Your activity: 125 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email:

Sleep-wake disturbances and sleep disorders in patients with dementia

Sleep-wake disturbances and sleep disorders in patients with dementia
Ariel B Neikrug, PhD
Sonia Ancoli-Israel, PhD
Section Editors:
Cathy A Goldstein, MD
Ruth Benca, MD, PhD
Deputy Editors:
April F Eichler, MD, MPH
Janet L Wilterdink, MD
Literature review current through: Dec 2022. | This topic last updated: Sep 19, 2022.

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 and an approach to sleep disorders in patients with Parkinson disease (PD) are reviewed separately. (See "Management of neuropsychiatric symptoms of dementia" and "Evaluation and treatment of insomnia, daytime sleepiness, and other sleep disorders in Parkinson disease".)

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.

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 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), 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 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].


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.

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:


Frequent limb movements

Rubbing or kneading the limbs


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 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".)

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?

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

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.)

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 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 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.

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 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.

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 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 caregivers. 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'.)

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".)


Symptom spectrum – 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.)

Evaluation – 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.)

Diagnosis – 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.)

Sleep testing – 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.)

Insomnia management – Poor sleep in adults with dementia is closely related to environmental disturbances, particularly in hospital and nursing home settings.

Environmental restructuring – 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.)

Behavioral therapies – 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.)

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 – Pharmacotherapy for insomnia is poorly studied in patients with dementia and is associated with a high risk of side effects. (See 'Pharmacotherapy' above.)

Sleep apnea management – 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.)

Other sleep disorders – Rapid eye movement (REM) sleep behavior disorder (RBD) and RLS occur with increased frequency in patients with dementia and are readily treatable. (See 'Rapid eye movement sleep behavior disorder' above and 'Restless legs syndrome and periodic limb movement disorder' above.)

