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doi:10.1111/psyg.12069
REVIEW ARTICLE
Sleep disturbances and dementia
Gabriele CIPRIANI, Claudio LUCETTI, Sabrina DANTI and Angelo NUTI
Division of Neurology, Versilia Hospital, Lido di
Camaiore, Italy
Correspondence: Dr Gabriele Cipriani MD, U.O. di
Neurologia, Ospedale della Versilia, via Aurelia 335,
55043 Lido di Camaiore, Lucca (Lu), Italy. Email:
cprgrl@gmail.com
Received 17 February 2014; revision received 15 August
2014; accepted 18 August 2014.
Key words: Alzheimer’s disease, dementia with
Lewy bodies, dementia, frontotemporal dementia,
sleep disorders.
INTRODUCTION
Sleep is a complex phenomenon that is rooted in
neurologic function. It is an active process generated
and modulated by a complex set of neural systems
located mainly in the hypothalamus, brainstem, and
thalamus. Sleep serves a restorative function in the
brain and has a critical role in cognitive functions.
Fortunate are those who rise out of bed to greet the
morning light well rested with the energy and enthu-
siasm to drive a productive day.1 Disturbed sleep can
mean different things to different people. Nearly half of
older adults report difficulty initiating and maintaining
sleep. Sleep decreases physiologically in quantity
and quality with age,2,3 and insomnia and excessive
daytime sleepiness are frequently reported in the
elderly.4 Sleep becomes more fragmented as we age,
with more night-time awakenings and greater ten-
dency for daytime sleep.5 Comorbid insomnia and
other sleep disturbances are common in patients
with neurodegenerative disorders, such Alzheimer’s
disease (AD) and other dementing disorders. Further-
more, studies of incident dementia suggest that sleep
problems increase the risk of dementia.6–8
EPIDEMIOLOGY
Not all dementia patients develop sleep problems.
According to Guarnieri et al.,9 individuals suffering
© 2014 The Authors
Psychogeriatrics © 2014 Japanese Psychogeriatric Society
PSYCHOGERIATRICS 2014; ••: ••–••
Abstract
Sleep is a complex behavioural state, the ultimate functions of which remain
poorly understood. It becomes more fragmented as we age, with more
night-time awakenings and greater tendency for daytime sleep. The magni-
tude of disordered sleep among individuals affected by dementia has been
clearly demonstrated, and disturbed sleep is a major clinical problem in
dementia. Comorbid insomnia and other sleep disturbances are common in
patients with neurodegenerative disorders, such Alzheimer’s disease and
other dementing disorders. How and when sleep problems manifest them-
selves can depend on the type of dementia involved as well as the stage of the
dementia. However, differences in sleep pattern presentation show more
variation during the initial stages of dementias than they do during the later
stages. Effective, pragmatic interventions are largely anecdotal and untested.
