Context Insomnia is a prevalent health complaint in older
adults. Behavioral and pharmacological treatments have their benefits
and limitations, but no placebo-controlled study has compared their
separate and combined effects for late-life insomnia.
Objective To evaluate the clinical efficacy of behavioral and
pharmacological therapies, singly and combined, for late-life insomnia.
Design and Setting Randomized, placebo-controlled clinical trial,
at a single academic medical center. Outpatient treatment lasted 8
weeks with follow-ups conducted at 3, 12, and 24 months.
Subjects Seventy-eight adults (50 women, 28 men; mean age, 65
years) with chronic and primary insomnia.
Interventions Cognitive-behavior therapy (stimulus control, sleep
restriction, sleep hygiene, and cognitive therapy)
(n=18), pharmacotherapy (temazepam)
(n=20), or both (n=20) compared with
placebo (n=20).
Main Outcome Measures Time awake after sleep onset and sleep
efficiency as measured by sleep diaries and polysomnography; clinical
ratings from subjects, significant others, and clinicians.
Results The 3 active treatments were more effective than placebo
at posttreatment assessment; there was a trend for the combined
approach to improve sleep more than either of its 2 single components
(shorter time awake after sleep onset by sleep diary and
polysomnography). For example, the percentage reductions of time awake
after sleep onset was highest for the combined condition (63.5%),
followed by cognitive-behavior therapy (55%), pharmacotherapy
(46.5%), and placebo (16.9%). Subjects treated with behavior therapy
sustained their clinical gains at follow-up, whereas those treated with
drug therapy alone did not. Long-term outcome of the combined
intervention was more variable. Behavioral treatment, singly or
combined, was rated by subjects, significant others, and clinicians as
more effective than drug therapy alone. Subjects were also more
satisfied with the behavioral approach.
Conclusions Behavioral and pharmacological approaches are
effective for the short-term management of insomnia in late life; sleep
improvements are better sustained over time with behavioral
treatment.
Sleep disturbance
is a prevalent problem in late life. Between 12% and 25% of healthy
seniors report chronic insomnia, and these estimates are even higher
among older adults with coexisting medical or psychiatric
illness.1-4 In addition to normal age-related changes in
the physiological aspects of sleep, the increased incidence of health
problems and medication use, combined with lifestyle changes associated
with retirement, place older adults at increased risk for disrupted
sleep.5 Insomnia, the most common sleep disorder, may
involve trouble falling asleep, frequent or prolonged nocturnal
awakenings, or early morning awakenings with an inability to return to
sleep.6 Older adults report primarily, although not
exclusively, difficulty in maintaining sleep. Although not all sleep
changes are pathologic in late life,7,8 severe sleep
disturbances are associated with daytime fatigue and impaired
functioning, reduced quality of life, and increased health care
costs.9,10 When left untreated, chronic insomnia may
increase vulnerability to major depression2 and, among
older adults with cognitive impairments, may hasten nursing home
placement.11 Despite its high prevalence and negative
impact, less than 15% of individuals with chronic insomnia receive
treatment.4
When treatment is initiated, pharmacotherapy is the most common
method for insomnia management.3,12,13 Although short-term
use of hypnotic
medications may be useful and indicated for acute
insomnia,14,15 there is little information on long-term
efficacy or on whether changes in sleep are sustained when the
medication is discontinued. A meta-analysis16 of 22
placebo-controlled hypnotic trials (n=1894) concluded
that benzodiazepines and zolpidem produced improvements in sleep
latency, number of awakenings, total sleep time, and sleep quality.
However, median treatment duration was only 1 week and follow-up was
often limited to evaluating withdrawal effects 1 or 2 nights after drug
discontinuation. Thus, although the acute effects of benzodiazepine
receptor agents are well documented, controlled evaluations of hypnotic
effects beyond the acute treatment phase are warranted. Also, as older
adults consume a disproportionate number of hypnotic medications, often
for prolonged periods and despite being at greater risk for residual
daytime effects,4,15,17,18 additional studies of the short- and
long-term effects of hypnotics are particularly needed.
