INTENSIVE SLEEP RETRAINING FOR CHRONIC INSOMNIA
http://dx.doi.org/10.5665/sleep.1584

A Randomized Controlled Trial of Intensive Sleep Retraining (ISR): A Brief
Conditioning Treatment for Chronic Insomnia
Jodie Harris, PhD1,2; Leon Lack, PhD1,2; Kristyn Kemp, PhD3; Helen Wright, PhD1; Richard Bootzin, PhD4
1
3School of Psychology, Flinders University, South Australia; 2Adelaide Institute for Sleep Health, Repatriation General Hospital, South Australia;
Adelaide Insomnia Clinic, Adelaide, South Australia; 4University of Arizona, Tucson, AZ

Study Objective: To investigate the effectiveness of intensive sleep retraining in comparison and combination with traditional behavioral intervention for chronic primary insomnia.
Participants: Seventy-nine volunteers with chronic sleep-onset insomnia (with or without sleep maintenance difficulties) were randomly assigned
either to intensive sleep retraining (ISR), stimulus control therapy (SCT), ISR plus SCT, or the control (sleep hygiene) treatment condition.
Intervention: ISR treatment consisted of 50 sleep onset trials over a 25-h sleep deprivation period.
Measurements and Results: Treatment response was assessed with sleep diary, activity monitoring, and questionnaire measures. The active
treatment groups (ISR, SCT, ISR+SCT) all resulted in significant improvements in sleep onset latency and sleep efficiency, with moderate to large
effect sizes from pre- to post-treatment. Wake time after sleep onset decreased significantly in the SCT and ISR+SCT groups. Total sleep time increased significantly in the ISR and ISR+SCT treatment groups. Participants receiving ISR (ISR, ISR+SCT) experienced rapidly improved SOL and
TST during treatment, suggesting an advantage of rapid improvements in sleep in response to ISR. Although there were few statistically significant
differences between groups on individual variables, ISR+SCT resulted in consistently larger effect sizes of change than other treatments, including
questionnaire measures of sleep quality, sleep self-efficacy, and daytime functioning. The combination treatment group (ISR+SCT) showed trends
to outperform other active treatment groups with fewer treatment dropouts, and a greater proportion of treatment responders with 61% reaching“good sleeper” status. Treatment gains achieved at post-treatment in the active treatment groups were largely maintained throughout follow-up
periods to 6 months.
Conclusion: This 25-hour intensive conditioning treatment for chronic insomnia can produce rapid improvements in sleep, daytime functioning,and psychological variables. Adding ISR to traditional interventions seems to result in a superior treatment response.
Keywords: Chronic insomnia, classical conditioning, behavioral treatment, intensive sleep retraining
Citation: Harris J; Lack L; Kemp K; Wright H; Bootzin R. A randomized controlled trial of intensive sleep retraining (ISR): a brief conditioning treatment for chronic insomnia. SLEEP 2012;35(1):49-60.

INTRODUCTION
Chronic insomnia is a pervasive, unrelenting sleep disorder,
and is associated with considerable consequences for sufferers.
Various conceptual models contribute an understanding of thedevelopment and maintenance of insomnia, in addition to helping inform treatment choice. Of those, a conditioning model
offers a theoretical basis for the efficacy of behavioral intervention. This model suggests that the wakeful state associatedwith insomnia may be learned through a process of conditioning.1 According to this model, transient sleep disturbance may
be triggered by acute periods of stress or heightened arousal.
With repeated episodes of wakefulness and distress in bed, an
individual may rapidly associate the bedroom, bedtime, andother associated cues with anxiety and sleeplessness. Thus
both temporal and contextual stimuli may become cues for apprehension, worries, and fear of being unable to sleep, in addition to the sleeplessness itself. Research suggests that once
insomnia is established, it may persist over many years.2,3

Although a significant body of research supports cognitive
behavioral treatments for insomnia, this common sleep disorderoften remains untreated, or treated only with pharmacotherapy.4
Of the behavioral interventions, stimulus control therapy (SCT)
is the most widely studied and endorsed single component
treatment method. Indeed, SCT is currently recommended withthe highest standard of support by the American Academy ofSleep Medicine.5 SCT is considered effective for both sleep onset and sleep maintenance insomnia symptoms.6,7 The assumed
mechanism involved in successful SCT implementation is theeventual conditioning of a rapid sleep onset, countering thelearned psychophysiologic arousal (or absence of de-arousal8)
associated with the insomnia response.
Nevertheless, the administration of behavioral treatment for
insomnia is typically associated with a lag in treatment response,
some early treatment sleepiness and/or fatigue, and some difficulties with treatment compliance. Consequently, the rapid treatment response associated with intensive sleep retraining (ISR)9
may improve the response to and compliance with non-drug interventions. ISR is a brief 25-h conditioning treatment, involving
the use of acute sleep deprivation to facilitate a series of rapid
sleep onsets in an effort to counteract the conditioned insomnia
response. In a case series study, this brief conditioning treatment
has shown rapid and sustained improvements in sleep variables.9
The current study aims to compare the treatment response toboth ISR and SCT treatments alone, in addition to evaluating
a combination of the 2 treatment methods in comparison to acontrol (sleep hygiene intervention only) group.

A commentary on this article appears in this issue on page 11.
Submitted for publication September 2010
Submitted in final revised form August, 2011
Accepted for publication September, 2011
Address correspondence to: Prof. Leon Lack, School of Psychology,
Flinders University, GPO Box 2100, Adelaide, South Australia 5001; Tel:
618 8201 2391; Fax: 618 8201 3877; E-mail: leon.lack@flinders.edu.au
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Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et alTable 1—Sample demographic and clinical characteristics, mean (standard deviation)
VariableAge (SD)
Gender (M:F)
Length of insomnia (yr)SOL at screening (min)Pre-treatment WASO (min)Insomnia Severity (Mild: Severe)
Body Mass Index (BMI)
Respiratory Disturbance Index (RDI)
Mean BDI-II Depression score (adjusted)

ISR (N = 19)
38.53 (13.3)
8:11
16.8 (12.8)
74.5 (31.4)
83.4 (58.2)(9:10)
25.2 (5.4)
4.89 (4.5)
8.63 (6.2)

SCT (N = 20)
42.2 (13.1)
5:15
12.1 (10.7)
82.6 (53.5)
74.3 (47.2)(10:10)24.2 (2.5)
6.27 (4.9)
9.05 (7.2)

MATERIALS AND METHODSControl (N = 20)
43.8 (13.8)
7:13
16.2 (15.4)
92.1 (63.8)
94.6 (69.9)(10:10)25.8 (6.2)
6.77 (4.9)
7.47 (5.7)

All (N = 79)
40.9 (13.8)
23:56
16.0 (13.6)
81.7 (50.3)
84.5 (56.9)(39:40)25.6 (5.5)
6.17 (4.4)
8.55 (6.5)

fied by severity. The demographic and clinical characteristicsof the treatment groups are presented in Table 1. There were no
significant differences between treatment groups on age, lengthof insomnia, BMI, RDI, SOL at screening, pre-treatment waketime after sleep onset (WASO), or BDI-II adjusted score.
All participants signed informed consent forms prior to research participation. Ethical approval was obtained from theSocial and Behavioural Research Ethics Committee at Flinders
University of South Australia.