from dementia with Lewy bodies (DLB) and Parkin-
son’s disease (PD) with dementia have the highest
frequency of occurrence of any sleep disturbances,
with 90% of patients affected. The same authors
observed that insomnia frequency was identical in AD
and frontotemporal dementia (FTD) patients but was
about 2.5 and 1.5 times more frequent in vascular
dementia (VaD) and DLB/PD with dementia patients,
respectively. Nocturnal and daytime sleep distur-
bances are common in persons with AD, affecting up
to 44% of patients in clinic and community-based
samples.10,11 Using logistic regression analyses,
McCurry et al. observed that the factors most strongly
associated with night awakenings among patients
with AD were male gender, greater memory problems,
and decreased functional status.10
DISORDER OUTCOMES
Sleep disturbances negatively affect patients’ quality
of life and functional abilities,12 and they are associ-
ated with a greater risk of psychiatric symptoms.13
Poor sleep among persons with AD may lead to
increased daytime irritability and decreased attention,
motivation, and cognitive performance.14,15 Further-
more, poor sleep results in an increased risk of sig-
nificant morbidities and even mortality in demented
patients.16 In fact, sleep problems, or more specifi-
1
G. Cipriani et al.
cally, sleep debt, may represent one of the biological
pathways associated with sympathovagal imbalance
and elevated heart rate, leading to early mortality in
middle-aged subjects.17 Also, the rate of falls in older
persons with disordered sleep has been shown higher
than in healthy older persons.18
In addition to being prominent in neurodegenerat-
ive diseases, sleep disturbances could exacerbate a
fundamental process leading to neurodegeneration:
researchers found a relationship between sleep depri-
vation for just 3 weeks and accelerated development
of amyloid plaques (aggregation of extracellular
amyloid-β, which is thought to play a major part in the
pathogenesis of AD) in the brains of lab mice.19
When patients with long-term neurological ill-
nesses have disrupted sleep, this becomes a
problem, not only for the patient, but also for their
carers. Nocturnal sleep disruption is reported as a
major source of caregiver physical and psychological
burden.20 In some cases, caretakers may even
develop clinical depression as a result.21 Furthermore,
sleep disturbances are often the catalyst and the
primary reason for institutional care.22–24 Institutional-
ization has been shown to exacerbate sleep–wake
disruption,25 and to increase the speed of deteriora-
tion.26 Even in nursing homes, circadian rhythm dis-
turbances in AD patients can be disruptive for the
staff. In addition, caregivers experiencing emotional or
mental strain in conjunction with their caregiving role
have been reported to have an increased risk of mor-
tality when compared with non-caregiving controls.27
AETIOLOGY
The origin of sleep disorders in dementia is usually
multifactorial, resulting from pathophysiological
changes associated with the disease itself and envi-
ronmental factors.28 For example, in a nursing home,
noise and light exposure occur intermittently through-
out the night and contribute to sleep disruption.29
Other factors involve medical or psychiatric morbidity.
Medications used to lessen the negative behavioural
symptoms of dementia and to slow disease progres-
sion are often associated with side effects that nega-
tively affect sleep and wakefulness. It is also known
that longer periods in bed are associated with more
fragmented sleep;30 therefore, the chronic bed rest
that often characterizes the routine care of AD
patients, particularly patients at more advanced
stages, may in itself contribute to insomnia.31 It is
2 © 2014 The Authors
highly plausible that the diffuse brain damage that
characterizes dementia might extend over the cogni-
tive brain areas to involve the neural networks that
control sleep function (i.e. the anterior hypothalamus,
reticular activating system, suprachiasmatic nucleus,
and pineal gland).32 The hypothalamic suprachias-
matic nucleus (SCN) is the central biological clock of
the brain; it generates and synchronizes the overt
biochemical, physiological, and behavioural rhythms
throughout our body.33 It is thought to induce a single
circadian oscillation in mammals.34 The SCN has input
pathways that link it to the retina, limbic forebrain,
other hypothalamic nuclei, the raphe nuclei, and
reticular formation, and it also responds to various
hormones. Light entering the retina travels along the
optic nerves to the SCN, which triggers the pineal
gland to stop producing the neurohormone melatonin,
an essential component in sleep; its production is
highest during the night, when light stimuli are minimal
or absent. Disruptions anywhere along this pathway
can cause disruptions in the circadian rhythm and,
ultimately, sleep disturbances.35 Dementia patients
have been noted to have abnormalities in their
rhythms of melatonin secretion.36 This dysfunction
has been noted not only in patients with clinical diag-
nosis of AD,37 but it has also been confirmed after
post-mortem analysis. The observed functional dis-
connection between the SCN and the pineal gland
from the earliest AD stage onwards seems to account
for the pineal clock gene and melatonin changes, and
it underlies circadian rhythm disturbances in AD.38
Though not clear, genetic risk factors, such as in AD
patients who are negative for the APOε4 allele, have
also been implicated in the development of sleep
problems.39 There have been few studies of sleep
per se in relation to apolipoprotein E status, and the
findings are somewhat fragmentary. According to
Yesavage et al.,40 apolipoprotein E status was associ-
ated with the progression of sleep–wake disturbances
in AD. They observed a greater deterioration on sleep
parameters in patients negative for the ε4 allele.
SLEEP DISTURBANCES AND
DEMENTIA SUBTYPES
Sleep disorders seem to be different in each form of
dementia, and this may be a consequence of how the
brain’s varying pathological involvement character-
izes each type of dementia.41–43 However, few studies
have compared the presence of disturbed sleep
Psychogeriatrics © 2014 Japanese Psychogeriatric Society

between neurodegenerative conditions. How and
when sleep problems manifest themselves can
depend on the type of dementia involved as well as
the stage of dementia; differences in sleep pattern
presentation show more variation during the initial
stages of dementia than they do during the later
stages. The pathology of AD (amyloid-β accumulation
in the brain) emerges prior to any symptoms, with the
first identifiable changes occurring ∼10–15 years
before cognitive symptoms. Changes in sleep seem
to precede the onset of cognitive symptoms in
patients with AD, and the further decline of sleep
quality and/or circadian function parallels both cogni-
tive dysfunction and the progression of AD pathology.