Several nonpharmacological interventions have been shown
effective for the clinical management of insomnia. Behavioral treatment
methods seek to change poor sleep habits, alter faulty beliefs and
attitudes about sleep, and promote better sleep hygiene practices. Two
meta-analyses19,20 of more than 50 treatment studies
(>2000 patients) concluded that behavioral interventions produce
improvements of sleep in about 70% to 80% of patients with primary
insomnia. With an average treatment duration of 5 hours, implemented
over a 4-week period, sleep latency and time awake after sleep onset
were reduced to near normative values (ie, <30 minutes). One
particular strength of behavioral therapies is that sleep improvements
are maintained over time. The efficacy of nondrug interventions has
also been documented for late-life insomnia. When older adults are
screened for other primary sleep disorders (eg, sleep apnea and
periodic limb movements), their treatment response is similar to that
of younger adults.21-25 Despite these promising results,
behavioral interventions remain underused in primary care
settings.26
Only 3 studies have directly compared the efficacy of behavioral and
pharmacological treatments for insomnia.27-29 These
preliminary studies have shown that drug treatment (triazolam in all 3)
produced faster improvements, while behavioral treatment yielded more
durable benefits. Behavioral and pharmacological treatments are not
mutually exclusive, and their combined use may prove the most
successful approach for persistent insomnia. The present study was
designed to evaluate the separate and combined effects of behavioral
and pharmacological treatments for insomnia in older adults. The main
objective was to evaluate which treatment or combination produces the
best short- and long-term outcomes on subjective and objective sleep
parameters.
Prospective subjects were recruited through newspaper
advertisements and letters to physicians. Inclusion criteria were (1)
age 55 years or older; (2) sleep-onset or maintenance insomnia, defined
as sleep-onset latency and/or wake after sleep onset longer than 30
minutes per night at least 3 nights per week; (3) insomnia duration of
at least 6 months; and (4) a complaint of at least 1 negative effect
during waking hours (eg, fatigue, impaired functioning, mood
disturbances) attributed to insomnia. Exclusion criteria were (1)
evidence that insomnia was directly related to a medical disorder or
adverse effects of medication; (2) presence of sleep apnea
(apnea-hypopnea index >15) or periodic limb movements during sleep
(myoclonic index with arousal >15); (3) regular use of a hypnotic
medication or other psychotropic medication with an inability or
unwillingness to discontinue medication; (4) currently in
psychotherapy; (5) presence of major depression or other severe
psychopathologic conditions based on a brief self-report screening
measure (ie, Brief Symptom Inventory30) and the Structured
Clinical Interview for DSM-III-R31; and (6)
cognitive impairment as suggested by a score lower than 23 on the
Mini-Mental State Examination.32 These selection criteria
are consistent with those of the International Classification of Sleep
Disorders33 and the Diagnostic and Statistical Manual
for Mental Disorders34 for primary and chronic
insomnia.
Prospective subjects underwent a multistep screening evaluation,
which consisted of (1) telephone screening and (2) a sleep history
interview, a psychological assessment, and a medical history taking
with physical examination. These evaluations were conducted
respectively by a board-certified sleep specialist, a clinical
psychologist, and by a physician. Team meetings were regularly held to
ascertain that subjects met the study criteria. Forty-eight persons of
the 163 who underwent step 2 evaluation were excluded because of
psychopathology (n=9), another suspected sleep disorder
(n=9), lack of interest or inability to avoid taking
sleeping medication prior to randomization (n=21),
medical problems (n=6), or not meeting criteria for
insomnia (n=3). One hundred fifteen individuals
underwent the final screening phase of polysomnography. After this
final evaluation, another 37 subjects were excluded owing to sleep
apnea (n=23), periodic limb movements during sleep
(n=6), a combination of these 2 conditions
(n=2), no evidence of insomnia (n=3),
or for other medical or psychiatric reasons or lack of interest
(n=3).
The remaining 78 subjects were randomly assigned to either
cognitive-behavior therapy (CBT, n=18), pharmacotherapy
(PCT, n=20), combined CBT and PCT
(n=20), or a placebo condition (n=20).
