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Correspondence: Daniel J. Taylor, PhD, CBSM, ABSM, Department of Psychology, University of North Texas, 1155 Union Circle #311280, Denton, TX
76203-1280, USA. Tel: 940-565-2655. E-mail: djtaylor@unt.edu
Cognitive and behavioural therapy for insomnia (CBT-I) in psychiatric
populations: A systematic review
DANIEL J. TAYLOR
1 & KRISTI E. PRUIKSMA
2
1 Department of Psychology, University of North Texas, Denton, Texas, and
2 Department of Psychiatr y, University of Texas
Health Science Center at San Antonio, Texas, USA
Abstract
Insomnia is highly co-morbid with psychiatric disorders, making it a frequent issue in treatment planning in psychiatric
clinics. Research has also shown that although insomnia may originally precede or be a consequence of a psychiatric dis-
order, insomnia likely becomes semi-independent, and may exacerbate those disorders if it is not addressed, leading to
reduced treatment response. Cognitive behavioural therapy for insomnia (CBT-I) is now recommended as the fi rst line of
treatment of primary insomnia. The research reviewed below indicates that CBT-I in patients with co-morbid depression,
anxiety, post-traumatic stress disorder (PTSD), and substance abuse disorders is generally effective for insomnia and
sometimes the co-morbid disorder as well. Although more research is needed before defi nitive recommendations can be
made, it appears as though CBT-I is a viable approach to treating the patient with co-morbid insomnia and psychiatric
disorders.
Cognitive behavioural therapy for insomnia in
psychiatric populations
Insomnia is included in the diagnostic criteria for
various psychiatric disorders in the new DSM-5
(APA, 2013) including depressive disorders, anxiety
disorders post-traumatic stress disorder (PTSD),
and alcohol and substance use disorders. Research
in has generally indicated high levels of psychiatric
co-morbidity in people with insomnia (Buysse et al.,
1994; Mendelson, 1997; Ohayon et al., 1998; Taylor
et al., 2003, 2005, 2011, 2013). Current estimates
are that 80 – 90% of depression and anxiety patients,
70% of PTSD patients, and as many as 91% of
recovering alcoholics report signifi cant sleep disrup-
tion (Cohn et al., 2003; Ohayon & Roth, 2003;
Ohayon & Shapiro, 2000; Ohayon et al., 2000).
In the past decade, research has shown that
although insomnia may originally precede or be a
consequence of a psychiatric disorder (Ohayon &
Roth, 2003), insomnia likely becomes semi-indepen-
dent. If it is not addressed, insomnia may exacerbate
co-morbid disorders and lead to reduced treatment
response (e.g. Belleville et al., 2011b; Buysse et al.,
1997; Dew et al., 1997; Kupfer et al. , 1980, 1981,
1982; Trivedi et al., 2005; Winokur & Reynolds,
1994), and increased relapse and recurrence (Brower
et al., 2001; Drummond et al., 1998; Gillin et al.,
1994). These fi ndings have challenged the assump-
tion that insomnia is a ‘ symptom of ’ or ‘ secondary
to ’ the psychiatric disorder, which would remit once
the ‘ primary ’ psychiatric disorders were successfully
treated.
In the past few decades, research in the treatment of
primary insomnia has coalesced to show that cogni-
tive-behavioural therapy for insomnia (CBT-I) has
comparable short-term effi cacy to pharmacotherapy,
and better long-term effi cacy (for a review see
Riemann & Perlis, 2009). Thus, CBT-I is recom-
mended as a fi rst line treatment for primary insomnia.
CBT-I is a collection of separate interventions that
target behavioural, cognitive, and physiological per-
petuating factors of insomnia which, when used
singly or in various combinations, have shown sig-
nifi cant effi cacy to varying degrees (Morin et al.,
1994, 1999, 2006; Murtagh
& Greenwood, 1995;
Smith et al., 2001). The components of CBT-I with
the strongest empirical support in primary insomnia
are stimulus control therapy, sleep restriction, relax-
ation, and cognitive therapy (Morgenthaler et al.,
2006; Morin et al., 2006). Although often included
in CBT-I, sleep hygiene alone was considered an
inadequate treatment.