Participants
Potential participants were recruited from the community,
primarily via newspaper advertisements, media releases, andpamphlet distribution to general medical practices. Figure 1
illustrates participant flow through screening and treatment.
Following an initial telephone interview, 142 respondents were
mailed and returned a one-week sleep-wake diary and comprehensive sleep questionnaire. Of these, 45 were excluded and 97
underwent screening overnight polysomnography.
Participants reported sleep onset insomnia, with or without concurrent difficulty maintaining sleep. Selection criteria,
based on screening stages included (i) age between 18-65 years,(ii) mean sleep diary sleep onset latency > 30 min, for ≥ 3 nights
per week, (iii) insomnia symptoms for ≥ 6 months, and (iv) reported daytime consequences of poor sleep. Exclusion criteria
were other sleep disorders (e.g., obstructive sleep apnea, delayed sleep phase disorder, periodic limb movement disorder),other medical or psychiatric disorders are likely to affect sleep
and daytime functioning (e.g., chronic pain, bipolar disorder,
chronic fatigue syndrome), pregnancy, being a heavy smoker,
or taking medications likely to affect sleep. Those with significant depression were excluded on the basis of an adjusted Beck
Depression Inventory (BDI-II) score > 28. The adjusted scoring
method involved excluding items 15, 16, and 20 from the total
score—items that reflect sleep disturbance, fatigue, and loss ofenergy—which are also symptoms of insomnia. Of note, individuals taking daily antidepressant medication (stable dosage
for 3 months) were considered suitable for inclusion, provided
they were willing to continue on the same dose for the period of
the study, and met inclusion criteria on the BDI-II. Participants
using sleep medication were considered for inclusion following
a withdrawal and wash-out period of ≥ 3 weeks (8-10 of theparticipants in each group).
A total of 79 participants (23 males, 56 females, mean age
40.9 years [SD 13.8], mean length of insomnia 16.0 years [SD13.6]) were considered appropriate for inclusion and were accepted into the treatment study.
Suitable participants were stratified according to the severity of their insomnia into a severe (average sleep onset latency[SOL] > 60 min), or mild to moderate classification (SOL ≤ 60min), on their one-week screening sleep diary. Participants wererandomly allocated to the 4 treatment conditions using a computer generated randomization program, with allocations stratiSLEEP,
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ISR+SCT (N = 20)
36.9 (11.5)
3:17
17.9 (13.2)
67.7 (24.5)
85.7 (52.4)(10:10)25.9 (5.2)
6.33 (3.3)
9.65 (7.2)

Apparatus and Materials
Sleep-wake diary

The current study employed a chart version of a sleep-wakediary to provide the primary outcome measures of subjective
sleep variables. The sleep-wake diary facilitates a graphicaldaily recording of lights out time, sleep onset time, estimatedperiods of sleep overnight, final wake-up time, and out of bed
time, as well as estimates of SOL and WASO. Across each 24-h
period, food, caffeine, daytime naps, and alcohol were recorded by means of symbols at the appropriate times. Sleep-wakediaries were completed daily for the 2-week baseline period,
throughout treatment, and during follow-up assessments.
Actigraphy

Given the discrepancy between objective and subjective sleepthat has been reported in insomnia, it was considered important
to include actigraphy in the assessment process, in order to provide a more objective estimate of nightly sleep. Participants
wore an Actiwatch AW-64 (Mini Mitter Co. Inc., Bend, Oregon)on their non-dominant wrist throughout the day and night. Eventmarkers provided the times of retiring to bed, and out of bed
times. Total sleep time (TST), WASO, and sleep efficiency (SE)were estimated using the Actiware Sleep Software version 3.4.
Although actigraphy has been validated in insomniacs, sleep
onset latency estimates derived from this measure have beensignificantly underestimated.10 Accordingly, two methods wereused in an attempt to provide a clinically useful measure in thecurrent study. Firstly, all Actiwatch recordings were scored using a manually adjusted sensitivity setting, derived for eachindividual by equating actigraphy-scored TST to that of theovernight screening PSG-scored TST on the same night. Secondly, the Actiwatch SOL was manually estimated as the startof the first period ≥ 20 consecutive minutes with no more than
one epoch of movement.
50

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et alScreening stage 1:
telephone (N = 800)

Screening stage 2: sleep diaryand questionnaire (N = 142)
Excluded N = 45
Screening stage 3:
polysomnography (N = 97)
Excluded N = 17
Randomization (N = 80)

Intensive Sleep
Retraining (ISR)

Stimulus Control
Therapy (SCT)SCT + ISR
(N = 20)

Placebo control(Sleep Hygiene)

Pre-Treatment
assessment

Pre-Treatment
assessment

Pre-Treatment
assessment

Pre-Treatment
assessment(N = 19)(N = 20)ISR(N = 20)

ISR

Treatment week 1

SH

SCT+SHSCT+SHSH

Treatment week 2

SH

SCT+SHSCT+SHSH

Treatment week 3

SH

SCT+SHSCT+SHSH

Treatment week 4

SH

SCT+SHSCT+SHSH

Post-Treatment
assessment

Post-Treatment
assessment

Post-Treatment
assessment

Post-Treatment
assessment

Follow-up 1(2 month)

Follow-up 1(2 month)

Follow-up 1(2 month)

Follow-up 2(6 month)

Follow-up 2(6 month)

Follow-up 2(6 month)Figure 1—Research design and participant flow.
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Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et al

Questionnaires

an arrival to the sleep laboratory on night 1 at 21:00. Following
an explanation, the signing of an informed consent form, electrode application, and a quiet settling period, treatment began at
22:30. Treatment trials were conducted every half hour, finishing after 23:00 on night 2. Thereby, the ISR treatment routine
allowed a series of 50 half-hourly sleep onset opportunities.
Prior to the beginning of each trial, participants completed the
Stanford Sleepiness Scale (SSS)17 in order to gauge subjective
sleepiness throughout treatment. Within each treatment trial,
the opportunity for sleep onset was limited to a 20-min period,
with the trial stopping if sleep onset had not occurred by thistime. For those trials in which sleep was initiated, 3 consecutive
minutes of sleep were permitted, prior to being awoken. Upon
awakening, treatment participants first rated their perception ofwhether sleep onset had occurred (on a Likert scale of 1 “No,definitely not” to 7 “Yes, definitely”). Following this response,
participants were provided with information as to whether sleep
onset had or had not occurred.
Participants then arose from bed following each treatment
trial, to maintain quiet alertness in a bedside chair, undertaking
activities such as reading or watching DVD movies. At the culmination of the treatment session, participants were provided
with detailed treatment feedback regarding the number of treatment trials, their sleep status for each trial, perceived sleep attainment, sleep onset latencies, and total sleep time for eachtrial. Participants then traveled home via a taxi, in order to havea recovery night’s sleep (with a maximum of 8 h in bed). Following this weekend component of treatment, participants werebooked to attend a series of 5 further treatment sessions, involving sleep hygiene alone or in combination with SCT. In order tocreate a degree of experimental treatment blindness, the SCT/
sleep hygiene therapist was blind to the presence or absence of
the ISR treatment component.
Stimulus Control Therapy (SCT): Stimulus control therapy was implemented and monitored over a series of 5 weekly
appointments with a clinical psychologist experienced in thetreatment of sleep disorders. Although improvements havebeen demonstrated in as little as one week in some patients,18,19
an average of 5 weeks for psychological therapies have beenreported in meta-analyses.6 SCT was administered concurrently
with sleep hygiene treatment.
Treatment sessions lasted for approximately 30 min each.
Session one was devoted to providing treatment instructions
and explaining the rationale behind SCT. Written therapy instructions were provided at this session. Sessions 2 to 4 weredevoted to treatment support and encouragement, a review of
the implementation of treatment instructions, and troubleshooting barriers to effective implementation of treatment. Session
5 was devoted to relapse prevention, with recommendations toreapply SCT instructions as required following treatment.
ISR plus SCT: The combination ISR and SCT group received treatment in the same manner that each were provided
separately. The SCT (plus sleep hygiene) component of treatment began on the day following ISR treatment, after the recovery sleep period.
Control (Sleep Hygiene Only): The minimal treatment
control utilized in the current study was sleep hygiene (SH)treatment only. Given that there is not sufficient evidence tosuggest that SH is effective as a stand-alone treatment,20 pre-Subjects completed sleep, cognition, and daytime functioning questionnaires at the completion of each 2-week assessment period. Measures included the Pittsburgh Sleep Quality
Index (PSQI),11 a 19-item questionnaire assessing sleep quality. The overall “global” score ranges from 0 to 21, with higherscores being indicative of poorer sleep quality. A score > 5 has
been used to identify significant sleep disturbance in insomnia
studies.12 The sleep Self-Efficacy Scale (SES), a 9-item scale,
was used to assess perceived self-efficacy for sleep-related
behaviors.13 Responses were scored on a 5-point scale from
1 (“Not confident at all”) to 5 (“Very confident”). The Dysfunctional Beliefs and Attitudes about Sleep (DBAS) scale,a 30-item questionnaire, was completed to assess cognitions
about sleep, including sleep loss, sleep need, and the causes
and sequelae of insomnia.14 In addition, the Daytime Feelingand Functioning Scale (DFFS) was completed, a 12-item scalethat assesses the frequency of specific daytime deficits commonly reported in insomnia (e.g. “felt lethargic,” “been unable
to concentrate”). Each item is scored on a 0-3 scale, where
0 indicates “never or seldom” and 3 indicates “frequently or
almost all the time,” resulting in a total score between 0 and
36. The DFFS shows good internal consistency in insomnia
samples (α = 0.89-0.94), reliably discriminates between goodand poor sleepers, and reflects treatment-related improvements
in sleep variables in insomniacs.15
Sleep Onset Determination
In-laboratory polysomnography (PSG) was utilized for participants undergoing the ISR procedure. These were conductedwith a Compumedics P-Series (Melbourne, Australia), configured to record 2 EEG channels (C3-O1, C4-A1), 2 EOG channels, EMG, and light level in order to calculate lights out time(LOT) and SOL for each sleep trial. EEG1 utilized a standard
bipolar recording method, with C3 and O1 sites referenced toan A2 reference site. A referential recording was utilized between C4 and A1 sites.
PSG was utilized to determine sleep onset, in accordancewith Rechtschaffen and Kales16 sleep scoring criteria. The online display was also the method by which wakefulness between sleep trials was monitored and recorded.
Procedure
Pretreatment