Of the 78 participants, 50 (64.1%) were women and 28 (35.9%) men,
with a mean age of 65 years (SD, 7 years). The average education
level was 14.4 years (SD, 2.5 years). All subjects were
community-dwelling residents; 70 (89.7%) were white, 7 (9%), black,
and 1 (1.3%), Native American; 53 (67.9%) were married, 37 (47.4%),
retired. Most (49; 62.8%) of the subjects reported mixed sleep-onset
and maintenance insomnia; 22 (28.2%) reported sleep maintenance
insomnia and 5 (6.4%) reported sleep onset insomnia only. The average
insomnia duration was 16.8 years (SD, 16.9 years) and 60 (76.9%) had
previously used sleeping medication. Table 1 presents illustrates data for demographic
and clinical variables. Figure 1
illustrates participant flow in the study protocol. All subjects
provided written informed consent prior to study
entry. The study protocol was approved by the institutional review
board of the Medical College of Virginia/Virginia Commonwealth
University.
All participants completed the same outcome measures, including daily
sleep diaries, polysomnography, and clinical rating scales. Subjects
receiving active or placebo medications completed the posttreatment
(end-of-treatment) assessment while they were still taking medication
(prior to tapering).
Sleep Diaries. Participants kept daily sleep diaries for at least 2 weeks prior to
treatment, during the 8 weeks of treatment, and for 2 weeks at each of
the follow-ups. Several parameters were monitored in the diaries (eg,
bedtime, arising time, sleep-onset latency, wake after sleep onset,
medication intake). The main outcome variables were wake after sleep
onset (amount of time awake from the initial sleep onset to the last
awakening), total wake time (summation of sleep-onset latency, wake
after sleep onset, and early morning awakening), total sleep time, and
sleep efficiency) ratio of total time spent asleep to the actual time
spent in bed and multiplied by 100). The subjects were instructed to
complete their diaries every morning at breakfast time and bring them
to each session during treatment; they were mailed in for follow-ups.
Although sleep diary data do not reflect absolute values obtained from
results of electroencephalography, they provide a reliable index of
insomnia35 and are used as standard outcome assessment in
insomnia research. In addition to allowing for prospective monitoring
of sleep in the subject's home environment and over extensive periods
of time, sleep diary data reflect an important dimension of chronic
insomnia, ie, the subjective perception of sleep.
Polysomnography. Subjects underwent 3 consecutive nights of sleep laboratory evaluation
both prior to (within 2 weeks) and at the end of treatment. Bedtime and
arising time in the sleep laboratory were within half an hour of the
subjects' typical sleep schedule. The polysomnographic montage
included electroencephalographic, electromyographic, and
electro-oculographic monitoring. Sleep stages, respiratory
disturbances, and limb movements were scored according to standard
criteria36 by an experienced technician who was blind to
subjects' condition. Respiration (air flow, tidal volume, and oxygen
saturation) and anterior tibialis electromyographic readings were
recorded during the first night to detect sleep apnea or periodic limb
movements. Outcome measures (wake after sleep onset, total wake time,
total sleep time, and sleep efficiency) were based on the average of
pretreatment nights 2 and 3 and posttreatment nights 5 and 6. To allow
for an adaptation to the laboratory, data from the first night of each
assessment phase were not used in computing baseline and posttreatment
means.
Clinical Outcome Ratings. The Sleep Impairment Index is a 7-item scale that yields a quantitative
index of insomnia severity; it was used as a collateral measure of
treatment outcome.6 Ratings on a 5-point scale were
obtained on the
perceived severity of sleep onset, sleep
maintenance, and early morning awakening problems; interference with
daytime functioning; noticeability of impairment caused by the sleep
problem; distress/concern caused by the sleep problem; and satisfaction
with current sleep pattern. A composite score was obtained by summing
the 7 ratings, and higher scores indicated more severe insomnia (total
range, 5-35). Several items were added to this scale at posttreatment
assessment and at follow-ups to assess overall degree of improvement,
treatment compliance, and satisfaction with the treatment received.
Parallel versions of the Sleep Impairment Index were completed by
subjects, significant others (eg, spouses), and by a clinician (before
and after treatment only). The Sleep Impairment Index has adequate
psychometric properties and has been shown sensitive to changes in
previous treatment studies of insomnia.24,25
A 4 (condition) × 2 (assessment) placebo-controlled randomized design
was used, with repeated measures on the second factor. After completing
baseline assessments, subjects were randomly assigned to 1 of 4
conditions: CBT (n=18), PCT (n=20),
combined (n=20), and placebo (n=20).