What is less clear is how best to treat insomnia
when co-morbid with psychiatric disorders. Random-
ized clinical trials of CBT-I in co-morbid populations
have become much more common in the past few
decades, as has an increased focus on measuring
International Review of Psychiatry, April 2014; 26(2): 205–213
ISSN 0954– 0261 print /ISSN 1369–1627 online © 2014 Institute of Psychiatry
DOI : 10.3109/ 09540 261.2 014.902808
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206 D. J. Taylor & K. E. Pruiksma
psychiatric symptom severity in studies of primary
insomnia. The primary objective of the current sys-
tematic review was to evaluate the effects of CBT-I
on sleep in patients with co-morbid psychiatric
disorders. The secondary objective was to evaluate
the effect of CBT-I on other psychiatric outcomes in
patients with and without co-morbid psychiatric
disorders. This is an update to a review by Smith
et al. (2005) that also included medical conditions.
Method
Data sources and study selection
Published studies were identifi ed by using the
following Keywords: insomnia, cognitive, behav-
ioural, therapy, treatment, psychiatric, depression,
anxiety, post-traumatic stress disorder, alcohol, sub-
stance, and hypnotic in a search of PubMed and
PsycINFO on 1 September 2013 and updated on
12 February 2014. References in the resulting
articles were also reviewed and relevant studies were
included in this review. The intent was to capture a
broad range of randomized clinical trials that had
attempted to treat insomnia with CBT-I in psychiatric
populations.
Outcome variables
Due to the varied nature of the studies identifi ed,
outcome variables with the greatest usage between
studies and the greatest clinical utility to the practis-
ing clinician were chosen. Outcome measures were
largely dependent on the co-morbid disorder, but
included self-reported sleep effi ciency (derived from
diaries), depression, anxiety, PTSD, and hypnotic
usage. Sleep effi ciency was chosen as the primary
sleep diary outcome variable because it was the most
consistently reported variable and because it encom-
passes many of the other components of sleep often
reported. Specifi cally, sleep effi ciency ⫽ total sleep
time/time in bed time in bed ⫻ 100, and total sleep
time ⫽ time in bed ⫺ sleep onset latency ⫺ wake time
after sleep onset ⫺ morning wake time. Other vari-
ables of interest (e.g., insomnia severity, depression,
anxiety, PTSD, alcohol use, and hypnotic use) were
included, when a validated measure was used, in an
effort to determine whether treating insomnia alone
resulted in concomitant improvement in the co-
morbid disorders.
Calculation of effect sizes and data extraction
The current study reports effect sizes for the time
(pre-treatment versus post-treatment) X group
(treatment versus control) interaction alone. Within
subject effect sizes were not calculated because they
suffer from regression to the mean biases. Several
authors (Manber et al., 2008; Margolies et al., 2013;
Talbot et al., 2014; Taylor et al., 2010, 2014;
Ulmer et al., 2011) reported interaction effect sizes
and these were used in our calculations. More com-
monly, authors only reported within and between
subject effect sizes, signifi cant interactions only, or
no effect sizes at all. In these cases, a standardized
effect size score was calculated for each outcome
variable by using the formula ES ⫽ (M1
c – M2
c ) ⫺
(M1
t – M2
t ) / SD
c , where ES ⫽ effect size, M1 ⫽
pre-treatment mean, M2 ⫽ post-treatment mean,
SD ⫽ standard deviation, c ⫽ control condition, and
t ⫽ treatment condition (Cohen, 1988). When the
standard error of the mean was provided, the stan-
dard deviation was calculated (SD ⫽ SEM ⫻ square
root of N) for comparability between studies (Cohen,
1988). Individual effect sizes were weighted to
account for individual sample sizes. The overall
weighted effect size was calculated according to the
formula Σ (di ⫻ Ni) / Σ (Ni) assuming random effects.
Cohen defi ned effect sizes of 0.2 – 0.3 as small, 0.5
as medium, and ⱖ 0.8 as large (Cohen, 1988).