Following screening, participants were scheduled to attend
an orientation and education visit to the sleep laboratory approximately 2 weeks prior to their scheduled treatment startdate. At this session, participants were provided with the paperwork and equipment required to complete their pre-treatment
assessments, and an appointment schedule for all appointments
throughout the study program.
Treatments

Intensive Sleep Retraining (ISR): On the night prior to attending the laboratory, participants undergoing ISR treatment
were required to restrict their bed period to a total of 5 h, withthe aid of an alarm clock, in an attempt to increase homeostatic
sleep drive for the treatment period. Treatment then started withSLEEP,
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Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et alParticipant Attrition
Of the 79 participants randomized to a treatment condition, 71 (89.9%) were classified as treatment completers,
having attended all 5 treatment sessions. The proportion oftreatment completers for each treatment group were as follows: ISR (84%), SCT (84%), ISR+SCT (100%), and control(90%). Following treatment, the proportions of participants
who completed the Follow-up 1 were as follows: ISR (84%),
SCT (75%), ISR+SCT (95%). The reasons for dropout included illness, unwillingness due to time commitments, an inability/unwillingness to follow treatment recommendations, andmedication changes.

vious investigators have also used SH treatment as a control
condition.5,21-24 The SH control group was chosen over the alternative of a wait-list control due to its ability to control forvariance in outcomes explained by the measurement process(i.e., monitoring via sleep diary) and nonspecific factors suchas therapist attention.25
Sleep hygiene instructions involved education regarding
healthy sleep behaviors and sleep-conducive environmental
conditions, and are applied under the assumption that poor
sleep, at least in part, results from a violation of these rules.24
The SH treatment in the current study consisted of instructions addressing caffeine, nicotine, alcohol, eating behaviors,
exercise, pre-bed “wind down” periods, and addressing environmental considerations of noise, light and temperature in the
bedroom. These basic instructions were similar to those recommended by Morin26 for treatment, in addition to incorporatingsome relaxing, resting time prior to retiring to bed. Sleep hygiene treatment was administered and monitored over a seriesof 5 weekly appointments of approximately 30 min in length.
For those receiving SH treatment in the control condition, participation continued until the completion of the Post-treatment
assessment, after which time all participants were offered further treatment.

RESULTS
Statistical Overview
All analyses were conducted using SPSS version 14.0
(2005). The degree of change in outcome variables in responseto treatment was assessed for each treatment condition separately via the use of one-way repeated measures ANOVAs andeffect sizes. The effect size calculation utilized was a Cohen’sd index (d = [M1-M2]/SDpooled) where M1 = Pre-treatment
mean, M2 = Post-treatment mean, and SDpooled = pooled
standard deviation, obtained by pooling the Pre-treatment SD
across groups.
Between-group comparisons on outcome variables were undertaken between the 3 active treatment groups and the control
group via the use of maximum likelihood linear mixed model
analyses, hereafter referred to as linear mixed model analyses(these analyses are also known by the terms mixed effects models
or random effects models). Linear mixed models are considered
to be flexible and robust with respect to handling missing data inrepeated measures research, and are considered superior to traditional ANOVA analyses for repeated measures designs.27-29
For each dependent variable, 2 linear mixed model analyses were undertaken, a preferred statistical approach forlongitudinal clinical trials.30 Firstly, all 4 treatment groups,
including the SH control, were compared throughout treatment(sleep variables only) and the immediate Post-treatment assessment, using their baseline mean values as a covariate control.
The 3 active treatment groups were then compared throughout
Post-treatment and Follow-up periods, again controlling forbaseline differences. Planned comparisons within these analyses were conducted between treatment groups at both Week 1
and at Post-treatment, in order to make a comparison of both
immediate treatment response and final treatment outcome.
Power calculations indicated that with the current sample sizeof approximately 20 per group, large effect sizes of d = 0.80
with a probability of above 0.80 (P < 0.05) might be detected.
Smaller differences between active treatment groups were unlikely to be detected in the current study. Therefore, analyses
were primarily aimed to detect differences between each of theactive treatment groups with the control.

Treatment Response Determination
Each assessment period involved 2 consecutive weeks ofsleep diary and activity monitoring, with questionnaires completed at the completion of each assessment period. Assessment
periods were scheduled for 2 weeks immediately prior to treatment start (Pre-treatment), immediately following treatment(Post-treatment), 6 weeks after treatment completion (Followup 1), and at a 6-month follow-up (Follow-up 2). Treatment
response was assessed via change on both measures of sleep(sleep diary and actigraphy) for the variables of SOL, TST,WASO, and SE. Questionnaires scores also provided an important index of various psychological and subjective daytime
functioning aspects of treatment response.
Treatment Fidelity
The SCT and sleep hygiene treatment components were
provided by experienced clinical psychologists. The therapists
were provided with written instructions as to how to explain thetherapeutic rationale and each treatment recommendation. Furthermore, each client was provided with written treatment instructions to ensure they were aware of all treatment components.
Therapy sessions were audio recorded by the psychologist using a small portable digital recording device. Of these files, a randomly selected subset of 6 recordings of each of the 5 treatment
sessions was selected for scrutiny as a check on treatment fidelity. Reviews suggested that all treatment items were addressed intreatment implementation and review for each treatment.
Furthermore, this process allowed a check on treatment sessions length. The mean session lengths were as follows: session 1, 35:05 minutes (SD 13:49); session 2, 21:40 minutes (SD
10:49); session 3, 20:13 minutes (SD 8:01); session 4, 19:48
minutes (SD 10:42); session 5, 17:20 minutes (SD 8:12). Oneway ANOVAs indicated that there were no significant differences between all treatment groups on overall mean session
length (at P > 0.05).
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Intensive Sleep Retraining Treatment Application
In-laboratory ISR was successfully applied, with data demonstrating an increased and sustained objective sleepiness throughout the procedure, as indicated by repetitive rapid sleep attainment
throughout the procedure. Figure 2 plots the mean subjective
53

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et al(Stanford Sleepiness Scale) and objective (SOL) values throughout the 25-h procedure. After the first 2-3 h, the majority of participants obtained short sleep onset latencies (< 5 min).

ments resulted in a significant reduction in SOL and increased
sleep efficiency, compared to non-significant changes in the control group. Treatment groups undergoing ISR (ISR, ISR+SCT)
resulted in increased TST time from Pre-treatment, whereas
those treated with SCT (SCT, ISR +SCT) and the control groupall showed significant reductions in WASO. The combined
ISR+SCT group showed trends towards greater response as indicated by effect sizes. Actigraphy showed some minor trends
towards improved sleep (i.e., greater SE and reduced SOL in
active treatment groups), however, failed to indicate any statistically significant treatment-related changes in sleep variables
other than a decreased TST in the SCT and control groups.