This is consistent with the finding that brain regions
involved in sleep and circadian control are affected
early in the pathogenesis of the condition.44 In a
population-based sample of AD, the most common
sleep-related behaviour problems reported by care-
givers were sleeping more than usual (40%) and
awakening early (31%), whereas being awakened at
night (24%) was the most distressing problem for
caregivers.10 Nocturnal sleep disturbance in AD
patients is often accompanied by increased daytime
napping,45 frequently in direct association with the
extent of dementia.46,47
DLB is a common form of dementia in old age,
sharing clinical and pathological features with both
AD and PD. Sleep profiles in DLB differ from those
in AD. Both groups suffer from sleep problems,
but DLB patients seem to suffer from more overall
sleep disturbance. Whether synucleinopathies or
amyloidopathies are the neurobiological substrates
for the preferential association of sleep disturbance
remains unknown, but they are thought to involve the
primacy of brainstem degeneration in parkinsonian-
like conditions.48,49 DLB patients have a greater ten-
dency to fall asleep at inappropriate times during the
day and to also have more night-time sleep distur-
bances.50 Ferman et al. found characteristics to sig-
nificantly differentiate AD from DLB.51 Among the
composite features, they included daytime drowsi-
ness and lethargy and daytime sleep of 2 h or more.
Rapid eye movement sleep behaviour disorder
(RBD) occurs frequently in patients with α-synuclein
pathology, including DLB, PD, and multiple system
atrophy.52 RBD is characterized by repeated episodes
of arousal during sleep associated with vocalization
and/or complex motor behaviours, which may be suf-
© 2014 The Authors
Psychogeriatrics © 2014 Japanese Psychogeriatric Society
Sleep disturbances and dementia
ficient to result in injury to the individual or bed
partner. Affected patients have excessive motor activ-
ity such as punching, kicking, or crying out in asso-
ciation with dream content.53 Most patients view their
dreams as nightmares, and the dream content often
involves insects, animals, or people chasing or attack-
ing them, their relatives, or their friends.52
In idiopathic RBD, the risk of developing neuro-
degenerative disease is substantial. The interval
between RBD onset and disease onset averages
10–15 years, suggesting a promisingly large window
for intervention into preclinical disease stages.54
Among the types of sleep disorders that patients with
PD can experience (insomnia, parasomnias, sleep
fragmentation, increased daytime drowsiness),55 there
is particular interest in impairments associated with the
rapid eye movement (REM) phase. Dementia is seen in
40–70% of PD patients, and it typically occurs 10 years
or more after the initial motor signs. Sleep disorders
during the REM phase may be combined with cognitive
impairments or precede their development. Marion
et al. reported a study of 65 patients with PD compli-
cated and not complicated by dementia and found that
77% of patients with dementia had sleep impairments
during the REM phase, while behavioural impairments
were present in only 27% of patients without demen-
tia.56 Although RBD secondary to a neurodegenerative
disease is commonly associated with synucleopathies
(PD, DLB, and multiple system atrophy), it has also
been reported in patients with AD.53
In 2012, RBD was described in a patient with
FTD for the first time.57 Anderson et al. first demon-
strated significant sleep–wake disturbance in non-
institutionalized FTD patients, which differed from that
seen with AD. FTD subjects showed increased noc-
turnal activity and decreased morning activity com-
pared with controls, suggesting possible phase
delay.58 Sleep diary data confirmed decreased sleep
efficiency and decreased total sleep in all FTD
patients. The disturbances of sleep within the cohort
of FTD subjects were less marked than those with
moderately severe AD, but changes were present in
the FTD group as a whole rather than in only those
who had more marked cognitive and behavioural
impairment.