  1. Pollak CP, Perlick D, Linsner JP, et al. Sleep problems in the community elderly as predictors of death and nursing home placement. J Community Health 1990; 15:123.
  2. Van Cauter E, Leproult R, Plat L. Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA 2000; 284:861.
  3. Ohayon MM, Carskadon MA, Guilleminault C, Vitiello MV. Meta-analysis of quantitative sleep parameters from childhood to old age in healthy individuals: developing normative sleep values across the human lifespan. Sleep 2004; 27:1255.
  4. Cribbet MR, Carlisle M, Cawthon RM, et al. Cellular aging and restorative processes: subjective sleep quality and duration moderate the association between age and telomere length in a sample of middle-aged and older adults. Sleep 2014; 37:65.
  5. Foley D, Ancoli-Israel S, Britz P, Walsh J. Sleep disturbances and chronic disease in older adults: results of the 2003 National Sleep Foundation Sleep in America Survey. J Psychosom Res 2004; 56:497.
  6. Foley DJ, Monjan AA, Brown SL, et al. Sleep complaints among elderly persons: an epidemiologic study of three communities. Sleep 1995; 18:425.
  7. Vitiello MV, Moe KE, Prinz PN. Sleep complaints cosegregate with illness in older adults: clinical research informed by and informing epidemiological studies of sleep. J Psychosom Res 2002; 53:555.
  8. Foley DJ, Monjan A, Simonsick EM, et al. Incidence and remission of insomnia among elderly adults: an epidemiologic study of 6,800 persons over three years. Sleep 1999; 22 Suppl 2:S366.
  9. Bliwise DL. Sleep disorders in Alzheimer's disease and other dementias. Clin Cornerstone 2004; 6 Suppl 1A:S16.
  10. Vitiello MV, Prinz PN. Alzheimer's disease. Sleep and sleep/wake patterns. Clin Geriatr Med 1989; 5:289.
  11. Tandberg E, Larsen JP, Karlsen K. A community-based study of sleep disorders in patients with Parkinson's disease. Mov Disord 1998; 13:895.
  12. Nebes RD, Buysse DJ, Halligan EM, et al. Self-reported sleep quality predicts poor cognitive performance in healthy older adults. J Gerontol B Psychol Sci Soc Sci 2009; 64:180.
  13. Xu L, Jiang CQ, Lam TH, et al. Short or long sleep duration is associated with memory impairment in older Chinese: the Guangzhou Biobank Cohort Study. Sleep 2011; 34:575.
  14. Ferrie JE, Shipley MJ, Akbaraly TN, et al. Change in sleep duration and cognitive function: findings from the Whitehall II Study. Sleep 2011; 34:565.
  15. Hahn EA, Wang HX, Andel R, Fratiglioni L. A change in sleep pattern may predict Alzheimer disease. Am J Geriatr Psychiatry 2014; 22:1262.
  16. Blackwell T, Yaffe K, Laffan A, et al. Associations of objectively and subjectively measured sleep quality with subsequent cognitive decline in older community-dwelling men: the MrOS sleep study. Sleep 2014; 37:655.
  17. Blackwell T, Yaffe K, Ancoli-Israel S, et al. Poor sleep is associated with impaired cognitive function in older women: the study of osteoporotic fractures. J Gerontol A Biol Sci Med Sci 2006; 61:405.
  18. Lutsey PL, Misialek JR, Mosley TH, et al. Sleep characteristics and risk of dementia and Alzheimer's disease: The Atherosclerosis Risk in Communities Study. Alzheimers Dement 2018; 14:157.
  19. Ju YE, McLeland JS, Toedebusch CD, et al. Sleep quality and preclinical Alzheimer disease. JAMA Neurol 2013; 70:587.
  20. Sprecher KE, Koscik RL, Carlsson CM, et al. Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults. Neurology 2017; 89:445.
  21. Insel PS, Mohlenhoff BS, Neylan TC, et al. Association of Sleep and β-Amyloid Pathology Among Older Cognitively Unimpaired Adults. JAMA Netw Open 2021; 4:e2117573.
  22. Lucey BP, Wisch J, Boerwinkle AH, et al. Sleep and longitudinal cognitive performance in preclinical and early symptomatic Alzheimer's disease. Brain 2021; 144:2852.
  23. Bliwise DL, Mercaldo ND, Avidan AY, et al. Sleep disturbance in dementia with Lewy bodies and Alzheimer's disease: a multicenter analysis. Dement Geriatr Cogn Disord 2011; 31:239.
  24. Prinz PN, Vitaliano PP, Vitiello MV, et al. Sleep, EEG and mental function changes in senile dementia of the Alzheimer's type. Neurobiol Aging 1982; 3:361.
