Archives of Gerontology and Geriatrics
31 (2000) 65 – 76
www.elsevier.com/locate/archger

Melatonin for treatment of sundowning in
elderly persons with dementia – a preliminary
study
Jiska Cohen-Mansﬁelda,b,*, Doron Garﬁnkelc, Steve Lipsona
a

Society for the Inhibition of Age-Related Processes Research Institute,
Hebrew Home of Greater Washington, 6121 Montrose Road, Rock6ille, MD 20852, USA
b
George Washington Uni6ersity Medical Center, Washington, DC, USA
c
Aging Research and Department of Medicine ‘E’, The E. Wolfson Medical Center, and Society for the
Inhibition of Age-Related Processes, Holon, Israel
Received 29 February 2000; received in revised form 5 June 2000; accepted 6 June 2000

Abstract
This pilot study investigated the impact of melatonin administration as a clinical intervention for improving sleep and alleviating sundowning in 11 elderly nursing home residents
who suffer from dementia. Melatonin is a hormone produced and secreted by the pineal
gland in response to darkness, which plays a major role in the induction and regulation of
sleep. Melatonin production decreases with age. Age-related sleep disorders are frequently
associated with disruption of circadian cycle rhythms, and sometimes with ‘sundowning’.
Sundowning refers to the manifestation of agitation and/or confusion in the evening hours.
Agitation has been linked to sleep disorders. Analysis revealed a signiﬁcant decrease in
agitated behaviors in all three shifts, and a signiﬁcant decrease in daytime sleepiness. There
was a nonsigniﬁcant decrease in latency (time to fall asleep) during the evening shift and no
signiﬁcant changes were reported in night-time sleep ratings. The results of this study are
important, because ﬁnding ways of decreasing sundowning in elderly persons may improve
their well being, alleviate the burden of the caregivers, and even enable caregiving in a less
restrictive environment. © 2000 Published by Elsevier Science Ireland Ltd.
Keywords: Melatonin; Agitation; Sundowning; Behavior problems in dementia

* Corresponding author. Tel.: +1-301-7708453; fax: + 1-301-7708455.
E-mail address: cohen-mansﬁeld@hebrew-home.org (J. Cohen-Mansﬁeld).
0167-4943/00/$ - see front matter © 2000 Published by Elsevier Science Ireland Ltd.
PII: S0167-4943(00)00068-6

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1. Introduction
The present study was undertaken in order to evaluate the possible therapeutic
effect of exogenous melatonin on sundowning, the agitated behavior manifested
during the evening hours, in a population of demented, elderly nursing home
residents.
Agitation refers to inappropriate verbal, vocal or motor behavior, which is not
explained by apparent needs or by confusion per se (Cohen-Mansﬁeld and Billig,
1986). Agitation is not a diagnostic term but is rather used by clinicians for a group
of symptoms which may reﬂect an underlying disorder. Whereas the term ‘disruptive behaviors’ refers to agitated behaviors, we prefer ‘agitation’ because this term
is more commonly used by professionals involved in long-term care for elderly
individuals. Agitation represents a major problem for elderly persons and for their
caregivers (Teri et al., 1988; Hamel et al., 1990). It affects the quality of life of
elderly persons in the community, their likelihood of entering a long-term care
facility and their speciﬁc needs in such a facility. Some of the practices currently
employed to deal with agitation in nursing homes residents include psychotropic
medication, physical restraints, a high ratio of staff to residents and special
environmental designs.
Although agitated behaviors are frequently considered as one entity by
caregivers, our previous research indicated that these behaviors differ in their
clinical manifestations and signiﬁcance. At least three main subgroups of behaviors
can be deﬁned separately: verbally agitated behaviors such as constant repetitive
talk or complaining; physically nonaggressive behaviors such as aimless wandering
or inappropriate disrobing; and aggressive behaviors such as hitting or kicking
(Cohen-Mansﬁeld et al., 1989a). All types of agitation are related to cognitive
impairment, though they peak at different levels of cognitive decline (CohenMansﬁeld et al., 1995a).
The relationship between agitation and sleep needs to be examined within the
context of the well-documented age-related changes in sleep patterns in the elderly
(Miles and Dement, 1980; Spiegel, 1981; Zepelin, 1983; Bliwise, 1993). Sleep
disturbances in the elderly have been linked to cognitive impairment (Loewenstein
et al., 1982). Sleep disturbances in elderly persons with Alzheimer’s disease include
fragmented sleep with frequent awakenings, reduced stage three (NREM) non rapid
eye movement and (REM) rapid eye movement sleep, and no stage four NREM
sleep (Prinz, 1982a; Prinz et al., 1982; Allen et al., 1983; Vitiello et al., 1990).
Several studies have shown a relationship between agitation and sleep in elderly
persons (Cohen-Mansﬁeld and Marx, 1990; Cohen-Mansﬁeld et al., 1995b). In
general, increased levels of agitation are observed along with an increased incidence
of sleep disturbances (e.g., frequency of awakenings, late sleep onset times, early
wake-up time). Furthermore, agitated behaviors may be exacerbated by fatigue
(Cohen-Mansﬁeld et al., 1995b).
The correlation between agitation and sleep disturbances may explain the related
concept of sundowning. This concept indicates episodes of agitation which are more
frequent and/or severe in the evening hours (Cohen-Mansﬁeld et al., 1989b; Bliwise,