Sleep Variables
Pre- to post-treatment sleep variables

16
14
12
10
8
6
4
2
0

SOL

1

5

9

13 17

21 25 29 33 37 41

SSS

45 49

5.0
4.5
4.0
3.5
3.0
2.5
2.0
1.5
1.0
0.5
0.0

Sleep onset latency

Figure 3 illustrates changes in sleep diary SOL throughout andfollowing treatment in the various treatment groups. Using linear
mixed model analyses and controlling for the log transformed
baseline SOL, between-group comparisons were carried out on
SOL values (with a log transformed sleep diary SOL variable)
during treatment (Weeks 1-4) and Post-treatment. There was amain effect for treatment group (F3,71.4 = 7.33, P < 0.001), witha marginally significant interaction (F12,68.6 = 1.82, P = 0.06) andmain effect for time (F4,68.0 = 2.42, P = 0.06). Paired comparisons
between groups indicated ISR+SCT reported a decreased SOL
during the treatment weeks and Post-treatment period in comparison to both the control group (P ≤ 0.001), and the SCT group(P < 0.05). ISR alone also demonstrated a consistently shorter
SOL than the control group across this period (P < 0.01). The
SCT group did not differ significantly from the control group.

Mean Stanford Sleepiness
Scale (SSS) Score

Mean Sleep Onset Latency(SOL; mins)

The average sleep parameters of SOL, WASO, TST, and SE
were calculated from the sleep diaries and activity monitor data.
The averages are from 2-week periods for each assessment period, and a 1-week average for treatment weeks. Table 2 presents mean diary and actigraphy sleep values at Pre-treatment
and Post-treatment (from ANOVA analyses), and the associatedeffect sizes (d). For the sleep diary measures all active treat-

Trial Number

Figure 2—Mean sleep onset latency (SOL) and Stanford Sleepiness
Scale (SSS) score by trial number during the intensive sleep retraining(ISR) treatment procedure.

Table 2—Mean (SD) sleep diary, actigraphy and questionnaire values from Pre-treatment (Pre-T) to Post-treatment (Post-T), and change effect sizes (d )ISR
Variable
Sleep Diary
SOL

SCT

ISR+SCTCONTROL

Pre-T

Post-Td

Pre-T

Post-Td

Pre-T

Post-Td

Pre-T

Post-Td

61.41(25.21)38.41**(16.24)

0.61

68.33
(44.04)38.94*** 0.78
(29.39)60.79(42.79)24.70*** 0.96
(12.83)71.87(37.23)68.65(37.72)0.09

TST

368.59(62.71)403.23**(55.37)0.53

370.65(54.13)387.95(57.36)0.26

357.41(65.61)411.91*** 0.83
(50.91)348.76(78.83)350.26(76.76)

0.02

WASO

75.57
(56.00)60.71(59.01)

0.26

72.34
(44.47)42.66**(37.53)

0.52

87.24
(53.30)42.42*** 0.79
(25.32)

99.25(70.48)80.31*(57.38)

0.33

SE

70.02
(11.08)79.85*** 0.65
(8.84)

70.64(9.40)

81.57*** 0.91
(7.34)

68.08(11.89)84.20*** 1.34
(5.68)

65.96(14.89)68.24(14.14)

0.24

38.53
(17.18)28.05(15.29)

0.35

34.17
(23.73)28.36(15.60)

0.19

40.53
(26.46)31.89(32.04)

0.29

47.54
(45.70)43.01(42.64)0.15

TST386.61(69.92)392.38(62.54)0.09

375.86(55.32)365.12*(65.98)0.17

388.84(58.22)378.24(71.41)0.17

379.40(73.84)368.50*(72.74)

0.17

WASO

90.04
(66.90)90.31(69.04)

0.01

93.85
(49.46)92.47(44.00)

0.03

85.37
(50.48)84.20(50.90)

0.02

99.47
(43.11)

100.19(46.49)

0.01

SE

75.32
(12.27)76.57(11.91)

0.11

74.33
(10.96)75.61(9.82)

0.11

75.55(10.03)

77.59(11.63)

0.18

72.26
(12.58)71.92(11.91)

0.03

Actigraphy
SOL

SOL, sleep onset latency; TST, total sleep time; WASO, total wake time overnight after sleep onset; SE, sleep efficiency (total sleep time/time in bed ×100). Data is derived from participants within each condition with available data at both assessment points. ANOVA (P) statistics for Pre-Treatment to PostTreatment change, *** < 0.001, ** < 0.01, * < 0.05.
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54

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et al

*†

360

*†

300

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Control

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Figure 4—Mean sleep diary total sleep time (TST) prior to, during, andfollowing treatment. *Mean values are significantly different (P < 0.05) fromcontrol, †Mean values are significantly different (P < 0.05) from SCT.

Figure 3—Mean sleep diary sleep onset latencies (SOL) prior to,during, and following treatment. * Mean values are significantly different(P < 0.05) from control.

and the ISR+SCT group (P < 0.01) in Week 1. In addition, theISR and ISR+SCT treatment groups demonstrated a significantly greater TST than those in the SCT group at Week 1 (ISR:
P < 0.001; ISR+SCT: P < 0.01). By Post-treatment, participantsreceiving ISR and ISR+SCT maintained a superior response,with a greater mean TST than the control group (ISR: P < 0.01;
ISR+SCT: P < 0.001). Comparisons between active treatmentgroups at Post-treatment found the only significant difference tobe a greater mean TST in the ISR+SCT group than in the SCT
treatment group (P < 0.05).
Analyses following treatment were conducted between active
treatment groups, indicating no main effect for treatment group(F2,47.5 = 1.55, P = 0.224), time (F2,45.1 = 0.43, P = 0.66), or interaction effect (F4,45.1 = 1.74, P = 0.16). This suggests that following treatment, all groups were comparable on the TST variable.
A main effect for treatment group on actigraph TST(F3,70.4 = 3.02, P < 0.05) indicated a greater TST in the ISRgroup during treatment than the SCT group (P < 0.01). Following treatment, there were no significant between group effects
for actigraphically measured TST (F2,47.7 = 0.34, P = 0.72).