Results
Included studies
This review returned results using a variety of
research designs (e.g. case series and randomized
clinical trials) and treatment formats (e.g. in-person,
self-help). The following analyses focused on out-
comes from randomized clinical trials that compared
active in-person CBT-I components to some sort of
control, most often a waiting list. Studies included in
this review fell into several categories. Some focused
on treating insomnia specifi cally in co-morbid
psychiatric populations (e.g. depression, anxiety,
PTSD, alcohol use, and hypnotic use), while others
focused on treating primary insomnia, but also
included psychiatric outcomes (e.g. depression and
anxiety symptoms). Studies with primarily co-
morbid medical disorders (e.g. pain, cancer, fi bromy-
algia) were excluded from these analyses. Studies
were also excluded if they did not report data using
a sleep diary or validated symptom questionnaire or
weekly hypnotic use.
Sixteen studies satisfi ed the criteria for entry into
this review. Studies spanned the years from 1999 to
2014 and summarized outcomes for 571 subjects.
Table 1 displays the clinical characteristics of sub-
jects by group, treatment components, number of
sessions, co-morbid disorders if applicable, and effect
sizes for reported outcomes. When multiple groups
were involved in the study, we chose to compare only
the active treatment most similar to CBT-I alone ver-
sus the control condition, which was most often a
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CBT-I in Psychiatric Populations 207
waiting list. Percentage of female participants ranged
from 10 – 90%. Participants were largely middle-aged,
but means ranged from 20 – 70. Co-morbid disorders
included depression, PTSD, alcohol dependence,
hypnotic dependence, or a variety of psychiatric dis-
orders (i.e. mixed). The mean number of therapy
sessions was six (SD ⫽ 2) and included a variety of
active components, including stimulus control
(n ⫽ 14), sleep restriction (n ⫽ 13), cognitive therapy
(n ⫽ 12), and relaxation (n ⫽ 6). Several also
included sleep hygiene, but as mentioned, this is
not considered an active therapy.
Table 1. Characteristics of 16 randomized clinical trials testing cognitive behavioural therapy of insomnia in co-morbid psychiatric disorders
or on psychiatric symptoms.
Study N
a
Age
(M) Female
Treatment
n
b
Control
n
b
Treatment
components
Number
of sessions
Co-morbid
psychiatric disorder Variable ES
Manber et al., 2008 30 35 61% 15 15 SC, SR, CT 7 Depression SE
Ins
Dep
0.76
1.03
0.25
Margolies et al., 2013 37 38 10% 20 17 SC, SR, CT 4 PTSD SE
Ins
PTSD
Dep
1.70
1.36
1.64
1.15
Talbot et al., 2014 45 37 69% 29 16 SC, SR, CT 8 PTSD SE
INS
Dep
PTSD
1.06
1.41
0.40
0.35
Ulmer et al., 2011 21 46 32% 12 9 SC, SR, CT 6 PTSD SE
INS
Dep
PTSD
1.27
1.76
0.34
1.76
Wagley et al., 2013 30 44 – 48 70% 20 10 SC, SR, CT 2 Mixed Dep 0.72
Arnedt et al., 2011 17 46 35% 9 8 SC, SR, CT 8 Alcohol dependence SE
Ins
Dep
Anx
0.45
1.20
0.29
0.26
Currie et al., 2004 40 43 30% 20 20 SC, SR,
CT, RT
5 Alcohol dependence SE
Ins
Dep
0.74
1.45
0.64
Lichstein et al., 1999 20 55 60% 10 10 RT 3 Hypnotic dependence SE
Dep
Anx
Hyp
0.26
0.36
0.52
⫺ 0.62
Lichstein et al., 2013 47 64 71% 24 23 SC, RT, CT 8 Hypnotic dependence SE
Dep
Anx
Hyp
0.63
0.20
0.03
⫺ 0.17
Morin et al., 2004 29 63 50% 24 25 SC, SR, CT 10 Hypnotic dependence SE
Ins
Hyp
0.42
0.29
0.30
Okajima et al., 2013 63 47 67% 34 29 SC, SR, RT,
CT
6 Hypnotic dependence Ins
Dep
Hyp
0.88
0.83
1.01
Soeffi ng et al., 2008 47 N/A 64% 20 27 SC, RT 8 Hypnotic dependence SE 0.75
Taylor et al., 2010 46 54 54% 24 22 SR 8 Hypnotic dependence SE
Hyp
1.16
1.05
Arnedt et al., 2013 30 39 90% 15 15 SC, SR, CT 8 None Dep
Anx
0.07
0.37
Germain et al., 2006 35 70 71% 17 18 SC, SR 2 None Dep
Anx
0.67
0.34
Taylor et al., (2014) 34 20 59% 17 17 SC, SR,
CT, RT
6 None Dep
Anx
0.73
0.25
M, mean; ES, effect size; SC, stimulus control; SR, sleep restriction; RT, relaxation therapy; CT, cognitive therapy; SE, sleep effi ciency;
Ins, Insomnia Symptom Scale; Dep, Depression Symptom Scale; PTSD, Post-Traumatic Stress Disorder Symptom Scale; Anx, Anxiety
Symptom Scale; Hyp, weekly hypnotic usage.