Because CBT treatment was provided in a group format, participants were
randomly assigned to conditions in clusters of 4 to 6 subjects at one
time. All treatments were administered based on a manual6
over 8 weekly outpatient therapy sessions. The PCT and placebo
conditions were administered in a standard double-blind fashion, and
the combined condition was blinded only for the medication component.
Due to the nonpharmacological nature of CBT, neither subjects nor
therapists were blinded to it.
Cognitive-Behavior Therapy. Subjects receiving CBT attended 8 weekly 90-minute therapy
sessions conducted in small groups of 4 to 6 individuals. Treatment
consisted of a structured, multifaceted intervention involving
behavioral, cognitive, and educational components that targeted
different facets of late-life insomnia.6 The behavioral
component incorporated sleep restriction therapy37 and
stimulus control procedures.38 Sleep restriction consists
of curtailing time in bed to the actual sleep time. For example, if an
individual reported sleeping an average of 6 hours per night out of 8
spent in bed during baseline assessment, the initial "sleep window"
prescribed for the first week of treatment was 6 hours. This sleep
window was gradually altered according to the subject's sleep
efficiency (ratio of total sleep time to time in bed) based on the
sleep diary data from the previous week. Allowable time in bed was
increased by 15 to 20 minutes when sleep efficiency exceeded 85%,
decreased by the same amount when sleep efficiency was lower than 80%,
and kept stable when sleep efficiency fell between 80% and 85%.
Implementation of these rules was flexible, and adjustments were made
on the basis of subjects' acceptance and willingness to comply. The
allotted time in bed was never less than 5 hours per night, regardless
of the subject's total sleep time from the week before. The stimulus
control procedures were designed to regulate the sleep-wake schedules
and to bring subjects to reassociate the bed/bedroom and bedtime
stimuli with sleep rather than with the frustration and anxiety
associated with lying in bed trying to sleep. These procedures are as
follows: (1) go to bed only when sleepy; (2) use the bed and bedroom
only for sleep and sex (ie, no reading, TV watching, or worrying in bed
or the bedroom during the daytime or at night); (3) get out of bed and
go to another room when unable to fall asleep within 15 to 20 minutes;
(4) repeat this step as often as necessary, either when trying to fall
asleep or to get back to sleep; and (5) arise at the same time every
morning regardless of the amount of sleep obtained the previous night.
Daytime napping was made optional during the initial sleep restriction
phase, as long as it was limited to less than 1 hour and occurred
before 3:00 PM.
The cognitive therapy component was designed to alter faulty
beliefs and attitudes that often serve to exacerbate
insomnia.6 Examples of faulty beliefs included (1)
unrealistic expectations about sleep requirements (eg, the need to
sleep 8 hours every night); (2) misattributions or amplifications of
the consequences of insomnia (eg, all daytime impairments are due to
poor sleep); and (3) erroneous beliefs about strategies to promote
sleep (eg, spending excessive time in bed). In addition to formal
cognitive therapy, there was an educational component about sleep and
aging aimed at distinguishing normative from pathologic sleep changes
occurring in late life, and at reviewing sleep hygiene principles about
the effects of diet, exercise, caffeine, alcohol, and environmental
factors.
Pharmacotherapy. Subjects assigned to the active medication condition were
prescribed temazepam (Restoril) to be taken 1 hour before bedtime. The
initial dosage was 7.5 mg per night, and the dosage was gradually
increased, based on treatment response and adverse effects, up to 30 mg
per night, maximum. Subjects were instructed to use sleep medication a
minimum of 2 to 3 nights per week, but the medication was made
available 7 nights if they chose to use it more frequently. Subjects
met once a week with the study physician for a 20-minute consultation
on medication management. During these sessions, the physician
monitored medication intake over the previous week (pill count) and
reviewed therapeutic response and adverse effects. Aside from providing
support and encouragement to comply with treatment and discussing
general information about sleep changes in late life, no behavioral
recommendations were allowed in this treatment condition.
The rationale for selecting temazepam for this study was based on its
documented efficacy for older adults39 and minimal daytime
residual effects. Temazepam has a moderate to slow absorption rate and
an intermediate half-life elimination. It has no active metabolite,
produces minimal accumulation with multiple doses, and is well
tolerated by elderly persons.40,41 For these reasons,
temazepam it was the best hypnotic medication for treating
sleep-maintenance insomnia in older adults.