Planned paired comparisons were performed between thecontrol group and active treatment groups in Week 1 and at
Post-treatment. In Week 1, only the ISR+SCT group reported
a mean SOL that was significantly shorter than the control
group (P < 0.01). No significant differences between any of
the active treatment groups were apparent at this stage. By
Post-treatment, all active treatment groups reported a significantly reduced SOL in comparison to the control group (ISR:
P < 0.05; SCT: P < 0.01; ISR+SCT: P < 0.001). Again, there
were no significant differences between active treatmentgroups.
Further analyses were undertaken on the active treatmentgroups during the Post-Treatment and Follow-up periods.
Again, linear mixed model analyses (controlling for Pre-treatment mean SOL values) were performed between the treatmentgroups during the Post-treatment, Follow-up 1, and Followup 2 assessments only. There was a main effect for treatmentgroup (F2,45.3 = 3.26, P < 0.05), with ISR+SCT outperforming
both SCT (P < 0.05) and ISR alone (P < 0.05). There was no
main effect for time (F2,47.1 = 1.59, P = 0.22) or interaction effect (F4,47.1 = 0.44, P = 0.78), indicating that following the treatment period, all active treatments maintained their response.
Actigraphy measures failed to indicate a significant main effect for treatment group (controlling for baseline differences)
for mean SOL either during treatment (F3,68.1 = 2.56, P = 0.06)
or following treatment (F2,55.9 = 2.25, P = 0.09).

Wake time after sleep onset

During treatment and Post-treatment, linear mixed model analyses resulted in a main effect for treatment group(F3,72.7 = 6.5, P ≤ 0.001) for the WASO variable, illustrated
by Figure 5. There were, however, no significant main effects for time (F4,70.5 = 1.33, P = 0.267) or interaction effects(F12,76.7 = 0.87, P = 0.58). Both the SCT and ISR+SCT treatmentgroups reported significantly lower mean WASO values thanthe control group (P ≤ 0.001). In addition, the ISR+SCT groupreported a decreased mean WASO compared with ISR group(P < 0.05). Overall, ISR treatment alone was not significantly
different from SCT or control groups on the WASO variable.
Planned comparisons indicated that improvements in WASO
were rapid in those treatment groups receiving SCT. In Week 1,
both ISR+SCT (P < 0.05) and SCT (P < 0.05) showed decreased
mean WASO values in comparison to the control group, withno other significant differences between treatment groups. By
Post-treatment, ISR+SCT (P < 0.01) and SCT (P < 0.05) groups
maintained their gains relative to control. Between active treatment groups, only the ISR+SCT group showed a significantly
reduced WASO in comparison to the ISR group (P < 0.05) at
Post-treatment.

Total sleep time

During treatment and Post-treatment, linear mixed model
analyses of TST (controlling for baseline values) indicated amain effect for group (F3,73.3 = 11.59, P < 0.001), a main effectfor time (F4,68.3 = 3.47, P < 0.05), and a significant interaction effect (F12,74.8 = 2.01, P < 0.05). Between-group significant effects
were found between the control group and both ISR+SCT treatment group (P < 0.001) and ISR treatment group (P < 0.001).
In addition, both ISR+SCT (P < 0.001) and ISR (P < 0.001)
outperformed SCT treatment, producing significantly increased
TST throughout treatment, illustrated in Figure 4.
When comparing treatment groups to the control group at
Week 1 in planned comparisons, the ISR treatment groups
showed rapidly increased TST, with significantly increased
TST relative to the control group in the ISR group (P < 0.001)
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*†
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ISR

t

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Mean Sleep Diary Total
Sleep Time (TST; mins)

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Mean Sleep Diary Sleep Onset
Latency (SOL; mins)

SCT

ISR

80
70
60
50
40
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55

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et al

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Mean Sleep Diary Wake Time
After Sleep Onset (WASO; mins)

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Figure 5—Mean sleep diary wake time after sleep onset (WASO) prior to,during, and following treatment. *Mean values are significantly different(P < 0.05) from control, °Mean values are significantly different (P < 0.05)
from ISR.

Figure 6—Mean sleep diary sleep efficiency (SE) prior to, during andfollowing treatment. *Mean values are significantly different (P < 0.01)
from control. °Mean values are significantly different (P < 0.05) from ISR.
†
Mean values are significantly different (P < 0.05) from SCT.

Following treatment, there were no main effects for time
(F2,45.4 = 0.36, P = 0.70), treatment group (F2,49.8 = 1.93, P = 0.16),
or interaction effects (F4,45.5 = 0.80, P = 0.54) on the sleep diary
WASO variable. These data indicate no differential response on
WASO to treatment or change in response over time following
treatment, based on Post-treatment and follow-up assessments.
There were no significant between-group effects for objective WASO as measured by actigraphy either during treatment(F3,71.9 = 1.75, P = 0.16) or following treatment (F2,50.6 = 0.23,
P = 0.80).

treatment (P < 0.05). These data suggest no significant changes
within groups over time following treatment.
Objective actigraph-measured sleep efficiency failed to indicate any main effects for treatment group either during treatment(F3,69.8 = 2.45, P = 0.07) or following treatment (F2,48.7 = 0.10,
P = 0.91).
Questionnaire Variables
Pittsburgh Sleep Quality Index

Table 3 outlines mean changes (and effect sizes) on questionnaire variables over time. Within groups, using ANOVA
analyses, there was a significant change from Pre-treatment toPost-treatment on mean global Pittsburgh Sleep Quality Indexscores in all active treatment groups (P < 0.001), with no significant change in the control group. Comparisons between allgroups at Post-treatment indicated a main effect for treatmentgroup (F3,63 = 10.66, P < 0.001) on global PSQI scores, whencontrolling for baseline values. The combination ISR+SCT
treatment group reported lower overall PSQI scores than ISR(P < 0.001), SCT (P < 0.01) and control (P < 0.001) groups. At
Post-treatment, SCT also had significantly lower mean PSQI
scores than the sleep hygiene control group (P < 0.05).
Linear mixed model analyses between active treatmentgroups, following treatment, indicated a significant main effect for treatment group (F2,47.91 = 6.66, P < 0.01) and time
(F2,36 = 4.28, P < 0.05) on Global Sleep Quality. Participants in
the ISR+SCT treatment group reported a significantly higher
sleep quality across assessments following treatment than thosein the SCT only group (P < 0.05) and the ISR group (P < 0.01).
Significant changes across time indicated a significantly decreased PSQI score from Post-treatment to Follow-up 1 in theactive treatment groups. The interaction effect was non-significant (F4,36 = 1.49, P = 0.23).

Sleep efficiency

Figure 6 illustrates changes in subjective SE across and following treatment in the various treatment conditions. Acrosstreatment to Post-treatment, linear mixed model analyses indicated a significant main effect for treatment group (F3,72.9 = 18.15,
P < 0.001), with ISR (P < 0.001), SCT (P < 0.001), and ISR+SCT(P < 0.001) outperforming the control group on the SE variable.
In addition, the combination ISR+SCT treatment group produced higher overall sleep efficiencies than SCT (P ≤ 0.01) andISR (P < 0.01). ISR and SCT were not significantly different.
There were no significant main effects for time (F4,68.5 = 2.18,
P = 0.08) or interaction effects (F12,68.6 = 0.96, P = 0.49) up to
Post-treatment.
Planned comparisons between treatment groups at the beginning and end of treatment indicated that all active treatment groups showed increased SE in comparison to the control
group at both Week 1 and Post-treatment (P < 0.01). ISR+SCT,
however, outperformed SCT in Week 1 (P < 0.05), with noother differences between active treatments at this time. By
Post-treatment, ISR+SCT was superior to ISR treatment alone(P < 0.05). This data indicates that all treatments were effective in rapidly increasing SE and maintaining those changes
throughout treatment, although ISR+SCT outperformed otheractive treatments.
Following treatment, after controlling for baseline differences, there were no main effects for treatment group (F2,49.2 = 2.69,
P = 0.08), time (F2,44.2 = 0.54, P = 0.59), or interaction effects(F4,44.2 = 0.96, P = 0.44). Nevertheless, as was the case during
treatment, the ISR+SCT treatment group maintained a significantly higher mean SE than the ISR treatment group following
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Sleep Self Efficacy Scale

Mean scores on the SES questionnaire variable increased
significantly, indicating improved self-efficacy in all active
treatment groups (P < 0.001), with little change in the control
group. Using linear mixed model analyses, controlling for baseline values, at Post-treatment there was a significant treatment
56