Huntington’s disease is an inherited neurodege-
nerative disorder characterized by behavioural and
cognitive disturbances and chorea. The sleep pheno-
type of Huntington’s disease includes insomnia,
3
G. Cipriani et al.
advanced sleep phase, periodic leg movements,
RBD, and reduced REM sleep. Reduced REM sleep
may precede chorea.59 Fuh et al. explored the
neuropsychiatric manifestations in patients with AD
and cortical and subcortical VaD.60 Patients with cor-
tical VaD had significantly higher mean composite
scores in the sleep disturbance domain. This is con-
sistent with a previous small group study showing that
VaD patients had more disrupted sleep–wake cycles
and decreased sleep quality compared with AD
patients.61 Cheng et al. investigated the association
between sleep disturbance, subcortical ischemic vas-
cular dementia, and white matter hyperintensity.62
They showed that manifestations of sleep disturbance
were significantly associated with white matter
hyperintensity severity, with most symptoms related
to daytime hypersomnolence. In their opinion, disrup-
tion of the frontal–subcortical neuronal circuit might
play a role in sleep disturbance in patients with
subcortical ischemic vascular dementia.
Fatal familial insomnia is an inherited (autosomal
dominant) prion disease that was originally described
in 1986.63 It is linked to a mutation at codon 178 of the
prion protein gene; it is clinically characterized by a
disordered sleep–wake cycle, dysautonomia, demen-
tia and motor signs, and is pathologically character-
ized by preferential thalamic degeneration.64 Patients
appear apathetic and unable to pay sustained atten-
tion to their surroundings. When not stimulated, they
tend to become sleepy and manifest recurrent
behavioural episodes mimicking a dream (oneiric
stupor). The insomnia is not the trivial difficulty in
initiating or maintaining sleep, but rather a severe,
persistent, and complete disorganization of sleep
cycles and a drastic reduction in total sleep time.65
Death occurs after a disease duration of 7–36
months.66
PSYCHOPATHOLOGY AND SLEEP
DISORDERS IN DEMENTIA
The influence of sleep problems on the behavioural and
psychological symptoms of dementia in AD has also
been studied. Depressive symptoms are common in
older adults, and insomnia is 2.5 times more frequent
in older adults with depressed mood.67 Research
has confirmed the association between depression,
depressive symptoms, and sleep disorders in persons
with dementia.9 One study concluded that sleep dis-
turbance is a predictive factor of depressive symptoms
4 © 2014 The Authors
in AD,68 and another study revealed an association
between apathy and sleep problems in AD.69 The
co-occurrence of sleep complaints in adults without
dementia who have anxiety disorders is well known.
McCurry et al. provided information about the relation-
ship between anxiety and night-time awakenings in a
community-residing sample of individuals with AD. 70 In
that study 56% of patients showed symptoms of
anxiety, and 29% awakened their caregiver at least
once per night during the past week. Moran et al.
showed that sleep disturbance in AD is associated with
other behavioural symptoms, notably aggressive-
ness.71 In line with previous results,72,73 García-Alberca
et al. demonstrated that sleep disturbances are also
significantly associated with daytime behavioural dis-
turbances, namely aberrant motor behaviour and
disinhibition.74 Findings suggest that night-time sleep
is important for cognitive function and for behavioural
and psychological symptoms of dementia in AD, and
that sleep problems should be considered when treat-
ing AD patients because their treatment might improve
cognitive function as well as behavioural and psycho-
logical symptoms of dementia.75
ASSESSMENT AND MANAGEMENT
The goal of managing sleep disturbance in dementia
should be to improve both night-time sleep and
daytime functioning. Clinical assessment of individu-
als with sleep disturbances must always include
screening for secondary causes, including medical
and psychiatric conditions (e.g. depression) and
medication side-effects, and for specific sleep disor-
ders. For instance, sleep problems have been related
to physical disabilities, respiratory symptoms, cardio-
vascular problems such as hypertension and cardiac
insufficiency,76 and decreased immune functions.77 If
a patient has a psychiatric disorder or comorbid
causes, the disorder or cause should be treated. If
sleep disorder is related to medication or drug abuse,
the offending medication or drug must be slowly
tapered and withdrawn.
An objective baseline measure of a patient’s sleep
disturbance may be helpful in identifying specific
target areas and gauging the efficacy of a proposed
intervention. Tractenberg et al. proposed an instru-
ment to assess symptoms of sleep disturbance and
disorder, the Sleep Disorders Inventory.78 It is an
expanded version of an item from the Neuro-
psychiatric Inventory that describes the frequency,
Psychogeriatrics © 2014 Japanese Psychogeriatric Society

severity, and caregiver burden of sleep-disturbed
behaviours during a period prior to assessment.79 The
Sleep Disorders Inventory covers a wide range of
sleep behaviours and provides information indepen-
dent of sleep time and sleep quality ratings kept in a
diary by caregivers.