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67

1993, 1994; McGafﬁgan and Bliwise, 1997). The sundowning syndrome is associated with increased burden on caregivers because it occurs during the hours in
which caregivers are least available, when family caregivers are tired and ready to
rest, and when institutional caregiving staff are at the lowest stafﬁng levels.
Therefore, if a phaseshift of this behavior is induced, it would alleviate the burden
and cost the caregivers.
Sundowning is associated with increased daytime sleep and disrupted night sleep
(Hess, 1997). This phenomenon may be related to dysfunction of circadian rhythmicity (Okawa et al., 1991), which may, in turn, be secondary to either spontaneous
or induced awakening from sleep. Alternatively, circadian changes in both sleep
and behavior may be related to a primary defect in translating the external
light/dark to the internal sleep/wake cycles.
Melatonin (5-methoxy-N-acetyltryptamine) is a hormone secreted principally by
the pineal gland in response to darkness under normal environmental conditions
(Arendt, 1988; Geoffriau et al., 1998; Pierpaoli, 1998). Melatonin affects sleep onset
in humans by its synchronizing effect on the internal biological clock (Arendt, 1988;
Dawson & Encel, 1993; Gross & Gysin, 1996). Endogenous serum melatonin levels
are usually lower in older people than in younger adults; however, serum melatonin
levels induced by low oral doses of exogenous melatonin are higher and more
variable in older adults as compared to young adults (Zhdanova et al., 1998).
Several studies have demonstrated that melatonin can improve sleep and affect
the circadian rhythm in humans, though the results are not unanimous. Okawa et
al. (1998) found that 1 – 3 mg of melatonin given before sleep, corrected circadian
rhythm sleep disorders in over half (six out of 11) of the patients (eight males and
three females aged 16 – 46). In a series of studies with young adults (Zhdanova et
al., 1995, 1996, 1998), low oral doses of melatonin (0.3 or 1.0 mg) were found to
decrease sleep onset latency and latency to stage two sleep. In a 16-day trial, Singer
et al., (1995a) did not ﬁnd any effect of 0.2 mg sustained release melatonin on
healthy elderly persons with no sleep disorders; however, they did ﬁnd modest
improvement in sleep efﬁciency and wake after sleep onset (WASO) in eight healthy
elderly persons without sleep disorders when using 50 mg dose of melatonin for 16
days (Singer et al., 1995b). Effects were more pronounced during the last days of
trial than during the ﬁrst days. Haimov et al. (1995) investigated the effect of
melatonin administration in melatonin-deﬁcient elderly insomniacs. They found
that a 1 week treatment with 2 mg sustained-release melatonin was effective for
sleep maintenance, while sleep initiation was improved by regular melatonin. Both
sleep maintenance and initiation were improved by prolonged (2 months) administration of 1 mg sustained release melatonin. Garﬁnkel et al. (1995) found that
administration of 2 mg controlled release melatonin tablets improved sleep quality
in community-dwelling elderly persons who had decreased endogenous melatonin
production and suffered from sleep problems. Similar beneﬁcial effects were found
in elderly insomniacs who had been chronically treated with benzodiazepine (Garﬁnkel et al., 1997). A review of the use of controlled-release melatonin for insomnia
in elderly people is provided in Zisapel and Garﬁnkel (1998).