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et alTable 3—Mean (SD) questionnaire values from Pre-treatment (Pre-T) to Post-treatment (Post-T), Follow-up 1 (6-weeks) (FU1), and Follow-up 2 (6-months)
and change effect sizes (d) from Pre- to Post-treatment
Variable
PSQI
Control
ISR
SCT
ISR+SCT

Pre-T

Post-T

d

FU1

FU2

12.22 (3.02)
11.13 (2.31)
11.73 (1.75)
11.47 (1.98)

11.11 (2.72)
8.88 (3.05)***8.73 (2.71)***
6.37 (2.59)***

0.48
0.97
1.29
2.20

–
7.93 (3.65)
6.81 (2.93)
5.78 (3.54)–
8.53 (5.02)
8.39 (2.60)
5.89 (3.27)

DBAS
Control
ISR
SCT
ISR+SCT

81.56 (13.6)
77.44 (10.1)
77.87 (13.8)
84.37 (11.4)

77.56 (13.4)
67.63 (12.7)***67.87 (12.3)***68.84 (13.2)***

0.32
0.79
0.81
1.26

–
63.87 (9.86)
64.19 (14.7)
63.00 (15.4)–
64.93 (11.8)
60.15 (14.1)
61.14 (11.8)

Daytime Impairment
Control
ISR
SCT
ISR+SCT

13.61 (7.72)
12.94 (5.54)
14.53 (5.71)
15.74 (7.29)

12.56 (6.92)
9.13 (5.33)*
10.00 (7.75)**
7.79 (6.00)***

0.16
0.57
0.68
1.20

–
8.13 (4.50)
9.56 (6.98)
7.22 (6.38)–
8.40 (5.84)
7.00 (6.11)
8.67 (6.08)

Sleep Self-Efficacy
Control
ISR
SCT
ISR+SCT

20.56 (5.16)
21.06 (4.48)
19.60 (3.14)
20.37 (5.30)

21.22 (5.45)
26.13 (5.60)***28.87 (6.16)***28.59 (5.91)***

0.15
1.10
1.58
1.79

–
27.33 (5.67)
30.88 (6.20)
30.44 (7.06)–
28.40 (6.01)
29.69 (7.29)
30.94 (8.16)

PSQI, Pittsburgh Sleep Quality Index; DBAS, Dysfunctional Beliefs and Attitudes about Sleep Scale; Daytime Impairment, DFFS, higher scores indicate
greater impairment. ANOVA (P) statistics for Pre-Treatment to Post-Treatment change, *** ≤ 0.001, ** < 0.01, * < 0.05.

group effect (F3,63 = 7.38, P < 0.001), with all treatment groups
being significantly different from control group self-efficacy
values (P < 0.01) There were no differences between active
treatment groups at this time point.
Linear mixed model analyses compared active treatmentgroups on SES scores across time, following treatment. Results indicated that there were no significant main effects fortreatment group (F2,47.8 = 1.62, P = 0.21), and no interaction
effects (F4,44.4 = 1.50, P = 0.23) when controlling for baseline
values. There was, however, a significant main effect for time
(F2,44.4 = 3.23, P < 0.05), with continued improvements on thisvariable from Post-treatment to Follow-up 2 (P < 0.05). These
data suggest a comparable treatment response across active interventions.

for time (F2,43.5 = 7.28, P < 0.005), with continued reductions
across treatment groups in DBAS scores from Post-treatment
to Follow-up 1 (P < 0.01) and to Follow-up 2 (P < 0.001). Theinteraction effect was non-significant (F4,43.6 = 1.13, P = 0.36).
Daytime feelings and functioning scale

Statistically significant improvements in various aspects ofdaytime feeling and functioning explored in the DFFS wereobserved in all treatment groups from Pre-treatment to Posttreatment (P < 0.05), but not in the control group. Comparisons
between treatment groups at Post-treatment using linear mixed
model analyses, controlling for baseline values, indicated a significant main effect for group (F3,63 = 4.02, P < 0.05). The combined ISR+SCT treatment group was the only active treatmentgroup to significantly differ from control (P < 0.001), with noother differences between groups at this time.
Linear mixed model analyses between active treatment groups
following treatment demonstrated no significant main effects fortreatment group (F2,44.2 = 1.46, P = 0.24), time (F2,42.9 = 1.56,
P = 0.86), or interaction effects (F4,42.9 = 0.48, P = 0.84). Results
indicate a trend for similar response to treatment on aspects ofdaytime functioning for active treatment groups.

Dysfunctional Beliefs and Attitudes about Sleep Scale

ANOVA analyses indicated a significant decrease on DBAS
scores from Pre-treatment to Post-treatment (P < 0.001), withno significant change in the control group. Using linear mixed
model analyses at Post-treatment, comparisons across all treatment groups resulted in a main effect for treatment group(F3,63 = 3.53, P < 0.05), with ISR (P < 0.05), SCT (P < 0.05) and
ISR+SCT (P < 0.01) all resulting in mean DBAS scores thatwere significantly lower than the control group. There were noother differences between the three active treatment groups at
Post-treatment.
After treatment, linear mixed model analyses compared treatment groups across time. Analyses indicated that there wereno significant main effects for treatment group (F2,46.4 = 1.39,
P = 0.26), showing a similar DBAS change in response to thedifferent interventions. There was a significant main effect
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Responder Analysis
In addition to demonstrating statistically significant changes,
and reporting change effect sizes, the clinical significance oftreatment-related change is important in assessing treatment response. Although there are no currently agreed upon criteria forassessing clinically significant change, many studies use a percentage change in SOL, or characterize treatment responders asreaching an outcome within a normative range for sleep vari57

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et almain advantage of ISR treatment appears to be the immediacyof treatment response. Under the assumption that the ISR technique acts via a conditioning effect, the treatment response to
the ISR procedure provides evidence for the explanatory valueof the conditioning etiologic model, and supports the use of
conditioning treatments in insomnia. In addition, it must be noted that the sleep/wake state feedback during the ISR treatment
may constitute sleep perception or sleep/wake discrimination
training, which has been found to improve sleep in individuals suffering from insomnia.32,33 More systematic explorationof sleep perception improvements with ISR treatment may assist in clarifying treatment mechanisms in future studies. Furthermore, this treatment also provides exposure to the single
element that is most feared by individuals with insomnia, theexperience of sleep deprivation. Indeed, the sleep deprivation
alone, with an acutely increased homeostatic drive, may be responsible for the generation of some improvements in sleep.
Further research will be needed to explore the effective components of this ISR treatment.
Participants undergoing stimulus control therapy (SCT) also
experienced significantly improved sleep from Pre- to Posttreatment. However, treatment response indicated by SOL and
TST were slower to eventuate over the treatment weeks in comparison to those groups receiving ISR. It must be noted thatan early response to SCT has been indicated in some research,with significant effects emerging in some sleep variables after
only one week of treatment in some patients.18,34 Although thecurrent study did not investigate individual response, a rapid
mean response was not apparent across all sleep variables
following SCT. However, consistent with this previous
research, the WASO and SE variables did demonstrate immediate improvements in the SCT group.
The combination ISR+SCT treatment group showed trends
for outperforming single treatments, producing immediate
treatment gains that were impressively maintained. The combination ISR+SCT group was associated with the strongest
treatment response, resulting in SOLs close to the 30-minutecutoff criterion for “good sleeper” status, larger effect sizes, anda somewhat greater proportion of treatment responders. Indeed,
61% of participants in the ISR+SCT treatment group achieved aclinically significant treatment response according to the sleep
diary criterion, achieving “good sleeper” status, in comparison
to 47% of ISR only recipients and 38% of SCT recipients. In
addition, this combination group produced fewer treatment
dropouts than other treatment conditions. The changes up
to Post-treatment in subjective sleep and daytime functioning variables for the combination ISR+SCT treatment group,as indicated by effect sizes, were consistently greater than in
the other treatment groups. The results obtained in this groupwere consistent, and even superior in some cases, to those reported in meta-analytic studies of insomnia treatments.6,7 For
instance, the ISR+SCT treatment group showed increases in
TST that were close to one hour. Reductions in mean WASO
in the ISR+SCT group were comparable to the improvements
obtained with SCT, reduced to around 40 minutes.
Nevertheless, there were relatively few statistically significant differences between active treatment groups, suggestingthat these groups often improved to a similar extent, and at asimilar rate, over time. Alternatively, it must be recognized that