  25. Schenck CH, Bundlie SR, Mahowald MW. Delayed emergence of a parkinsonian disorder in 38% of 29 older men initially diagnosed with idiopathic rapid eye movement sleep behaviour disorder. Neurology 1996; 46:388.
  26. Ohayon MM, Vecchierini MF. Normative sleep data, cognitive function and daily living activities in older adults in the community. Sleep 2005; 28:981.
  27. Prinz PN, Vitiello MV, Raskind MA, Thorpy MJ. Geriatrics: sleep disorders and aging. N Engl J Med 1990; 323:520.
  28. Blackwell T, Yaffe K, Ancoli-Israel S, et al. Associations between sleep architecture and sleep-disordered breathing and cognition in older community-dwelling men: the Osteoporotic Fractures in Men Sleep Study. J Am Geriatr Soc 2011; 59:2217.
  29. Song Y, Blackwell T, Yaffe K, et al. Relationships between sleep stages and changes in cognitive function in older men: the MrOS Sleep Study. Sleep 2015; 38:411.
  30. Pase MP, Himali JJ, Grima NA, et al. Sleep architecture and the risk of incident dementia in the community. Neurology 2017; 89:1244.
  31. Petit D, Gagnon JF, Fantini ML, et al. Sleep and quantitative EEG in neurodegenerative disorders. J Psychosom Res 2004; 56:487.
  32. D'Rozario AL, Chapman JL, Phillips CL, et al. Objective measurement of sleep in mild cognitive impairment: A systematic review and meta-analysis. Sleep Med Rev 2020; 52:101308.
  33. Bugalho P, Salavisa M, Marto JP, et al. Polysomnographic data in Dementia with Lewy Bodies: correlation with clinical symptoms and comparison with other α-synucleinopathies. Sleep Med 2019; 55:62.
  34. Montplaisir J, Petit D, Lorrain D, et al. Sleep in Alzheimer's disease: further considerations on the role of brainstem and forebrain cholinergic populations in sleep-wake mechanisms. Sleep 1995; 18:145.
  35. Prinz PN, Peskind ER, Vitaliano PP, et al. Changes in the sleep and waking EEGs of nondemented and demented elderly subjects. J Am Geriatr Soc 1982; 30:86.
  36. Reynolds CF 3rd, Kupfer DJ, Houck PR, et al. Reliable discrimination of elderly depressed and demented patients by electroencephalographic sleep data. Arch Gen Psychiatry 1988; 45:258.
  37. Touitou Y. Human aging and melatonin. Clinical relevance. Exp Gerontol 2001; 36:1083.
  38. Czeisler CA, Dumont M, Duffy JF, et al. Association of sleep-wake habits in older people with changes in output of circadian pacemaker. Lancet 1992; 340:933.
  39. Dijk DJ, Duffy JF, Riel E, et al. Ageing and the circadian and homeostatic regulation of human sleep during forced desynchrony of rest, melatonin and temperature rhythms. J Physiol 1999; 516 ( Pt 2):611.
  40. Tranah GJ, Blackwell T, Stone KL, et al. Circadian activity rhythms and risk of incident dementia and mild cognitive impairment in older women. Ann Neurol 2011; 70:722.
  41. Musiek ES, Bhimasani M, Zangrilli MA, et al. Circadian Rest-Activity Pattern Changes in Aging and Preclinical Alzheimer Disease. JAMA Neurol 2018; 75:582.
  42. Bliwise DL. Sleep in normal aging and dementia. Sleep 1993; 16:40.
  43. van Someren EJ, Mirmiran M, Swaab DF. Non-pharmacological treatment of sleep and wake disturbances in aging and Alzheimer's disease: chronobiological perspectives. Behav Brain Res 1993; 57:235.
  44. Satlin A, Volicer L, Stopa EG, Harper D. Circadian locomotor activity and core-body temperature rhythms in Alzheimer's disease. Neurobiol Aging 1995; 16:765.
  45. Harper DG, Stopa EG, McKee AC, et al. Dementia severity and Lewy bodies affect circadian rhythms in Alzheimer disease. Neurobiol Aging 2004; 25:771.
  46. Swaab DF, Fliers E, Partiman TS. The suprachiasmatic nucleus of the human brain in relation to sex, age and senile dementia. Brain Res 1985; 342:37.
  47. Stopa EG, Volicer L, Kuo-Leblanc V, et al. Pathologic evaluation of the human suprachiasmatic nucleus in severe dementia. J Neuropathol Exp Neurol 1999; 58:29.
  48. Wang JL, Lim AS, Chiang WY, et al. Suprachiasmatic neuron numbers and rest-activity circadian rhythms in older humans. Ann Neurol 2015; 78:317.
  49. La Morgia C, Ross-Cisneros FN, Koronyo Y, et al. Melanopsin retinal ganglion cell loss in Alzheimer disease. Ann Neurol 2016; 79:90.