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Disruption of the circadian rhythm in dementia (Sloan et al., 1996) and melatonin’s efﬁcacy in resetting the circadian clock, suggest that melatonin may have
beneﬁcial effects in patients with dementia who suffer from this dysrhythmicity and
to their caregivers. Those experiencing sundowning would probably be the most
likely to beneﬁt from melatonin. One should remember, however, that the exact
nature and etiology of sundowning are far from being clear. Even the signiﬁcance
of sundowning in contrast to morning-time agitation has been questioned (CohenMansﬁeld et al., 1989b). Two plausible alternative explanations are that (1)
sundowning is agitation induced by fatigue in patients who have difﬁculty sleeping,
or (2) sundowning involves evening time agitation caused by other reasons which
occurs in the evening because the older person has been awake for several hours. If
the patient was to sleep at night and spend more time awake during the day, this
agitation might have been manifested during the day. The ﬁrst model would suggest
that if melatonin improves the quantity and quality of sleep during the evening and
night hours, the person would be less tired, and overall agitation would decrease.
According to the latter model, if evening and night-time sleep would improve
because of melatonin administration, agitation during that time would decrease
because the person would be asleep. However, agitation during the daytime would
increase because of decreased sleep-time during the day, and more time available to
manifest agitation.
This pilot study investigated the effect of melatonin as a clinical intervention for
improving sleep and alleviating sundowning in institutionalized elderly persons who
suffer from dementia. Our hypotheses were that with the administration of melatonin before night sleep time:
1. Sleep would occur more during night time and less during day time hours.
2. Agitated behaviors would decrease in frequency, at least during the evening and
night shifts.
3. Agitated behaviors would shift more to daytime hours.

2. Methods

2.1. Participants
Participants were 11 nursing home residents of a large suburban nursing home.
Eight of the participants were female. The mean age was 85, with a range of 79–92
years. Five of the participants were widowed, ﬁve were married, and one was single.
All suffered from cognitive impairment according to the minimum data set (Hawes
et al., 1995; Frederiksen et al., 1996): Four were rated as ‘modiﬁed independence’,
ﬁve were rated as ‘moderately impaired’, and two were rated as ‘severely impaired’.

2.2. Inter6ention
Participants received a tablet containing melatonin every evening for three weeks
as part of their medical treatment. The commercially available tablets of oral

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69

melatonin were supplied to the residents by the nursing home pharmacy. Most
residents received 3 mg of melatonin per evening; two residents received a reduced
dose of melatonin, the ﬁrst was started on 1 mg which was increased to 3 mg after
2 days, and the other received 3 mg melatonin only every other evening, alternating
with 5 mg Zolpidem Tartrate. Residents received their dose of melatonin approximately 1 h prior to their planned bed time with the exception of one resident for
whom the time was changed to 18:00 h on the 3rd week of melatonin
administration.

2.3. Design and procedure
The study design was an open label clinical trial undertaken to examine safety,
and to obtain preliminary data on melatonin’s effectiveness. The research staff
members were notiﬁed by the physicians on their intent to prescribe melatonin to
speciﬁc residents for the treatment of sleep disturbances and/or evening-time
agitation.
In order to explore the impact of melatonin, nursing staff members on all three
of the 8 h shifts (7:00 – 15:00, 15:00–23:00, 23:00–7:00 h) were asked to rate the
sleep and agitation of each resident. Ratings were completed independently by a
member of the nursing staff who was most closely involved with the resident at the
end of each nursing shift. They were asked to rate the resident during a baseline
week, then during the 3 weeks of melatonin administration.

2.4. Assessments
2.4.1. Agitation
Agitation as assessed by the short form Cohen-Mansﬁeld Agitation Inventory
(CMAI). The inventory consists of 14 agitated behaviors, each rated on a ﬁve-point
scale of frequency (‘one’ indicates that the resident never engages in the speciﬁc
agitated behavior and ‘ﬁve’ that the resident manifests the behavior on the average
of several times an hour) (Werner et al., 1994). Inter-rater reliability was assessed by
two independent nursing staff members, who rated 19 residents. The inter-rater
agreement rate was calculated two ways: It was 81.8% based on exact agreement,
and 92.3% when based on a 0- or 1-point discrepancy (Werner et al., 1994). Based
on previous ﬁndings (Cohen-Mansﬁeld et al., 1995c), four syndromes were used:
Physically aggressive behaviors (PAG) (such as hitting and kicking), physically
nonaggressive behaviors (PNAB) (such as pacing, disrobing and handling things
inappropriately), verbally agitated behaviors (VNAB) (such as repetitious vocalizations and complaining), and verbally aggressive behaviors (VAG) (such as cursing
or screaming). For each syndrome of agitation, an index estimating the overall
frequency of occurrence of the syndrome was calculated. The procedure for
calculating the index involved the following stages: First, we determined the most
frequently occurring behavior of those included in the syndrome; when two or more
behaviors occurred at a low frequency, we speciﬁed that a behavior occurred at the
next higher level. For example, if two physically aggressive behaviors occurred at a

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frequency of ‘several times a week,’ this was equated to a score of a single behavior
occurring ‘once or twice a day’. The highest score between any single behavior and
the aggregate scores formed an index of the syndrome that was used in subsequent
analyses.