Table 4—Within treatment group N and % of sleep diary “treatment
responders” at Follow-up 1
Responder Criteria 1

Responder Criterion 2

N

%

N

%

ISR

7

46.7%

7

36.8%

SCT

6

37.5%

6

30.0%

ISR+SCT

11

61.1%

13

65.0%

Criteria 1 = (a) reduction of SOL from Pre-treatment to Follow-up 1 toan average of < 30 min, or a reduction of SOL by ≥ 50%, and (b) sleep
efficiency increase to ≥ 85%. Criterion 2 = a reduction in SOL by 33% to< 35 minutes.

ables such as SOL and SE. For instance, Morin and colleagues31
outline various indicators of clinical significance, including (a)the proportion of clients who experience a reduction of 50% on
sleep variables of SOL or WASO, and reach an absolute valueof near or below the 30-min criterion used to define insomnia,(b) the proportion of clients whose sleep efficiency moves into
a normative range (i.e., > 80% to 85%), or (c) a reduction in
hypnotic drug use.
The current study utilized a dual sleep diary criterion for theassessment clinical significance. Classification of response required (a) reduction of SOL to an average < 30 min, or a reduction of SOL by ≥ 50%, and (b) SE increase to ≥ 85%. Clinicallysignificant treatment response was assessed at Follow-up 1(beginning 6 weeks following treatment). Table 4 reports the
proportion of clients who met these criteria for a “responder,”in addition to those meeting criteria utilized in meta-analyses(reduction in SOL by 33% to < 35 min as the criterion for clinically meaningful change).7 Given that data were not available
at Follow-up 1 for the control group, these analyses pertain
to active treatment groups only. Overall, this classification of
response resulted in 40% to 45% of participants showing aclinically significant response. These data indicate the greatest number and percentage of “responders” in the combination
ISR+SCT treatment group, with over 60% achieving a clinically significant change.
DISCUSSION
The aim of this study was to further explore the efficacy ofintensive sleep retraining (ISR) treatment for chronic insomnia.
This treatment approach is novel in attempting to treat insomnia in an intensive, single treatment period. ISR was compared
to, and combined with, stimulus control therapy, and comparedwith a “sleep hygiene only” control group, with participants
randomly allocated to treatment group. Outcome variables
included the primary outcome of subjective sleep parameters,in addition to objective sleep variables and psychological anddaytime functioning measures.
As predicted, participants in all three active treatment groups
experienced significant improvements in subjective sleep variables following treatment. This was in comparison to the minimal changes observed in the sleep hygiene treatment control
group. ISR seemed to produce immediate improvements insleep, as demonstrated by decreased SOL and increased TSTin the first week following the treatment weekend. Indeed, the
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58

Intensive Sleep Retraining for Chronic Primary Insomnia—Harris et alneed to prove to be both clinically effective and cost-effective.
The advantage, over and above traditional therapies, must be
demonstrated in order to justify its use.
These advantages may include the rapid treatment response,
treatment effectiveness in particular populations, or in addressing particular components of the sleep disorder, factors open
to further investigation. The superior treatment response forsleep onset problems (with less impact on WASO) may indicate suitable ISR treatment recipients. With the assumption of
conditioning-based treatment mechanisms, responses to ISR
may indicate that there is some difference between the conditioned insomnia episodes that occur prior to sleep onset fromthose occurring during the night. Further research may further
determine the sleep profile of those individuals with insomnia
that best respond to this procedure.
Given that ISR is an intensive, monitored, in-laboratory procedure lasting 25 hours, the administration of this treatment isvery costly. In order for this to become a treatment that is able
to be easily disseminated to the sleep disordered community,
alternative administration of the treatment routine may need to
be devised. One such possibility is a self-administered versionof ISR at home. Home administration of ISR treatment thenneed not require a transfer of the conditioning training to thehome environment, perhaps resulting in a superior treatment
response. Therefore, an ISR treatment version administered in
the home environment of individuals suffering from insomnia
is an important avenue for future research.
The findings of the current study suggest that a brief, intensive, conditioning treatment procedure may be a useful treatment
possibility for individuals suffering from primary insomnia, particularly when combined with traditional behavioral treatments.
ISR rivals SCT, presently the most supported single behavioral
intervention. Further investigations into determining appropriate treatment recipients, and alternative forms of implementation of such a brief conditioning treatment are warranted.

significant differences between active interventions are difficult to obtain with the typical small absolute differences in
response. It may be that a much larger sample size would havebeen required in order to establish any consistent differencesin outcome between treatments. Nevertheless, the sample size
is comparable to that in other treatment comparison research,31
and the clinical significance of such small between-group differences may not be particularly meaningful. With limited power
and a truncated participation of the control group (to Post-treatment) due to ethical and dropout considerations, longer-term
control comparisons were unable to be made in this study.
Actigraphy and questionnaire measures also provided interesting information about treatment-related change. Questionnaire measures supported significant changes in daytime
functioning, beliefs about sleep and confidence in sleep.
Whether these cognitive changes occur as a function of successful behavioral intervention, or are key processes in treatment outcome may be addressed by further research in thisarea. The actigraphy data failed to support significant changes
in sleep, despite using an adjusted manual scoring method anda sensitivity setting in the scoring algorithm that calibrated actigraphy TST to PSG TST. Actigraphy has similarly failed tomirror subjective sleep changes in other treatment studies ininsomnia,35 and objective measures (i.e., EEG) fail to replicate
the extent of subjective sleep changes in clinical insomnia treatment studies.36 The current findings are consistent with conclusions regarding the limited usefulness of actigraphy in assessing
sleep in insomnia.37 In addition, although the data were not presented, the actigraphic data derived from the automatic (withsensitivity setting) scoring method similarly failed to indicate atreatment response over time. Unfortunately, no follow-up PSG
comparisons were made in this sample. This may have provided
a validation of, and a corresponding preference for, either method of actigraphy scoring. Similarly, this kind of follow-up PSG
assessment may have provided information regarding whether
objective changes in sleep were apparent following treatment.
It remains possible that the lack of response to treatment indicated by actigraphy validly indicates a lack of objective change
in sleep. This would suggest that the changes in sleep diary data
reflect the subjective nature of both the complaint and change
in sleep variables.
This RCT represents the first comprehensive study into
the efficacy and comparative effectiveness of intensive sleep
retraining and, as such, represents a novel contribution to theinsomnia treatment literature. Although the creation and assessment of novel treatment ideas are important for the advancement of the field, ISR fails to fulfill all requirements of an idealintervention. Despite significant treatment benefits, ISR alone
did not normalize sleep parameters, on average. With a more
rapid and larger magnitude of response when combined with
SCT, this combined treatment approach may provide two advantages, a rapid treatment response (i.e., comparative to therapidity of drug therapy) and the maintenance and enhancement of treatment gains. Indeed, a synergistic effect may bepossible, with an initial rapid response to ISR improving consequent compliance to and therefore response to SCT. Further
studies may systematically measure compliance to treatment to
explore this possibility. However, if ISR is to provide an appealing supplemental treatment or treatment alternative, it will
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ABBREVIATIONSISR, intensive sleep retraining
SCT, stimulus control therapy
OSA, obstructive sleep apnea
DSPD, delayed sleep phase disorder
PLMS, periodic limb movements of sleep
BDI-II, Beck Depression Inventory-II
SOL, sleep onset latency
BMI, body mass index
RDI, respiratory disturbance index
WASO, wake time after sleep onset
SE, sleep efficiency
TST, total sleep time
PSQI, Pittsburgh Sleep Quality Index
SES, Sleep Self Efficacy Scale
DBAS, Dysfunctional Beliefs and Attitudes about Sleep
DFFS, Daytime Feeling and Functioning Scale
PSG, polysomnography
EEG, electroencephalography
EOG, electrooculography
EMG, electromyography
LOT, lights out time
SSS, Stanford Sleepiness Scale
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SH, sleep hygiene
ANOVA, analysis of varianceSD, standard deviation
RCT, randomized controlled trial