a Only compared two groups for all studies, even when more than one group was present, so reported N will not always equal overall N
from the parent study.
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208 D. J. Taylor & K. E. Pruiksma
Sleep
Sleep effi ciency. The primary objective of the current
systematic review was to evaluate the effects of
CBT-I on sleep in patients with co-morbid psychiat-
ric disorders. As can be seen in Table 1, 13 studies
reported sleep diary sleep effi ciency outcomes in
patients with co-morbid psychiatric disorders. These
studies varied in duration from three to eight sessions
and spanned a variety of co-morbid psychiatric dis-
orders. The mean effect size for the sleep effi ciency
outcomes was 0.758 (95% CI: 0.557 – 0.958), indi-
cating that CBT-I results in signifi cant improvement
in sleep effi ciency in patients with co-morbid psychi-
atric disorders, Z ⫽ 7.417, p ⬍ 0.001. These medium
to large effects were homogeneous across studies,
Q(12) ⫽ 12.597, p ⫽ 0.399.
Insomnia questionnaires. Given the added time
necessary for patients to complete prospective sleep
diaries and for clinicians to score them to develop
summary data (e.g. average sleep effi ciency), it is
likely they will not be used in most psychiatry prac-
tices. Therefore it was important to also report the
effects of CBT-I on other self-report measures of
insomnia. As can be seen in Table 1, nine studies
reported validated insomnia symptom questionnaire
outcomes in patients with co-morbid psychiatric
disorders. These studies varied in duration from
three to ten sessions and spanned a variety of co-
morbid psychiatric disorders. The mean effect size
for the insomnia symptom outcomes was 1.001 (95%
CI: 0.639 – 1.363), indicating that CBT-I results in
signifi cant improvement in sleep effi ciency in patients
with co-morbid psychiatric disorders, Z ⫽ 5.422,
p ⬍ 0.001. These relatively large effects were not
homogeneous across studies, Q(8) ⫽ 12.51, p ⫽ 0.0115.
Morin et al. (2004) and Lichstein et al. (2013)
appeared to be considerably lower than the other
studies. This was likely due to CBT ⫹ medication
withdrawal being compared to another medication
withdrawal condition, which may have truncated the
results. If these two studies are removed from the
analysis the outcomes become homogeneous
Q(6) ⫽ 3.857, p ⫽ 0.696, with an effect size of 1.227
(95% CI: 0.957 – 1.497).
Depression
To date, only one pilot randomized trial has exam-
ined CBT-I in individuals with co-morbid depression
and insomnia (Manber et al., 2008). Participants
receiving open label escitalopram (n ⫽ 30), were ran-
domized to receive concomitant CBT-I or control
treatment. The CBT-I intervention included sleep
restriction, stimulus control, stress management and
cognitive therapy over seven sessions. The CBT-I
group demonstrated signifi cantly greater baseline to
post-treatment improvements in diary measured
sleep effi ciency (p ⬍ 0.05, d ⫽ 0.76) and self-reported
insomnia (p ⬍ 0.05, d ⫽ 1.03) than the control group,
indicating that insomnia can be successfully treated
with CBT-I in patients with co-morbid depression.