2.4.2. Sleep
Sleep ratings were adapted from the nurses’ ratings of sleep patterns questionnaire (NRSPQ), which utilizes independent raters (nursing staff). The nursing staff
are required to routinely check on the residents every 2 h (Cohen-Mansﬁeld and
Marx, 1990). The instrument measures the following dimensions of sleep: Number
of hours of sleep; latency-length of time to fall asleep; frequency of spontaneous
awakenings; length of average wake period; hour of awakening in the morning; and
external disruptions to sleep. In the adapted version, the following items were
included:
2.4.2.1. The night shift (23:00 – 7:00 h) sleep questionnaire tapped the following
dimensions of sleep. Latency-length of time to fall asleep (after retiring to bed). This
item was rated on the following scale: 0, was asleep at the beginning of the shift; 1,
fell asleep immediately; 2, fell asleep in less than 30 min; 3, fell asleep between 30
and 60 min; 4, fell asleep between 1 and 2 h; and 5, took more than 2 h to fall
asleep; 6, did not sleep during shift.
Frequency of spontaneous awakenings. How often had the participant spontaneously woken up during the night. This was assessed using the following scale: 1,
never; 2, once; 3, several times; 4, awake most of the night; 5, did not sleep during
shift.
Length of average wake period. The participant’s average duration of wake
periods (spontaneous awakenings only) during the night was rated using the
following scale: 0, did not wake up; 1, less than 3 min; 2, from 3 to 15 min; 3, from
16 to 30 min; 4, from 31 to 60 min; 5, more than an hour; and 6, awake most of
the night.
The number of hours of sleep. The number of hours the resident slept during
each particular shift.
2.4.2.2. The e6ening shift (15:00 – 23:00 h) sleep questionnaire tapped the following
dimensions of sleep. Latency-length of time to fall asleep (after retiring to bed);
frequency of spontaneous awakenings; and length of average wake period. These
were rated in the same way as the night-time shift.
2.4.2.3. The daytime shift (7:00 – 15:00 h) sleep questionnaire tapped the following
dimensions of sleep. The hour at which each participant woke up in the morning.
Drowsiness of the participant. How frequently had the resident appeared
‘drowsy’ or sleepy during the day. This was rated on a six-point scale with one
indicating never, and six all or nearly all of the time.
Frequency of naps. How frequently had the participant fallen asleep during the
day. This was rated on a six-point scale with one indicating never and six all or
nearly all of the time.

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71

How long had the participant usually napped. The average duration of the
participants’ naps was rated on a ﬁve-point scale with one indicating less that 3 min
and ﬁve indicating more than an hour.

3. Results
No adverse effects were noted and no difﬁculty in procedures of handling the
melatonin were encountered. However, one resident was withdrawn from the study.
Prior to entering the study, this patient was severely agitated. During baseline, he
fractured his right shoulder. The staff tried to control his pain and agitation with
different medications but to no avail. His behavior included removing the arm
sling, bed alarm and night clothes. Therefore, only ten residents were available for
the hypothesis testing. During the study, the other participants did not have any
febrile or other acute diseases.
The testing of hypotheses is described below:
(i) With melatonin, sleep would occur more during night time and less during
day time.
Analyses involved paired t-tests comparing sleep variables during week 1 (baseline) to week 4 (after 3 weeks on melatonin). Results are presented in Table 1.
Generally, sleepiness during the daytime shift decreased signiﬁcantly but no signiﬁcant differences were found in evening and night-time sleep. There was a trend in
the hypothesized direction for latency to decrease, but this change was not
statistically signiﬁcant.
(ii) Agitated behaviors would decrease in frequency.
The change in the frequency of agitation manifested by the residents was
examined via paired t-tests comparing the levels of each syndrome of agitation
during the baseline week to that of the 4th week, following 3 weeks of melatonin
administration. The results are presented in Table 2. Reduction in the frequency of
agitated behavior was found in most indices: Five decreases were signiﬁcant at the
0.05 level, and nine at the 0.1 level, which was considered here because of the small
number of participants. Most impressive are the reductions in agitated behaviors
during the evening shift. Examining weekly changes for individual participants on
the evening shift, the following was noted: For physically nonaggressive behaviors
(PNAB), seven of the ten residents manifested such behaviors at baseline. Of these,
ﬁve manifested consistent decline after melatonin administration and two did not
show a consistent change. Out of the three who did not manifest any such behavior
at baseline, two remained the same throughout the follow-up period, and one
showed just a slight increase on week 4 from a rating of one to 1.2. The same ﬁve
residents who showed decreased PNAB also showed a decrease in verbally agitated
behaviors, as did another resident who did not change in his level of physically
nonaggressive behaviors. Concerning the other residents, two did not manifest any
verbally agitated behaviors during the trial and one showed some increase (this is
not the same individual as the one manifesting slight increase in physically
nonaggressive behaviors).