Treatment should start with behavioural therapy
and, if indicated, should be combined with
pharmacologic therapy.
Non-pharmacologic strategies
It seems that behavioural interventions pose a
minimal risk of adverse side-effects to patients and
should be considered the first line of therapy for sleep
disturbance in demented patients. Multifaceted
behavioural strategies for improving sleep in patients
with dementia have been recommended, but currently
there is a paucity of methodologically rigorous
research in the area of non-pharmacological sleep
interventions for persons with dementia. Many
behavioural treatments for insomnia, including stimu-
lus control, sleep restriction, progressive muscle
relaxation, biofeedback, sleep hygiene education,
paradoxical intention, and multicomponent cognitive-
behavioural therapy, are known to be effective with
older adults.80 Sleep hygiene practices to improve
sleep include establishing consistent daily times for
going to bed and arising from bed, establishing a
bedtime routine, and limiting napping to a brief time in
the morning or early afternoon.81
The American Academy of Sleep Medicine has pub-
lished practice parameters for the use of bright light to
treat sleep and circadian rhythm disorders.82,83 Lower
levels of light are associated with decreased amplitude
of the rest–activity cycle and more wakefulness at
night.84 The goal of light therapy is to expose the
patient to increased amounts of natural or artificial
light. This added light exposure may provide input to
the SCN that will facilitate entrainment of the individu-
al’s circadian clock to the 24-h day. Studies examining
the efficacy of light therapy have had mixed results. AD
patients, whose sleep–wake and rest–activity rhythms
are even more severely disrupted, responded well to
bright light treatment in many studies.85,86 However, no
response to bright light therapy in AD patients has
been reported by others.36,87
A report showed that acupuncture increases noc-
turnal melatonin secretion and reduces insomnia and
anxiety.88
© 2014 The Authors
Psychogeriatrics © 2014 Japanese Psychogeriatric Society
Sleep disturbances and dementia
Brown et al. provided a structured critical literature
review of the evidence for non-pharmacological inter-
ventions to reduce disordered sleep in persons with
dementia, and they concluded that there is a paucity
of conclusive research for non-pharmacological sleep
interventions for persons with dementia.89 Most of the
evidence about effective interventions is anecdotal
and untested.
Pharmacologic interventions
There is a full range of medications used to treat sleep
disorders, each with particular benefits and potential
for harm. Melatonin is synthetized in pineal cells, and
its synthesis and release are regulated by seasonal
fluctuations in the length of the day. Light exerts an
inhibiting effect. Several studies have showed that
melatonin levels are diminished in AD patients com-
pared to age-matched control subjects.90–92 It has
been suggested that a deficiency of this hormone in
the cerebrospinal fluid is critical for the development
of AD because an inadequate concentration of
melatonin allows production of free radicalsm which
can damage neurons.93 Singer et al. found that low-
dose melatonin (0.5 mg) had a robust effect relative to
placebo in two of five AD subjects monitored for a
2-week treatment period by wrist actigraphy,94 but
a follow-up study employing more subjects and a
longer monitoring period failed to find such an effect.95
Large interindividual differences between patients
suffering from a neurodegenerative disease are not
uncommon and can explain the erratic results seen
with melatonin in fully developed AD.96 It should be
also taken into account that melatonin, though having
some sedating and sleep latency-reducing properties,
does not primarily act as a sleeping pill; it acts mainly
as a chronobiotic.96 Ramelteon, a melatonin receptor
agonist, has high affinity for the melatonin (MT) recep-
tors MT1 and MT2. It acts on the MT1 and MT2 recep-
tors to stimulate the action of melatonin to induce and
shorten sleep latency.97 The subjective efficacy of
ramelteon was evaluated in clinical trials consisting of
829 elderly outpatients with chronic insomnia; 701
patients (128 patients discontinued) were treated for 5
weeks with 4-mg and 8-mg ramelteon.98 Patients in
both ramelteon groups reported significant reductions
in sleep onset latency and increases in total sleep
time.