This study failed to fi nd a signifi cant interaction on
depression due to the relatively small effect of d ⫽ 0.25
on the 17-item Hamilton Depression Rating Scale
(Hamilton, 1960) minus the sleep items. The effect
was likely truncated somewhat by the fact that both
groups were simultaneously receiving medications
for depression. Notably, the group with CBT-I aug-
mentation had more insomnia remission (50% ver-
sus 8%) and depression remission (61.5% versus
33.3%) than the control group, which suggests that
CBT-I provides benefi t above and beyond concur-
rent depression treatment for both the insomnia and
depression outcomes.
As can be seen in Table 1, 12 additional studies
reported depression outcomes using a variety of
self-report measures. These studies varied in dura-
tion (two to eight sessions) and spanned a variety of
co-morbid psychiatric disorders as well as three in
primary insomnia patients. The effect size data were
combined to provide a meta-analytic estimate of the
effect of treating insomnia on depression outcomes.
The mean effect size for the depression outcomes
was 0.505 (95% CI: 0.313 – 0.696), indicating that
CBT-I results in signifi cant small to medium effects
in depression symptomatology, Z ⫽ 5.159, p ⬍ 0.001.
The results were homogeneous across studies,
Q(12) ⫽ 10.864, p ⫽ 0.541.
Anxiety, trauma and stressor-related disorders
Surprisingly, we were unable to fi nd any randomized
controlled trials that specifi cally attempted to treat
insomnia in any anxiety disorders other than PTSD
(which, as of DSM-5, is no longer considered an
anxiety disorder). A recent meta-analysis examined
the impact of CBT-I on concomitant anxiety across
a variety of trials in patients with co-morbid medical
disorders and that used self-help interventions
(Belleville et al., 2011a). They used a broad opera-
tional defi nition anxiety which included arousal,
worry, and stress. They found a combined effect size
of 0.406 (95% CI ⫽ 0.318 – 0.493), indicating signifi -
cant small to moderate effects of CBT-I on anxiety.
They found a signifi cant amount of variability across
samples, Q(49) ⫽ 131.08, p ⬍ 0.001, likely due to
heterogeneity in populations and measures.
Restricting our sample to randomized clinical tri-
als of in-person CBT-I, we found six studies that
assessed anxiety symptoms (Table 1). These studies
varied in duration from three to eight sessions and
spanned a variety of co-morbid psychiatric disorders,
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CBT-I in Psychiatric Populations 209
with three that were in primary insomnia patients.
The mean effect size for the anxiety outcomes was
0.208 (95% CI: ⫺ 0.084 – 0.499), indicating that
CBT-I did not result in signifi cant improvements in
anxiety symptomatology, Z ⫽ 1.396, p ⫽ 0.163.
Although the results were homogeneous across stud-
ies, Q(5) ⫽ 2.513, p ⫽ 0.775, Lichstein et al. (2013)
was the only study to fi nd negative results on an
anxiety measure. When that study was removed from
the analyses, the effect size increased to 0.340 (95%
CI: 0.001 – 0.679), indicating that CBT-I results in
signifi cant small effects in anxiety symptomatology,
Z ⫽ 1.966, p ⬍ 0.05, with excellent homogeneity,
Q(4) ⫽ 0.259, p ⫽ 0.992.
PTSD. Insomnia in the context of PTSD is unique
in that it is often characterized by hypervigilance at
night and fear of going to bed or to sleep (DeViva
et al., 2004; Pruiksma et al., 2014). Patients may
report increased anxiety at night related to noises
around the house, checking locks frequently, or fear
of intrusive memories or nightmares of traumatic
experiences. Thus, much of the research examining
CBT-I in PTSD has included interventions for night-
mares or has implemented insomnia treatment after
PTSD treatment. One randomized controlled trial
has examined the effi cacy of CBT-I in individuals
with PTSD (Talbot et al., 2014), and another two
have examined the effi cacy CBT-I ⫹ imagery rehearsal
therapy (IRT) for nightmares (Margolies et al., 2013;
Ulmer et al., 2011).