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72

As for the aggressive behaviors, only four patients showed any physically
aggressive behaviors at baseline and all exhibited a decrease in these manifestations
following melatonin administration. The other six did not manifest any such
behaviors before or throughout the trial. For verbally aggressive behaviors, the
results were less distinctive, with two residents showing consistent decreases, two
residents never manifesting the behaviors, and the other six ﬂuctuating during the
trial.
(iii) Agitated behaviors would shift more to daytime occurrence. This hypothesis
was not conﬁrmed. Daytime agitation did not increase. (Table 2.)

4. Discussion
The present pilot study suggests that melatonin can be administered safely to this
population of elderly residents with dementia. It also presents some promise for
melatonin’s utility in decreasing sundowning, the evening time agitation.
Table 1
Sleep scores (unless otherwise noted n =10)
Day shift
Variable

Week 1 index

Week 4 index

t-test value

P-value
(1-tailed)

How often resident appeared
drowsy*
How long resident napped*
How often resident napped*
Time resident awoke in the
morning*
E6ening shift
Variable

3.10

2.24

3.092

0.0075

2.67
2.80
6.69

2.00
1.88
6.62

2.317
2.856
0.470

0.0245
0.0105
0.326

Week 1 index

Week 4 index

t-test value

How long resident took to fall
asleep (Latency)
How often resident awoke
How long resident was awake
Night shift
Variable

4.47

3.86

1.280

P-value
(1-tailed)
0.117

3.39
4.23

3.36
4.04

0.047
0.290

0.482
0.389

Week 1 index

Week 4 index

t-test value

How long resident took to fall
asleep (Latency)
How long resident actually
slept
How often resident awoke*
How long resident was
awake*

1.03

1.17

0.305

P-value
(1-tailed)
0.384

6.24

6.24

0.008

0.497

1.66
1.16

1.96
1.85

1.203
0.986

0.132
0.177

* n= 9

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73

Table 2
Comparison of levels of agitation at baseline and at week 4 of melatonin administration via paired
t-tests of CMAI Index (n= 10).
Day shift
Variable

Week 1 index

Week 4 index

t-test value

P-value (1-tailed)

Pnab*
Pag**
Vnab***
Vag****
E6ening shift
Variable
Pnab*
Pag**
Vnab***
Vag****
Night shift
Variable
Pnab*
Pag**
Vnab***
Vag****

2.0500
1.4550
2.3600
1.8200

1.8517
1.1150
2.1350
1.5216

1.407
1.738
1.886
2.216

0.097
0.058
0.046
0.027

Week 1 index
1.9250
1.2000
2.3000
1.5617

Week 4 index
1.4633
1.0000
1.7483
1.3967

t-test value
2.338
1.809
2.201
0.858

P-value (1-tailed)
0.022
0.052
0.028
0.207

Week 1 index
1.4817
1.0200
1.4133
1.2000

Week 4 index
1.0200
1.0200
1.1117
1.1617

t-test value
2.663
0.000
1.370
0.260

P-value (1-tailed)
0.013
0.500
0.102
0.401

* pnab, physically nonaggressive behavior
** pag, physically aggressive behavior
*** vnab, verbally nonaggressive behavior
**** vag, verbally aggressive behavior (n = 10) all t-tests excluded participant number 10, as they only
completed through week 3 of the study