Combined CBT and PCT. Subjects in the combined CBT and PCT treatment condition
received both the active medication (temazepam) and CBT. They attended
8 weekly individual therapy sessions with a psychiatrist to discuss
medication management issues and 8 weekly group therapy sessions with a
psychologist to review all cognitive behavioral procedures.
Placebo. Subjects in the placebo condition were treated according to a protocol
identical to those receiving the active medication. The placebo
medication was provided in identical gelatin capsules, and dosage was
adjusted according to perceived therapeutic response and adverse
effects. Subjects in this condition were offered an active treatment
after completing the 3-month follow-up.
The CBT sessions were led by a licensed clinical
psychologist or a postdoctoral fellow in clinical psychology.
Therapists had previously treated a minimum of 4 clinical subjects
using this protocol before their enrollment in this study. A
manual6 outlining each session was used. A third-year
psychiatry resident provided medication treatment for those in
conditions involving either an active or a placebo drug. A treatment
manual was also used for the PCT sessions. This manual outlined the
structure of each consultation, the issues that needed to be covered,
and the type of information that was not allowed to be discussed (ie,
behavioral recommendations). All therapy sessions were audiotaped and
reviewed regularly with the project director to ensure adherence to
protocol.
All treated participants were contacted by mail at 3, 12, and 24 months
after completing treatment. At each follow-up, they were sent sleep
diaries to keep for 2 weeks and were asked to complete the same rating
scales and questionnaires administered at baseline and posttreatment
assessment.
Multiple outcome measures were collected as part of this study, but the
present report focuses on selected sleep variables (ie, wake after
sleep onset, sleep efficiency, total wake time, and total sleep time)
that are most relevant to the problem of sleep-maintenance insomnia in
older adults. The main comparisons of interest were to determine
whether active treatments were more effective than placebo, whether a
combined behavioral and pharmacological approach was more effective
than either of its single components alone, and whether there were
differential improvement rates over time across treatment modalities.
Of the 78 subjects enrolled in the study, 71 completed the treatment
protocol, 6 dropped out prior to reaching the midtreatment phase
(CBT=0; PCT=3;
combined=1; placebo=2), and 1 subject
receiving placebo completed more than half of the intervention.
Midtreatment data for this latter subject were used for statistical
analysis. Of the 6 dropouts, 3 (PCT) discontinued treatment because of
adverse effects, and 3 (1 combined and 2 placebo) refused to continue
taking medication because of lack of efficacy. There were no
significant differences in the demographic or clinical variables
between subjects who completed and those who dropped out of the study.
The statistical analyses were computed with and without dropouts, and
both methods produced similar outcomes. The latter method was retained
to ensure that subjects included in the analyses had received an
adequate dosage of treatment (completed ≥50% of the treatment
protocol). Thus, the results are based on 72 subjects: 18 in CBT, 17 in
PCT, 19 in the combined group, and 18 placebo. There was no significant
baseline difference across conditions for demographic variables,
insomnia severity and duration, prior use of sleep medications, number
of physical illnesses, and medications used.
For each dependent measure, a 4 (group) × 2 (time; baseline to
posttreatment assessment) repeated-measures analysis of variance
(ANOVA) was conducted. Significant group × time interactions,
indicating a differential treatment effect across groups, were followed
by post hoc comparisons using the Tukey Honestly Significant Difference
test. Means and SDs for selected outcome measures are presented in
Table 2 (additional data on other
sleep variables are available on request from the corresponding
author).
Sleep Diary. Repeated-measures ANOVAs on sleep diary data, using wake after
sleep onset, sleep efficiency, total wake time, and total sleep time as
dependent measures, yielded significant time effects on all 4 dependent
measures (P<.001 for all 4). Significant group × time
interaction effects were obtained for total wake time
(F3,68=5.55;
P=.002) and sleep efficiency
(F3,68=5.52;
P=.002). Post hoc comparisons revealed that
subjects in all 3 active groups were significantly more improved than
those in the placebo condition at posttreatment assessment
(P<.05 for all 3). Likewise, posttreatment values for wake
after sleep onset were significantly lower for all 3 active treatment
conditions compared with the placebo condition (P<.01 for
all 3). Although there was no significant difference among the active
treatments, the data suggest a trend for the combined condition to
yield greater improvement rates than either of its single components (Figure 2). For example, the
percentage reduction of wake after sleep onset was highest (63.5%) for
the combined condition, followed by CBT (55%), PCT (46.5%), and
placebo (16.9%). Likewise, the improvement rate on sleep efficiency
was also highest (20.9%) for the combined condition, followed by CBT
(16.5%), PCT (10.3%), and placebo (4.4%).