Talbot et al. (2014) examined the effi cacy of
CBT-I compared to a waiting list control group in
45 veterans with co-morbid insomnia and PTSD.
The CBT-I intervention included stimulus control,
sleep restriction, and cognitive therapy over eight
sessions. CBT-I resulted in signifi cantly greater
baseline to post-treatment improvements in diary-
measured sleep effi ciency (p ⬍ 0.001, d ⫽ 1.06) than
the control group, indicating that insomnia can be
successfully treated with CBT-I alone in patients
with co-morbid PTSD. This study failed to fi nd
a signifi cant interaction on the 17-item PCL
(Blanchard et al., 1996) minus the sleep items, even
though they had a small effect (d ⫽ 0.35). The effect
was likely truncated by the fact that both groups
were simultaneously receiving active PTSD treat-
ment. Both groups showed signifi cant improve-
ments in PTSD and nightmares. Notably, the CBT-I
group had more insomnia remission than the
control group (41% versus 0%), which likely had
some quality of life benefi ts for these veterans.
Ulmer et al. (2011) examined the effi cacy of three
sessions of sleep restriction, stimulus control, and
cognitive therapy, followed by three sessions of IRT
in 22 veterans with PTSD. The treatment was com-
pared to a usual care group. CBT-I ⫹ IRT resulted
in signifi cantly greater baseline to post-treatment
improvements in diary measured sleep effi ciency
(p ⬍ 0.01, d ⫽ 1.27) than the control group. In addi-
tion, this study found a signifi cant interaction on
the 17-item PCL minus the sleep items (p ⬍ 0.01,
d ⫽ 1.76). The effect was likely strengthened by the
added IRT as well as the fact that most were not
simultaneously receiving active PTSD treatment.
Margolies et al. (2013) examined the effi cacy of
CBT-I ⫹ IRT in 40 Operation Enduring Freedom
(OEF)/Operation Iraqi Freedom (OIF) veterans with
PTSD in comparison to a waiting list control group.
They found treatment resulted in statistically sig-
nifi cant interactions for sleep effi ciency (p ⬍ 0.001,
d ⫽ 1.70) and the PTSD Symptom Scale self-report
(p ⬍ 0.001, d ⫽ 1.64). It is important to note that
only 40% of the treatment group elected to receive
adjunctive IRT. Thus, it is possible the effects found
were likely strengthened by added IRT treatment as
well as the fact that 35% of the sample was not simul-
taneously receiving active PTSD treatment.
Overall, the research indicates insomnia can be
meaningfully improved in the context of PTSD.
There is some indication that improvements in PTSD
may occur as well. The extent to which nightmare
interventions contributed to these gains is unclear.
Although four is typically the minimum acceptable
number of studies needed to perform meta-analyses,
it was decided an exploratory analysis was justifi ed
for PTSD. The mean effect size for the PTSD
outcomes was 1.192 (95% CI: 0.210 – 2.173),
indicating that CBT-I results in signifi cant small to
large effects, Z ⫽ 2.38, p ⬍ 0.05. However, the results
were not homogeneous across studies, Q(2) ⫽ 8.482,
p ⫽ 0.0144. Further, it was not clear how much of
those gains are the result of the addition of IRT and
how much are the result of CBT-I alone. Further
research is needed to tease this apart. Research is also
needed to determine whether sleep disturbances
should be treated before, during, or after treatment
for PTSD.
Alcohol dependence
Two randomized clinical trials have now been
conducted examining the effi cacy of CBT-I in indi-
viduals diagnosed with alcohol dependence. Currie
et al. (2004) randomized 60 individuals recovering
from alcohol dependence to either fi ve sessions
of in-person CBT-I, a self-help intervention with
telephone support, or a waiting list control. The in-
person treatment groups included stimulus control,
sleep restriction, relaxation, and cognitive therapy.
Overall, the in-person treatment resulted in more
signifi cant gains than the waiting list group on sleep
effi ciency (p ⬍ 0.05, d ⫽ 0.74). Alcohol relapse rates
did not differ between groups, but the follow-up rates
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210 D. J. Taylor & K. E. Pruiksma
were exceptionally low across groups (i.e. 15%), and
long-term follow-up was less than ideal.