  50. Mishima K, Tozawa T, Satoh K, et al. Melatonin secretion rhythm disorders in patients with senile dementia of Alzheimer's type with disturbed sleep-waking. Biol Psychiatry 1999; 45:417.
  51. van Someren EJ, Hagebeuk EE, Lijzenga C, et al. Circadian rest-activity rhythm disturbances in Alzheimer's disease. Biol Psychiatry 1996; 40:259.
  52. Martin J, Marler M, Shochat T, Ancoli-Israel S. Circadian rhythms of agitation in institutionalized patients with Alzheimer's disease. Chronobiol Int 2000; 17:405.
  53. Leng Y, Musiek ES, Hu K, et al. Association between circadian rhythms and neurodegenerative diseases. Lancet Neurol 2019; 18:307.
  54. McCurry SM, Reynolds CF, Ancoli-Israel S, et al. Treatment of sleep disturbance in Alzheimer's disease. Sleep Med Rev 2000; 4:603.
  55. Roth T, Ancoli-Israel S. Daytime consequences and correlates of insomnia in the United States: results of the 1991 National Sleep Foundation Survey. II. Sleep 1999; 22 Suppl 2:S354.
  56. Schutte-Rodin S, Broch L, Buysse D, et al. Clinical guideline for the evaluation and management of chronic insomnia in adults. J Clin Sleep Med 2008; 4:487.
  57. Simon GE, VonKorff M. Prevalence, burden, and treatment of insomnia in primary care. Am J Psychiatry 1997; 154:1417.
  58. Zee PC, Vitiello MV. Circadian Rhythm Sleep Disorder: Irregular Sleep Wake Rhythm Type. Sleep Med Clin 2009; 4:213.
  59. Sack RL, Auckley D, Auger RR, et al. Circadian rhythm sleep disorders: part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm. An American Academy of Sleep Medicine review. Sleep 2007; 30:1484.
  60. Ohayon MM, Roth T. Prevalence of restless legs syndrome and periodic limb movement disorder in the general population. J Psychosom Res 2002; 53:547.
  61. Lavigne GJ, Montplaisir JY. Restless legs syndrome and sleep bruxism: prevalence and association among Canadians. Sleep 1994; 17:739.
  62. Rothdach AJ, Trenkwalder C, Haberstock J, et al. Prevalence and risk factors of RLS in an elderly population: the MEMO study. Memory and Morbidity in Augsburg Elderly. Neurology 2000; 54:1064.
  63. Richards K, Shue VM, Beck CK, et al. Restless legs syndrome risk factors, behaviors, and diagnoses in persons with early to moderate dementia and sleep disturbance. Behav Sleep Med 2010; 8:48.
  64. Bliwise DL. Periodic Leg Movements in Sleep and Restless Legs Syndrome: Considerations in Geriatrics. Sleep Med Clin 2006; 1:263.
  65. Leng Y, Blackwell T, Stone KL, et al. Periodic Limb Movements in Sleep are Associated with Greater Cognitive Decline in Older Men without Dementia. Sleep 2016; 39:1807.
  66. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, 2014.
  67. Ancoli-Israel S, Gehrman P, Kripke DF, et al. Long-term follow-up of sleep disordered breathing in older adults. Sleep Med 2001; 2:511.
  68. Reynolds CF 3rd, Kupfer DJ, Taska LS, et al. Sleep apnea in Alzheimer's dementia: correlation with mental deterioration. J Clin Psychiatry 1985; 46:257.
  69. Ancoli-Israel S, Klauber MR, Butters N, et al. Dementia in institutionalized elderly: relation to sleep apnea. J Am Geriatr Soc 1991; 39:258.
  70. Onen F, Onen H. [Obstructive sleep apnea and cognitive impairment in the elderly]. Psychol Neuropsychiatr Vieil 2010; 8:163.
  71. Hoch CC, Reynolds CF 3rd, Kupfer DJ, et al. Sleep-disordered breathing in normal and pathologic aging. J Clin Psychiatry 1986; 47:499.
  72. Arnulf I, Konofal E, Merino-Andreu M, et al. Parkinson's disease and sleepiness: an integral part of PD. Neurology 2002; 58:1019.
  73. Zoccolella S, Savarese M, Lamberti P, et al. Sleep disorders and the natural history of Parkinson's disease: the contribution of epidemiological studies. Sleep Med Rev 2011; 15:41.
  74. Norlinah MI, Afidah KN, Noradina AT, et al. Sleep disturbances in Malaysian patients with Parkinson's disease using polysomnography and PDSS. Parkinsonism Relat Disord 2009; 15:670.
  75. Cochen De Cock V, Abouda M, Leu S, et al. Is obstructive sleep apnea a problem in Parkinson's disease? Sleep Med 2010; 11:247.