Polysomnography. Repeated-measures ANOVAs on polysomnographic data, using the same
dependent measures, yielded significant time effects for all 4
variables (P<.001 for all), and significant group × time
interaction effects for total wake time
(F3,66=2.76;
P=.05) and sleep efficiency
(F3,66=2.70;
P=.05). Post hoc comparisons showed that, for
both variables, only the combined condition produced greater
improvements than the placebo condition (P<.05 for both). A
near-significant group × time interaction
effect was obtained for wake after sleep onset (F3,66=2.53;
P=.07). Post hoc comparisons indicated that
the subjects in the 3 active treatment conditions spent less time awake
after sleep onset than subjects in the placebo condition. Although no
significant difference emerged among the 3 active treatment conditions,
the combined condition tended to yield higher improvement rates on most
measures. For example, the percentage reduction of wake time after
sleep onset was highest (63.3%) for the combined condition, followed
by CBT (48.5%), PCT (38.6%), and placebo (7.7%).
On the Sleep Impairment Index scale, significant group × time
interactions were obtained on composite scores for subjects
(F3,63=9.86;
P=.001), significant others
(F3,53=5.41;
P=.003), and clinicians' ratings
(F3,54=9.31;
P=.001). Post hoc comparisons indicated that
subjects in the CBT and combined conditions rated themselves as
significantly more improved (and less impaired) than subjects in either
PCT (P=.01) or placebo conditions
(P=.002) (Figure
3). There was no significant difference
between the 2 medication-only conditions. Combined and CBT subjects
were more satisfied, less distressed, and felt less interference with
daytime functioning than subjects in the PCT or placebo conditions
(P<.05 for all). Comparisons of significant others' ratings
showed that subjects in all 3 active treatment conditions were
perceived as more improved than control subjects (P<.05 for
all), but no between-group differences were obtained among the active
treatments. The same pattern of results was obtained for clinicians'
ratings, which showed all treated subjects as more improved than the
control subjects (P<.05 for all), with no difference among
the active treatments. Analyses of posttreatment global ratings of
improvement yielded significant group effects for subjects
(F3,68=7.54;
P=.001), significant others
(F3,62=10.35;
P=.001), and clinicians
(F3,61=16.37;
P=.001). The subjects in the CBT condition
rated their improvements higher than those in placebo, and those in the
combined group rated their improvements greater than those in PCT or
placebo (P<.05 for all).
Follow-up data were collected at 3, 12, and 24 months after
treatment completion. The number of subjects available at each
follow-up assessment is shown in Table 2. Follow-up analyses were
conducted with the 3 active treatment groups only
because placebo subjects were offered an active treatment after the
3-month follow-up, and too few subjects were left for meaningful
comparisons of long-term outcomes. In both the PCT and combined
conditions, there were 5, 6, and 7 subjects who resumed medication at
the 3-, 12-, and 24-month follow-up, respectively. In the CBT
condition, there were 3 to 4 subjects who used medication at each
follow-up.
Since polysomnographic assessment was conducted only at baseline and
posttreatment assessment, follow-up assessments for sleep variables
were based on daily sleep diary only. For each dependent measure,
within-group t tests were conducted to examine possible
changes from posttreatment assessment to each of the follow-up
assessments. For the CBT condition, there was no significant change on
any of the dependent variables at any follow-up, suggesting that
treatment gains achieved by posttreatment assessment were well
maintained (Figure 4). For the PCT
condition, significant worsening from the posttreatment period was
noted at the 24-month follow-up for total wake time (t11 =−1.92;
P=.04), sleep efficiency
(t11 =2.22;
P=.03), and wake after sleep onset
(t11 = −2.04; P=.03).
For the combined condition, significant changes were obtained at all 3
follow-ups on measures of total wake time, sleep efficiency, and wake
after sleep onset (P<.05 for all), indicating significant
worsening of sleep pattern over time.