In selected cases, treatment with hypnotics has
been useful, but the evidence is limited and care
5
G. Cipriani et al.
should be undertaken in terms of chronic use, the
risk of falls, daytime sedation, and confusion.99
Benzodiazepines and non-benzodiazepine hypnotics
such as zolpidem and zaleplon are frequently pre-
scribed as short-term sleep aids in the general popu-
lation. Benzodiazepines are associated with increased
incidence of sedation, confusion, anterograde
amnesia, daytime sleepiness, and rebound insomnia.
Even where effective for increasing sleep,
benzodiazepines can only be a very short-term solu-
tion for occasional use in crises – for example, to give
a carer short break from sleep disturbance.100
Triazolam has a half-life of approximately 2 to 6 h, has
clinically significant metabolites, and is rapidly
absorbed. However, this medication has been asso-
ciated with severe rebound insomnia,101 and its short
action may not be optimal for treating early morning
awakenings seen in the elderly population.
Antipsychotic medication has often been used for
sleep in agitated dementia patients. However, it may
aggravate sleep–wake cycle disturbances in AD.102
Sleep aids with anticholinergic activity such
as tricyclic antidepressants may exacerbate the
cholinergic abnormalities inherent to AD and should
be avoided.11 Trazodone offers a dual action on sero-
tonin receptors by blocking serotonergic receptor 2A
and inhibiting serotonin reuptake. Its classic indication
is for depression, particularly when anxiety and
insomnia are also present. It is also widely used for
insomnia, although virtually no evidence-based data
support its efficacy with older adults.103 When the
risk-benefit ratio of trazodone is assessed, its side-
effect profile, which is much more significant than that
of conventional hypnotics, should be considered.104
Acetylcholinesterase inhibitors are widely used as
treatment for AD. There is considerable evidence that
the neurotransmitter acetylcholine plays a prominent
role in the activation of REM sleep. In addition, there
are reciprocal interactions between the cholinergic
system and REM facilitatory and inhibitory neurons
that maintain the cycle between REM and non-REM
sleep.105 Their cholinomimetic action has the potential
to influence sleep quality. In two placebo-controlled
clinical trials, donepezil was found to be associated
with elevated rates of insomnia based on adverse-
event reports.106,107 Furthermore, case studies have
reported nightmares to be a consequence of
donepezil treatment.108 In contrast, there has been no
evidence of night-time sleep-related adverse events in
6 © 2014 The Authors
pivotal trials of rivastigmine or galantamine.109–113 The
favourable profile in relation to sleep of galantamine
treatment at dosages of 16 or 24 mg/day may be
linked to the drug’s short half-life, dual mechanisms of
action including effects on both muscarinic and nico-
tinic receptors, and/or timing of administration.114
There are currently no clear recommendations for
the treatment of sleep impairments in PD with demen-
tia. Positive results have been obtained in the treat-
ment of daytime drowsiness in patients with PD using
the selective noradrenaline reuptake inhibitor
atomoxetine.115 Litvinenko et al. evaluated the effects
of treatment with galantamine.116 They found that it
produced significant improvements in the quality of
nocturnal sleep (restoration of its structure, decreased
fragmentation), with reductions in the severity of REM
sleep behaviour disorder, daytime drowsiness, and
cognitive deficits and hallucinations.
CONCLUSIONS
The magnitude and significance of the issue of disor-
dered sleep among elderly individuals in general and,
particularly, among those affected by dementia has
been clearly demonstrated. The aetiology of sleep
disorders is complex, involving multiple factors,
such as neurodegenerative changes in the brain,
environment, medical or psychiatric morbidity, and
medications used to treat chronic illnesses and
dementia-related behavioural symptoms. Sleep distur-
bance occurs in many forms of dementia, but it is
possible that certain forms of dementia may be more
likely to be associated with disturbed sleep. Addition-
ally, the disordered sleep of dementia patients can
compromise the overall health of caregivers, as their
sleep is likely to be negatively impacted.
Effective, pragmatic interventions are largely anec-
dotal and untested. Treatment should target both the
sleep problem and any comorbidities in order to opti-
mize the chance for improvement in quality of life and
functioning in older adults. There is a need for rigorous
scientific inquiry, coupled with tacit knowledge and
clinical experience regarding effective interventions,
to build strong evidence on the non-pharmacological
interventions for disordered sleep for persons with
dementia. Pharmacologic options should be used
judiciously, with potential side-effects seriously con-
sidered before hypnotic and psychotropic agents are
prescribed. When drug therapy is used, short-term
use is recommended.
Psychogeriatrics © 2014 Japanese Psychogeriatric Society

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