16. Rechtschaffen A, Kales A. A manual of standardised terminology, techniques, and scoring system for sleep stages of human subjects. Los Angeles: Brain Information Service/Brain Research Institute, UCLA, 1968.
17. Hoddes E, Zarcone V, Smythe H, Phillips R, Dement WC. Quantificationof sleepiness: a new approach. Psychophysiology 1973;10:431-6.
18. Espie CA, Lindsay WR, Brooks N, Hood EM, Turvey T. A controlled
comparative investigation of psychological treatments for chronic sleeponset insomnia. Behav Res Ther 1989;27:79-88.
19. Turner RM, Ascher LM. A within-subject analysis of Stimulus Control Therapy with severe sleep-onset insomnia. Behav Res Ther
1979;17:107-12.
20. Chesson A, Anderson M, Littner M, et al. Practice parameters for the nonpharmacologic treatment of chronic insomnia. Sleep 1999;22:1-6.
21. Edinger JD, Sampson WS. A primary care “friendly” cognitive behavioral
insomnia therapy. Sleep 2003;26:177-82.
22. Guilleminault C, Palombini L, Poyares D, Chowdhuri S. Chronic insomnia, premenopausal women and sleep disordered breathing: part 2. Comparison of nondrug treatment trials in normal breathing and UARS post
menopausal women complaining of chronic insomnia. J Psychosom Res
2002;53:617-23.
23. Pallesen S, Nordhus IH, Kvale G, et al. Behavioral treatment of insomnia
in older adults: an open clinical trial comparing two interventions. Behav
Res Ther 2003;41:31-48.
24. Stepanski E, Wyatt JK. Use of sleep hygiene in the treatment of insomnia.
Sleep Med Rev 2003;7:215-25.
25. Morin CM, Bootzin RR, Buysse, DJ, Edinger JD, Espie CA, Lichstein
KL. Psychological and behavioral treatment of insomnia: update of therecent evidence (1998-2004). Sleep 2006;29:1398-414.
26. Morin CM. Insomnia; Psychological assessment and management. New
York: The Guilford Press, 1993.
27. Gueorguieva R, Krystal JH. Move over ANOVA: progress in analyzing
repeated-measures data and its reflection in papers published in the Archives of General Psychiatry. Arch Gen Psychiatry 2004;61:310-7.
28. Nich C, Carroll K. Now you see it, now you don’t: a comparison of traditional versus random-effects regression models in the analysis of longitudinal follow-up data from a clinical trial. J Consult Clin Psychol 1997;
65:252-61.
29. Schafer JL, Graham JW. Missing data: our view of the state of the art.
Psychol Methods 2002;7:147-77.
30. Chakraborty H, Gu H. A mixed model approach for intent-to-treat analysis in longitudinal clinical trials with missing values. Research Triangle
Park, NC: RTI Press. RTI Press Publication No. MR-0009-0903, 2009.
31. Morin CM, Colecchi C, Stone J, Sood R, Brink D. Behavioral and pharmacological therapies for late-life insomnia. JAMA 1999;281:991-9.
32. Mercer J, Lack LC, Bootzin RR. Feedback of sleep/wake state improves
subjective and objective sleep of insomniacs. Sleep 2005; 28(Abstract
Suppl.): pA242.
33. Tang NK, Harvey AG. Correcting distorted perception of sleep in insomnia: a novel behavioural experiment? Behav Res Ther 2004;42:27-39.
34. Lacks P, Bertelson AD, Sugerman J, Kunkel J. The treatment of sleepmaintenance insomnia with stimulus-control techniques. Behav Res Ther
1983;21:291-5.
35. Espie CA, MacMahon KM, Kelly HL, et al. Randomized clinical effectiveness trial of nurse-administered small-group cognitive behavior therapy for persistent insomnia in general practice. Sleep 2007;30:574-84.
36. Krystal AD, Edinger JD. Sleep EEG predictors and correlates of
the response to cognitive behavioural therapy for insomnia. Sleep
2010;33:669-77.
37. Verbeek I, Klip EC, Declerck AC. The use of actigraphy revised: the value
for clinical practice in insomnia. Percept Mot Skills 2001;92:852-6.

ACKNOWLEDGMENTS
This research was partially funded by a National Health andMedical Research Council (NH&MRC) grant.
DISCLOSURE STATEMENT
This was not an industry supported study. Dr Kemp is in a
directorship role with Adelaide Insomnia Clinic (private business). Dr Bootzin has received research support from Takeda
Pharmaceuticals. The other authors have indicated no financial
conflicts of interest.
REFERENCES

1. Bootzin RR. Stimulus control treatment for insomnia. Proc Am Psychol
Assoc 1972;7:395-6.
2. Edinger JD, Wohlgemuth WK, Radtke RA, Marsh GR, Quillian RE. Does
cognitive-behavioral insomnia therapy alter dysfunctional beliefs about
sleep? Sleep 2001;24:591-9.
3. Mendelson WB. Long-term follow-up of chronic insomnia. Sleep
1995;18:698-701.
4. Mellinger GD, Balter MB, Uhlenhuth EH. Insomnia and its treatment.
Prevalence and correlates. Arch Gen Psychiatry 1985;42:225-32.
5. Morgenthaler T, Kramer M, Alessi C, et al. Practice parameters for thepsychological and behavioral treatment of insomnia: an update. An American Academy of Sleep Medicine report. Sleep 2006;29:1415-9.
6. Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions
for insomnia: A meta-analysis of treatment efficacy. Am J Psychiatry
1994;151:1172-80.
7. Murtagh DR, Greenwood KM. Identifying effective psychological treatments for insomnia: A meta-analysis. J Consult Clin Psychol
1995;63:79-89.
8. Robertson JA, Broomfield NB, Espie CA. Prospective comparison of subjective arousal during the pre-sleep period in primary sleep-onset insomnia and normal sleepers. J Sleep Res 2007;16:230-8.
9. Harris J, Lack L, Wright H, Gradisar M, Brooks A. Intensive sleep retraining treatment for chronic primary insomnia: a preliminary investigation. J
Sleep Res 2007;16:276-84.
10. Lichstein KL, Stone KC, Donaldson J, et al. Actigraphy validation withinsomnia. Sleep 2006;29:232-9.
11. Buysse DJ, Reynolds CF, Monk TH, Berman SR, Kupfer DJ. The Pittsburgh Sleep Quality Index: a new instrument for psychiatric practice andresearch. Psychiatry Research 1989;28:193-213.
12. Mimeault V, Morin CM. Self-help treatment for insomnia: Bibliotherapy with and without professional guidance. J Consult Clin Psychol
1999;67:511-9.
13. Lacks P. Behavioral Treatment for Persistent Insomnia. New York: Pergamon Press, 1987.
14. Morin CM, Stone J, Trinkle D, Mercer J, Remsberg S. Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychol Aging 1993;8:463-7.
15. Gradisar M, Lack LC, Richards H, Harris J, Gallasch J, Boundy M. Psychometric properties of two new scales for measuring daytime functioning for insomnia. Sleep 2006;29 (Abs. supp.):A339.

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