Paired t tests were also computed on clinical outcome
ratings from subjects and significant others at posttreatment
assessment and follow-up. For the CBT condition, subjects' ratings
were higher (less favorable) at 12-month follow-up than at
posttreatment assessment (t16
=−1.81; P=.04), whereas
significant others' ratings were lower (more improved) at the 3- and
12-month follow-ups than at posttreatment assessment (P<.05
for all). Subjects' ratings in the combined condition were higher at
the 12-month follow-up than their posttreatment ratings
(t14 =−2.32;
P=.02). There was no significant change in the
PCT condition.
Clinical Significance
of Sleep Improvements
To examine the clinical (as opposed to statistical) significance
of outcome, we computed the proportion of individuals in each condition
who reached a sleep efficiency greater than 85%. This criterion is the
typical cutoff score used to distinguish clinically impaired from
normal sleep. The proportions of subjects meeting this criterion at
posttreatment assessment were 55.6% (10/18) for CBT, 47.1% (8/17) for
PCT, 68.4% (13/19) for combined, and 22.2% (4/18) for placebo
(χ23=8.37;
P=.04). There were significantly more subjects
in the CBT (P=.04) and combined
(P=.005) conditions meeting this criterion
than in the placebo condition. When using polysomnographic data, there
were 10 subjects in the CBT condition, 10 in PCT, 13 in combined, and 6
in placebo meeting this criterion at posttreatment assessment
(P=.22). Another criterion, the proportion of
subjects who scored lower than 15 on the Sleep Impairment Index
(clinician's version) at posttreatment assessment, provides an
estimate of the number of subjects no longer meeting insomnia
diagnostic criteria. Those proportions were 78% (CBT), 56% (PCT),
75% (combined), and 14% (placebo), respectively
(χ23=15.77;
P=.001). There were significantly more
subjects in each treatment condition meeting this criterion than in the
placebo group (P<.05 for all).
Treatment Attendance
and Compliance
The number of treatment sessions attended averaged 7.78 per
subject (range, 6-8 sessions), for an overall attendance rate of
97.1%. Make-up sessions either in person or via telephone were
conducted whenever possible. There were no significant differences
between conditions for treatment attendance. One-way (group) ANOVAs on
subjects' self-ratings of compliance with treatment revealed no
significant group difference. Subjects in all 4 conditions rated their
degree of compliance equally high (group means >4.2 on a 5-point
scale). Likewise, there was no significant difference on compliance
ratings provided by significant others. No difference was noted between
conditions on ratings of therapist competence, empathy, and support. We
examined compliance with medication use by comparing the proportion of
medicated nights and average dosage used. No significant differences
were found among the 3 groups in the percentage of medicated nights
(placebo, 79%; PCT, 75%; combined, 70%) or in the average dosage
used during the treatment period (placebo, 20 mg/night; PCT, 20
mg/night; combined, 16 mg/night). Urine drug screens were performed at
baseline and posttreatment assessment. At baseline, 1 subject in the
combined condition had traces of benzodiazepine; at posttreatment
assessment, all PCT and combined subjects had positive screen findings,
and all but 1 subject in the placebo condition had negative urinalysis
findings for benzodiazepines.
The present findings indicate that behavioral and pharmacological
therapies, alone or in combination, are effective in the short-term
management of late-life insomnia. Their main effects are to improve
sleep continuity and efficiency. Subjects who received an active
treatment were able to maintain sleep more efficiently than
placebo-control subjects. There was a nonsignificant trend for the
combined condition to produce slightly higher improvement rates on
sleep continuity measures than either treatment alone during the
initial treatment phase. Follow-up results showed that behavior therapy
yielded the most durable improvements in sleep patterns; PCT gradually
lost its clinical benefits over time; and the combined approach yielded
more variable long-term outcomes.
These results extend those from previous studies21-25,39,41
and provide additional evidence that chronic insomnia is a treatable
condition even in late life. Once older adults are well screened for
other sleep disorders such as sleep apnea and periodic limb movements,
2 conditions particularly prevalent in the elderly, their treatment
response is similar to that of younger adults.16,19 For
example, the percentages of reduction of time awake after sleep onset
were 64% for the combined condition, 55% for the CBT, and 47% for
PCT, with all 3 conditions reducing their posttreatment values on this
variable below the 30-minute criterion typically used to define
sleep-maintenance insomnia. These clinical benefits were also
corroborated with objective electroencephalographic measures. As
illustrated in Figure 2, the magnitude of clinical improvements
obtained on polysomnographic measures is slightly smaller but clearly
in the same direction as those obtained on subjective daily sleep diary
measures.