Arnedt et al. (2011) followed with a randomized
controlled trial of CBT-I versus a placebo control in
17 patients with co-morbid alcohol dependence. The
CBT-I included stimulus control, sleep restriction,
and cognitive therapy. Similar to the Currie et al.
(2004) study, the CBT-I group had signifi cantly
better sleep post-treatment sleep effi ciency (p ⬍ 0.05,
d ⫽ 0.45), but there were no differences with regard
to relapse prevention.
These studies indicate that CBT-I for insomnia
can help recovering alcoholics improve their sleep,
obviating the need for hypnotic medications. How-
ever, the treatment may not improve long-term
alcohol relapse rates. Although the small sample sizes
may account for the failure to fi nd relapse improve-
ments, it is more likely that alcohol relapse is very
complex and diffi cult to address. Two studies are not
enough to justify meta-analysis at this point.
Hypnotic dependence
Many patients (24 – 53%) in primary care and sleep
medicine clinics report using hypnotics for insomnia
(Hohagen et al., 1993; Rosenthal et al., 2008).
Although rarely discussed, many physicians are not
comfortable prescribing hypnotic medications long-
term (e.g. ⬎ 6 – 12 months). Increasingly, studies are
showing that CBT-I alone or in combination with a
hypnotic tapering programme can improve both
insomnia and reduce hypnotic use, often to absti-
nence (Baillargeon et al., 2003; Dolan et al., 2010;
Lichstein & Johnson, 1993; Morgan et al., 2003;
Morin et al., 1995, 2004; Soeffi ng et al., 2008; Taylor
et al., 2010).
Lichstein et al. (1999) performed one of the fi rst
randomized clinical trials examining the effi cacy of
insomnia interventions in 20 individuals with insom-
nia and hypnotic dependency. They compared three
sessions of relaxation therapy ⫹ hypnotic withdrawal
to hypnotic withdrawal alone. They reported that the
addition of relaxation therapy to hypnotic withdrawal
resulted in signifi cant improvements in sleep effi -
ciency (p ⬍ 0.05, d ⫽ 0.26). Although both groups
showed signifi cant reductions in hypnotic use, the
hypnotic withdrawal only group actually had greater
reductions in hypnotics from pre- to post-treatment
than the group with relaxation therapy augmentation
(d ⫽ ⫺ 0.62).
Morin et al. (2004) examined the effi cacy of 10
sessions of CBT-I in 29 older adults with chronic
insomnia and prolonged benzodiazepine medication
use (M ⫽ 19.3 years). Patients were randomly
assigned to either medication withdrawal, CBT-I, or
CBT-I ⫹ medication withdrawal. Comparing only the
CBT-I ⫹ medication withdrawal versus the medication
withdrawal only, to determine the additive effect of
CBT-I, the CBT-I ⫹ withdrawal resulted in a larger
improvement in sleep effi ciency (d ⫽ 0.42), but this
small to medium effect did not reach statistical sig-
nifi cance. Similar, but smaller results were seen for
hypnotic withdrawal (d ⫽ 0.30).
Taylor et al. (2010) examined the effi cacy of sleep
restriction therapy versus a sleep hygiene control in
46 hypnotic using patients with insomnia. These
authors found that sleep restriction resulted in sig-
nifi cant improvements in sleep effi ciency (p ⫽ 0.003,
d ⫽ 1.16). They also found signifi cant reductions in
hypnotic usage (p ⬍ 0.001, d ⫽ 1.05).
Okajima et al. (2013) compared the effi cacy of
CBT-I ⫹ behaviour analysis to treatment as usual in
63 people with insomnia resistant to pharmaco-
logical treatment. The CBT-I intervention included
sleep restriction, stimulus control, relaxation ther-
apy, and cognitive therapy over six sessions. CBT-I
resulted in signifi cantly greater baseline to post-
treatment improvements on insomnia severity
(p ⬍ 0.01, d ⫽ 0.88) and hypnotic usage (p ⫽ 0.01,
d ⫽ 1.01).
Lichstein et al. (2013) examined CBT-I ⫹ drug
withdrawal, placebo biofeedback with drug with-
drawal, and drug withdrawal only in 70 older adults.