  76. Aloia MS, Ilniczky N, Di Dio P, et al. Neuropsychological changes and treatment compliance in older adults with sleep apnea. J Psychosom Res 2003; 54:71.
  77. Décary A, Rouleau I, Montplaisir J. Cognitive deficits associated with sleep apnea syndrome: a proposed neuropsychological test battery. Sleep 2000; 23:369.
  78. El-Ad B, Lavie P. Effect of sleep apnea on cognition and mood. Int Rev Psychiatry 2005; 17:277.
  79. Sateia MJ. Neuropsychological impairment and quality of life in obstructive sleep apnea. Clin Chest Med 2003; 24:249.
  80. Leng Y, McEvoy CT, Allen IE, Yaffe K. Association of Sleep-Disordered Breathing With Cognitive Function and Risk of Cognitive Impairment: A Systematic Review and Meta-analysis. JAMA Neurol 2017; 74:1237.
  81. Elfil M, Bahbah EI, Attia MM, et al. Impact of Obstructive Sleep Apnea on Cognitive and Motor Functions in Parkinson's Disease. Mov Disord 2021; 36:570.
  82. Vetrugno R, Provini F, Cortelli P, et al. Sleep disorders in multiple system atrophy: a correlative video-polysomnographic study. Sleep Med 2004; 5:21.
  83. Trenkwalder C, Arnulf I. Parkinsonism. In: Principles and practice of sleep medicine, 5th ed, Kryger M, Roth T, Dement W (Eds), Elsevier, Philadelphia 2011. p.980.
  84. Boddy F, Rowan EN, Lett D, et al. Subjectively reported sleep quality and excessive daytime somnolence in Parkinson's disease with and without dementia, dementia with Lewy bodies and Alzheimer's disease. Int J Geriatr Psychiatry 2007; 22:529.
  85. Ghorayeb I, Loundou A, Auquier P, et al. A nationwide survey of excessive daytime sleepiness in Parkinson's disease in France. Mov Disord 2007; 22:1567.
  86. Paus S, Brecht HM, Köster J, et al. Sleep attacks, daytime sleepiness, and dopamine agonists in Parkinson's disease. Mov Disord 2003; 18:659.
  87. Leng Y, Redline S, Stone KL, et al. Objective napping, cognitive decline, and risk of cognitive impairment in older men. Alzheimers Dement 2019; 15:1039.
  88. Adler CH, Thorpy MJ. Sleep issues in Parkinson's disease. Neurology 2005; 64:S12.
  89. Bloom HG, Ahmed I, Alessi CA, et al. Evidence-based recommendations for the assessment and management of sleep disorders in older persons. J Am Geriatr Soc 2009; 57:761.
  90. Maglione JE, Liu L, Neikrug AB, et al. Actigraphy for the assessment of sleep measures in Parkinson's disease. Sleep 2013; 36:1209.
  91. Schnelle JF, Alessi CA, Al-Samarrai NR, et al. The nursing home at night: effects of an intervention on noise, light, and sleep. J Am Geriatr Soc 1999; 47:430.
  92. Cruise PA, Schnelle JF, Alessi CA, et al. The nighttime environment and incontinence care practices in nursing homes. J Am Geriatr Soc 1998; 46:181.
  93. Campbell SS, Kripke DF, Gillin JC, Hrubovcak JC. Exposure to light in healthy elderly subjects and Alzheimer's patients. Physiol Behav 1988; 42:141.
  94. Morin CM, Colecchi C, Stone J, et al. Behavioral and pharmacological therapies for late-life insomnia: a randomized controlled trial. JAMA 1999; 281:991.
  95. Buysse DJ, Germain A, Moul DE, et al. Efficacy of brief behavioral treatment for chronic insomnia in older adults. Arch Intern Med 2011; 171:887.
  96. Germain A, Moul DE, Franzen PL, et al. Effects of a brief behavioral treatment for late-life insomnia: preliminary findings. J Clin Sleep Med 2006; 2:403.
  97. Teri L, McKenzie G, Logsdon RG, et al. Translation of two evidence-based programs for training families to improve care of persons with dementia. Gerontologist 2012; 52:452.
  98. McCurry SM, Gibbons LE, Logsdon RG, et al. Nighttime insomnia treatment and education for Alzheimer's disease: a randomized, controlled trial. J Am Geriatr Soc 2005; 53:793.
  99. McCurry SM, Gibbons LE, Logsdon RG, et al. Training caregivers to change the sleep hygiene practices of patients with dementia: the NITE-AD project. J Am Geriatr Soc 2003; 51:1455.
  100. Alessi CA, Martin JL, Webber AP, et al. Randomized, controlled trial of a nonpharmacological intervention to improve abnormal sleep/wake patterns in nursing home residents. J Am Geriatr Soc 2005; 53:803.
  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.
  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 24.0