The clinical significance of these results is illustrated by the
proportion of patients who reached a normative sleep efficiency of 85%
or who obtained a normative score of less than 15 on the Sleep
Impairment Index measure. These findings were paralleled by collateral
ratings from patients and significant others. Patients who received
active treatments rated themselves and were judged by significant
others as more improved than control patients on measures of insomnia
severity, interference with daytime functioning, and level of distress.
Although all 3 active treatments were effective during the initial
intervention, sleep improvements were not equally well maintained
across conditions. Initial gains produced by behavioral and
pharmacological interventions were well maintained at the short-term
(3-month) follow-up. However, long-term (12- and 24-month) follow-up
data showed a different trajectory of change in that only behavioral
treatment produced durable changes. Clinical benefits obtained by
subjects treated with drug therapy alone were gradually lost. Only 1 of
12 subjects available at the 12-month follow-up had a sleep efficiency
greater than 85%; by the 24-month follow-up, subjects treated with
medication alone had returned to their baseline sleep difficulties. The
combined approach produced more variable outcomes across subjects.
Although about half of the subjects in the combined approach retained a
sleep efficiency greater than 85% at each follow-up, 3 subjects
(outliers) reported significant worsening of sleep difficulties, which
contributed to the overall deterioration of the combined treatment
condition.
These latter findings indicate that, while a combined approach
may produce slightly larger benefits initially, these gains are not
necessarily better maintained. One possible explanation is that
subjects treated with hypnotic medications, singly or combined, may
attribute their initial gains exclusively to the medication. These
subjects may be more vulnerable to relapse when the drug is
discontinued. While these findings are consistent with Hauri's
study,27 and may suggest that insomnia is best treated with
a behavioral approach alone, additional research is needed to determine
the optimal model for integrating behavioral and drug therapies. A
sequential approach, in which medication would be initiated first and
behavioral treatment introduced or continued when the drug is
discontinued, may prove a more effective method than concurrent
initiation and discontinuation of both treatment modalities together.
Some methodological limitations preclude more definite conclusions
about effectiveness of treatment for late-life insomnia. While this was
the largest controlled clinical trial comparing behavioral and
pharmacological therapies for insomnia, the sample size was relatively
small; this may have reduced power to detect more differences among the
conditions. Another limitation
concerns the generalizability of the findings. The
sample was composed mainly of subjects responding to newspaper
advertisements; in addition, many subjects were excluded because of
comorbid medical or psychiatric illness or because they were unable to
stop taking their hypnotic medications prior to enrollment. Future
studies should enroll more subjects from primary care settings and
examine outcome as a function of medical and psychiatric conditions
often associated with insomnia.2,42 Finally, long-term
follow-up data must be interpreted cautiously because of the increasing
attrition over time and because several subjects initiated or resumed
medication between posttreatment and follow-up assessments.
Despite these limitations, this study has implications for
clinical practice. Insomnia is a widespread complaint, particularly in
late life, and is associated with functional impairments, diminished
quality of life, and increased health care costs.2,4,9,10
In addition, insomnia is typically undertreated and nondrug
interventions are underused by health care practitioners. Our results
indicate that chronic insomnia can be effectively treated in late life
with structured and sleep-focused interventions aimed at changing poor
sleep habits and faulty beliefs and attitudes about sleep. Although
such behavioral intervention is more time consuming than drug therapy,
it is worth the investment because therapeutic gains are well
maintained. The results also indicate that PCT alone, although
effective in the short term, may not be sufficient for long-term
management of chronic insomnia. Because insomnia is often a recurrent
problem42 and because many older persons use hypnotic
medications for much longer than the standard recommended
period,18 more studies are needed to evaluate long-term
effects of hypnotics. Despite the intuitive appeal in combining drug
and nondrug interventions, the present results call for additional
research to further evaluate other models (eg, sequential approaches,
maintenance trials) for optimal integration of biobehavioral approaches
in the clinical management of insomnia.
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