Contrary to our expectations, changes in sleep behaviors were not statistically
signiﬁcant during the evening and night shifts, but were statistically signiﬁcant
during the daytime shift. There are several possible explanations for this ﬁnding. It
is obvious that daytime staff have much more contact with residents and it is
possible that this contact allows them to provide a more accurate rating of the
amount of sleep during their shift. Given the short half-life of melatonin, the main
anticipated effect was related to decreased latency in the evening shift. Latency did
show a decrease in the anticipated direction, but it was not statistically signiﬁcant.
Utilization of more accurate sleep assessments (e.g., wrist actigraphy) and a larger
sample are needed in order to elucidate whether the administration of melatonin
has a signiﬁcant effect on evening and night sleep in this population.
The effect of melatonin administration on agitation is promising. Decreased
agitation scores were noted in all shifts and for all types of agitation. Our results
support the hypothesis that agitation is, in part, related to sleep quality and may be
increased by fatigue. Therefore, the decrease in fatigue which supposedly occurred
because of improved night sleep due to melatonin (albeit undocumented improved
sleep), might have resulted in decreased levels of agitation. The alternative hypothesis, according to which agitation would increase during the daytime because of
increased opportunities resulting from increased time awake, was rejected. Al-

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though results do suggest increased time awake during daytime, this time was
accompanied by decreased levels of agitation.
There was much variability among residents in their response to the melatonin.
One resident seemed to have an immediate response to melatonin, with a signiﬁcant
decrease in latency during the evening shift (average ratings of: 6.0, 5.4, 3.8, 3.6,
during the baseline and ensuing weeks, respectively). The number of hours asleep
during the night shift also increased signiﬁcantly (average ratings of: 4.4, 5.8, 7.5,
6.3, for baseline and 3 weeks of melatonin treatment). Similarly, the levels of
agitation decreased. In contrast, another resident did not show any decrease in
latency, nor consistent changes in the number of hours asleep during the night shift.
Although there were some decreases in physical types of agitation during the
daytime shift, there were no overall consistent changes in the manifestation of
agitation in that resident.
Several limitations of the study need to be explicitly stated. Obviously, the study
is limited in its scientiﬁc merit by being an open label trial rather than a
double-blind placebo controlled study. Mitigating this limitation is the fact that
staff members continued to assess agitation for the full 4 weeks. A placebo effect is
more likely to be evident during the 1st week and decline by the 4th week, yet
effects seemed to be manifested at the 4 week assessment. The study is also limited
by the small number of participants, reducing both the power of the study to obtain
signiﬁcant results and its generalizability. Sleep ratings by staff are far from being
the ideal objective method for sleep assessment. Monitoring residents every 2 h may
not provide sufﬁciently accurate data for the type of sleep assessment required,
which is supposed to characterize the sleep of a resident within a given night. On
the other hand, if the normal melatonin output proﬁle is disrupted in these patients,
3 weeks of melatonin therapy may not sufﬁce to reset their circadian rhythm to the
normal day/night cycle.
In contrast to sleep, assessment of agitation is likely to be more accurate, because
physically nonaggressive behaviors are most frequently manifested (e.g., pacing in
the corridors) where staff members are likely to encounter them. Similarly, verbal
and vocal agitation is heard even without a speciﬁc inspection of a resident.
Improvement of sleep for nursing home residents is essential for improving their
quality of life. To the extent that their agitation is a manifestation of discomfort
resulting from fatigue, improvement of such fatigue and on the ensuing agitation is
of major signiﬁcance to their well-being. Beyond the direct suffering of the elderly
patients themselves, sleep problems pose major burden to caregivers-both formal
and informal. For family caregivers caring for an older person at home, sleep
problems associated with agitation may impose such an impact on their daily lives,
that they may be forced to seek institutionalization for the older person. Any
alleviation of the evening/night-time agitation will decrease the burden for
caregivers and, when applied in the community, may also decrease
institutionalization.
We recognize that no accurate decisive conclusion can be drawn from our present
results. A larger, double blind placebo-controlled study for a longer period of time
and preferable with controlled release melatonin is necessary in order to examine

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75

the impact of melatonin on agitated behaviors. We do believe that the results
obtained in this study provide sufﬁcient evidence to warrant such a study.

Acknowledgements
The authors would like to thank Nicola Netto and Burt Feldman, M.D. for their
help in this project. This study was supported in part by grant K01AG00547 from
the National Institutes of Aging.

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