The CBT-I intervention included relaxation training,
stimulus control, sleep hygiene and also integrated
cognitive therapy. Comparing only the CBT-I ⫹
medication withdrawal versus the placebo ⫹
withdrawal only, to determine whether CBT-I was
better than a credible control, we found that CBT-I
resulted in a larger improvement in sleep effi ciency
(d ⫽ 0.63), but this effect did not reach statistical sig-
nifi cance. Similar, but smaller results were seen for
hypnotic withdrawal and insomnia symptom severity
(d ⫽ 0.20). Although both groups showed signifi cant
reductions in depression, anxiety, and hypnotic use,
the placebo group actually had greater reductions
(d ⫽ ⫺ 0.33).
We performed a meta-analyses of these fi ve ran-
domized clinical trials that reported the quantity of
hypnotics taken at pre- and post-treatment (Table 1).
These studies varied in duration from three to eight
sessions and spanned a variety of co-morbid psychi-
atric disorders. The mean effect size for the hypnotic
quantity outcomes was 0.333 (95% CI: ⫺ 0.287 –
0.953). The results were non-signifi cant, Z ⫽ 1.053,
p ⫽ 0.293, largely due to the heterogeneity,
Q(4) ⫽ 19.633, p ⫽ 0.0006. Similar to the anxiety
analyses, only the Lichstein et al., studies (1999,
2013) reported negative results. If those studies
are removed from the equation, the effect size of
CBT-I on hypnotic reduction increased to 0.802
(95% CI: 0.402 – 1.202), which was signifi cant,
Z ⫽ 1.62, p ⬍ 0.001, and homogeneous, Q(2) ⫽ 2.863,
p ⫽ 0.239. Thus, it appears that the addition of CBT-I
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CBT-I in Psychiatric Populations 211
alone is signifi cantly better than waiting-list controls
at reducing hypnotic reduction, but does not add
much over tapering alone.
Conclusion
CBT-I is now considered a fi rst-line intervention for
primary insomnia (National Institutes of Health,
2005; Wilson et al., 2010). The results presented here
provide clear evidence that CBT-I is also highly effec-
tive in improving sleep in patients with co-morbid
psychiatric disorders. To our knowledge, no contrain-
dications have been reported for the use of CBT-I in
patients with depression, anxiety, PTSD, alcohol
dependence, or hypnotic medication dependence. In
addition, CBT-I signifi cantly improves depression
and anxiety symptoms in both co-morbid and pri-
mary insomnia populations. Although there are some
promising results regarding the effi cacy of CBT-I in
reducing PTSD symptoms and hypnotic withdrawal,
more studies are needed before defi nitive conclu-
sions can be drawn.
The evidence base does appear strong enough to
begin using CBT-I in clinical practice to augment
treatment for patients with co-morbid depression,
anxiety, PTSD, and substance abuse disorders. It
seems clear this augmentation should, at the very
least, result in improved sleep as well as depression
and anxiety symptoms. Several excellent manuals are
available describing in detail how to deliver these
interventions (e.g. Edinger & Carney, 2008; Morin
& Espie, 2003; Perlis et al. , 2005, 2010), including
one developed specifi cally for treating insomnia
in patients with depression or anxiety (Carney &
Manber, 2009).
One of the primary diffi culties with performing
the above meta-analysis was the inconsistency of
reporting means, standard deviations, interaction
effects and what types of analyses they use even
within the same study. A new movement within ran-
domized clinical trials is to performed mixed models
analyses, eliminating the need for imputation of
missing data, and reporting effect sizes for all inter-
actions within tables. This is a positive change that
will allow for greater assimilation of results across
studies in the future. In addition, more recent
studies are beginning to take heed of the recom-
mendations of Buysse et al., (2006) to include a
larger compendium of outcome measures, including
depression and anxiety.
Acknowledgement
We would like to offer special thanks to Katherine
Marczyk, who helped in compiling the large list of
manuscripts and in building Table 1.
Declaration of interest: The authors report no
confl icts of interest. The authors alone are respon-
sible for the content and writing of the paper.
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