationship(s) with ineligible companies to disclose. Janet L Wilterdink, MD No relevant financial
relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

Sleep-Wake Disturbances and Sleep Disorders in Patients With Dementia

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Sleep-wake disturbances and sleep disorders in patients

SLEEP CHANGES IN AGING AND DEMENTIA

Sleep quality and duration

● Age-related changes – Total sleep time decreases by an average of approximately 30

● Dementia-related changes – Patients with neurodegenerative dementias report and

In observational studies, subjective reductions in total sleep time, increased nighttime

● Age-related changes – Sleep generally becomes lighter and more fragmented as

Additional electrophysiologic changes associated with specific types of dementia include a

Circadian rhythms — Virtually every tissue in the body demonstrates a circadian rhythm,

Endogenous section of melatonin and other pathophysiologic mechanisms involved in

● Dementia-related changes – Circadian rhythm disturbances are more prominent and

The deterioration of circadian rhythms in patients with dementia is likely a multifactorial

Consequences of insomnia disorder may include mood disturbances, fatigue, worsening

Abnormal movements or behaviors during sleep

● Restless legs syndrome – RLS is a sleep-related movement disorder characterized by an

periodic limb movement disorder in adults", section on 'Periodic limb movements of

RBD is important to recognize in patients with dementia, since dream enactment

Abnormal breathing patterns during sleep — Sleep-related breathing disorders (SRBD)

● Nocturnal stridor – Nocturnal stridor is a form of respiratory dysfunction commonly seen

● Does the patient use any medications (prescribed or over-the-counter) or behaviors to

Habits, environment, and medications — Patients and caregivers should be questioned

● Length/type of daily physical activity and timing of the activity

● Type of sleep environment (roommate-related disturbances, noise, staff interruptions)

● Type of medications, administration times, and side effects

● Alcohol and tobacco use (frequency, quantity, and timing)

● Symptoms of depression or anxiety

Formulating a diagnosis — Most sleep-wake disturbances are diagnosed by history alone or

• Environmental, medical, psychiatric, and medication causes of EDS should also be

● Unusual sleep-related behaviors or movements – When the initial assessment indicates

• If behaviors are violent, aggressive, or involve vocalization and dream enactment,

Additional testing — Although many sleep-wake disorders are diagnosed by history alone,

A single intervention is rarely completely effective, and inclusion of multiple behavioral,

Insomnia and other sleep-wake disturbances — Management of difficulties in sleep initiation

In order to best gauge whether an intervention is working, we recommend regular outcome

Environmental restructuring — Poor sleep is closely related to environmental disturbances,

General recommendations for environmental restructuring include:

Addressing polypharmacy — Polypharmacy is common among patients with dementia and is

Multicomponent behavioral therapy — Behavioral therapy is best accomplished with a

Key aspects of a multicomponent approach include the following:

● Environmental restructuring (see 'Environmental restructuring' above)

● Sleep-wake scheduling – In our experience, stabilization and maintenance of a consistent

Supporting evidence for multicomponent behavioral sleep interventions in patients with

● Another randomized trial evaluated the effectiveness of a similar multicomponent

Pharmacotherapy — Pharmacotherapy does not have a role in the routine management of

Certain medications used for insomnia, such as nonbenzodiazepine benzodiazepine receptor

We strongly encourage a multicomponent, nonpharmacologic approach that should, over time,

A 2020 systematic review of placebo-controlled trials of insomnia medications in patients with

● Melatonin – The review found low-certainty evidence that melatonin doses of up to 10 mg

● Ramelteon – Ramelteon, an oral melatonin receptor agonist, showed no evidence of

● Orexin receptor antagonists – The review identified moderate-certainty evidence that

Medications known to cause or exacerbate RBD, such as serotonin reuptake inhibitors,

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● Poor sleep in adults with dementia is closely related to environmental disturbances,

• For patients with advanced dementia, nonpharmacologic interventions consist

• Pharmacotherapy for insomnia is poorly studied in patients with dementia and is

Use of UpToDate is subject to the Terms of Use.

Actigram from a patient with irregular sleep-wake rhythm disorder

Graphic 103995 Version 2.0

Diagnostic criteria for irregular sleep-wake rhythm disorder

Diagnostic criteria A-D must be met: