J. Sleep Res. (2007) 16, 276–284

Intensive Sleep Retraining treatment for chronic primary
insomnia: a preliminary investigationJ O D I E H A R R I S , L E O N L A C K , H E L E N W R I G H T , M I C H A E L G R A D I S A R and
AMBER BROOKSSchool of Psychology, Flinders University of South Australia, Adelaide, SA, Australia

Accepted in revised form 17 April 2007; received 17 October 2006

SUMMARY

The aim of this study was to assess the effectiveness of Intensive Sleep Retraining, anovel, short duration behavioural therapy in treating chronic primary insomnia.
Seventeen consecutive volunteers from the general public (mean age = 39.1 years),meeting selection criteria for chronic primary insomnia participated in the treatment
study. The study was performed as a case replication series. Assessment involved sleep
diary, actigraph and questionnaire measures of sleep and daytime functioning for aperiod of 2 weeks prior to, immediately after, and 6 weeks following the treatment.
Treatment involved a single night of sleep deprivation, facilitating short sleep latencies(mean: 6.9 min) to a series of 50 brief nap opportunities. Following treatment, Sleep
Onset Latency significantly decreased by a mean of 30.5 min (SD = 28.3), Wake Timeafter Sleep Onset significantly decreased by a mean of 28 min (SD = 34.0), and Total
Sleep Time significantly increased by 64.6 min (SD = 45.5). Significant improvements
were also seen in the daytime functioning and psychological measures of fatigue andvigour, cognitive sleep anticipatory anxiety and self-efficacy for sleep. This brief therapy
was effective in improving sleep and some daytime functioning and psychologicalquestionnaire measures. These improvements were maintained up to 2 months
following the treatment weekend. Further exploration of this brief therapy is needed,with larger, randomized, placebo-controlled trials over longer follow-up periods, and incomparison to other traditional therapies for insomnia.
keywords
insomnia

behavioural therapy, brief therapy, intensive sleep retraining, sleep onset

INTRODUCTION
With prevalence rates of 9–15% (Ancoli-Israel and Roth,
1999; Ohayon, 2002), chronic insomnia is the most common of
sleep disorders. Chronic insomnia is associated with significant
fatigue, irritability, decreased concentration and memory,increased risk of serious accidents ⁄ injuries and increased
healthcare use (Balter and Uhlenhuth, 1992; Chesson et al.,
2000; Kapur et al., 2002), resulting in both significantly
impaired quality of life and economic burden to society(Walsh and Engelhardt, 1999). The latest figures suggest
that, in Australia, insomnia results in AUD$30.4 m annually
Correspondence: Jodie Harris, School of Psychology, Flinders University, GPO Box 2100, Adelaide, SA 5001, Australia. Tel.: 618 8201
2349; fax: 618 8201 3877; e-mail: jodie.harris@flinders.edu.au

276

in GP costs alone, with pharmaceutical costs of managing
sleep disturbances exceeding AUD$10 m (Access Economics,
2004).
Pharmacotherapy remains the most common treatment for
insomnia (Ancoli-Israel and Roth, 1999). However, researchsuggests that cognitive behavioural therapies (CBT) for
insomnia produce significantly greater benefits than pharmacotherapy (Jacobs et al., 2004) and better long-term outcomes(Morin et al., 1994; Morin et al., 1999a). Although benefits
gained from pharmacological treatment are immediate, theseagents provide symptomatic relief that is not sustained beyond
the cessation of treatment (Edinger et al., 2001; Langer et al.,1999). The treatment benefits in response to CBT, in contrast,
remain beyond the termination of treatment (National Institutes of Health, 2005). But despite significant experimental
support for non-drug therapies, there is some suggestion that! 2007 European Sleep Research Society

Intensive Sleep Retraining treatment for chronic primary insomnia
they need to provide comparatively rapid improvement insleep if they are to be an appealing alternative to drug therapy(Guilleminault et al., 1995).
The non-pharmacological insomnia treatment literaturesuggests that the most notable improvements in insomnia
occur in response to Stimulus Control Therapy (SCT;
Bootzin, 1972) (Edinger et al., 2001). The goals of SCT areto strengthen the bed, bedroom, bedtime activities and thesleep attempt as cues for sleep, and to extinguish them ascues for wakefulness by curtailing any sleep-incompatible
activities (Bootzin and Rider, 2000). This is accomplishedby: going to bed only when sleepy, getting out of bed if
unable to initiate sleep quickly, arising at the same time eachmorning, avoiding using the bedroom for activities otherthan sleep (and sexual activity), and avoiding daytime naps
(Bootzin et al. 1991). SCT is the most validated behaviouralinsomnia treatment with the highest level of supporting
empirical evidence and is recommended as a !standard"
treatment by the American Academy of Sleep Medicine(Chesson et al., 1999).
Stimulus Control Therapy is supported theoretically by therationale that psychophysiological, or conditioned, insomnia
results when the bed and bedroom environment have lost theirdiscriminative ability to evoke sleepiness, and become insteada conditioned stimulus for arousal, thereby inhibiting sleep
onset. SCT can then reintroduce the sleep environment as acue for sleepiness, utilizing a build up of sleep pressure over the
early stages of the therapy to assist in the production of
sleepiness, resulting in more rapid sleep onsets. Sleep Restriction Therapy (Spielman et al., 1987) similarly uses mild sleep
deprivation induced homeostatic sleep pressure to promote
improvements in sleep (Morin et al., 1999b). However, effective behavioural treatment typically takes between 4 and8 weekly therapy sessions (Smith et al., 2002), and considerable investment of time and effort may be required for
optimum response to these strategies (Edinger and Wohlgemuth, 1999). These early stages of the therapy may involve
truncated sleep, increased sleepiness and fatigue, and resulting
problems with compliance.
The various cognitive behavioural treatments for insomnia
are a treatment option that takes longer than drugs to beeffective, and require considerable motivation to comply withthe often-difficult recommendations. Indeed, a lack of compliance to recommendations, a lack of understanding of theprocedures or rationale, experience of previous treatment
failure, and lack of partner support may all detrimentally
impact on the treatment response (Chambers, 1992). As aresult, it is desirable for research in this area to aim to provide
novel treatment approaches, with the aim of trying to improveupon or complement those currently offered (Harvey andTang, 2003).
Intensive Sleep Retraining (ISR), essentially a condensed
version of a behavioural conditioning treatment, may prove to
be one such therapy. A pilot study with four participants,
involved a treatment period of a single weekend of sleep
deprivation to facilitate the experience of multiple short sleep! 2007 European Sleep Research Society, J. Sleep Res., 16, 276–284

277

onset latencies at half hourly opportunities. This study
demonstrated an immediate improvement in sleep that lasted
for 2 months following therapy (Lack and Baraniec, 2002).
The current research aims to further explore this potentially
useful new therapy.

MATERIALS AND METHOD
ParticipantsRequests for volunteers for the treatment study were made to
the general public on radio, television and in local newspapers
for people aged between 18 and 60 years, to participate in astudy involving assessment and treatment. An initial telephoneinterview identified potential participants with a complaint of
sleep onset insomnia or a disorder of initiating and maintaining sleep of at least 6 months duration. Following the initialinterview, potential participants were sent a 1-week sleep diary
and a sleep history questionnaire with a symptom checklist.
Inclusion criteria, based on returned questionnaires and diaries
included (i) sleep latency of >30 min, three times in the week,(ii) Total Sleep Time (TST; average) of <7 h and (iii) daytime
consequences of poor sleep, including reports of tiredness ⁄ fatigue.
Exclusion criteria included any other reported ill health,severe depression [for example, scores of 20 or greater on the
Depression, Anxiety and Stress Scale (DASS-21, short form)
questionnaire] (Lovibond and Lovibond, 1995), excessive
alcohol or caffeine use, regular tobacco use, the use of
hypnotic medication or other medications known to affectsleep, and clinical indications of delayed sleep phase syndrome,
obstructive sleep apnoea, restless legs syndrome or periodic
limb movement disorder. Altogether, 29 applicants were
excluded from participation following screening due todepression (four), pain (three), OSA symptoms (two), sleep
maintenance insomnia only (four), regular use of sleep
medication (two), DPSP symptoms (six), insufficient SOL(five), restless legs symptoms (one) and other non-hypnotic
medication use (two). These selection criteria were designed torecruit chronic primary insomniacs with a principal difficultyof initiating sleep, with or without awakenings during thenight. In total, 17 consecutive primary insomniacs who met
criteria (five males, 12 females) with a mean age of 39.1 years(SD = 12.41) participated in the research. Participants presented with an average subjective pretreatment mean Sleep
Onset Latency (SOL) of 69.94 min, TST of 5 h, 17 min andSleep Efficiency (SE) of 62.44%. Fifty-nine percent of participants also reported sleep maintenance concerns, awake for an
average of >60 min overnight. Participants reported sufferingfrom insomnia for an average of 12.5 (SD = 8.75) years prior
to study entry. The 24% who had previously used hypnotic
medication ceased use at least 1 month prior to treatment.
Previous non-drug treatments reported included hypnosis(one), meditation (two), psychological intervention (one).
Seventy-seven percent of participants had not previously tried
any non-drug treatment methods.

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All participants signed informed consent forms prior tocommencing the pretreatment assessment period. Ethics
approval was obtained from the Social and Behavioral
Research Ethics Committee at Flinders University of South
Australia.

Apparatus and materials
Sleep-wake diary
The sleep-wake diary is an important index of a successfultreatment method (Langer et al., 1999). The diary used was agraphical version of a sleep log, and required the recording oflights-out-time, estimated SOL, number and length of awakenings during the night, periods of sleep overnight and final outof-bedtime. Mean SOL, Wake Time after Sleep Onset(WASO), TST and SE (Total Sleep Time ⁄ Time in
Bed · 100) were calculated for each 2-week assessment period.
Questionnaires
Although few studies have determined the effects of behavioural therapies on daytime functioning (Edinger and Wohlgemuth, 1999), it is important to assess this aspect of theinsomnia complaint. The DASS-21 was used as an indicator of
depression, anxiety and stress. The DASS-21 consists of three
7-item self-report scales taken from the full version of theDASS, both versions of which have been demonstrated to be avalid, reliable measure of these constructs in clinical and nonclinical groups (Antony et al., 1998). Items include !I was
unable to become enthusiastic about anything", !I felt scaredwithout any good reason" and !I tended to over-react tosituations", with scores added and doubled for each subscale.
The Dysfunctional Beliefs and Attitudes About Sleep(DBAS) is a frequently used 30-item questionnaire, utilized
to assess cognitions about sleep, including sleep loss, sleep
need and causes and sequelae of insomnia (Morin et al., 1993).
The 65-item Profile of Mood States (POMS) was administeredin order to obtain the Fatigue and Vigor subscale scores that
address these particular daytime functioning aspects (McNair
et al., 1971). Items included in the list are !listless", !lively" and!worn out", with responses ranging from 0 = !Not at all" to
4 = !Extremely" over the past week. The Sleep Anticipatory
Anxiety Questionnaire (SAAQ) was utilized as a measure ofpresleep anxiety, including both cognitive and somatic manifestations of anxiety related to the attempt to initiate sleep.
The SAAQ shows high reliability, and significantly differentiates insomniacs from the non-insomniac population (Bootzin
et al., 1994).
The sleep Self Efficacy Scale (SES) is a 9-item scale to assess
an individual"s confidence in the ability to influence their own
sleep behaviour, with possible scores ranging from 9 to 45(Lacks, 1987). Responders are required to indicate theirconfidence in being able to perform sleep-related behaviours,for example, !Fall asleep at night in under 30 min", on a 5-point
Likert scale, ranging from 1 (Not at all confident) to 5 (Veryconfident). Higher scores on this scale indicate a higher degreeof self-efficacy for sleep. Research indicates that changes on
this measure reflect treatment-related improvement in sleep(Spielman et al., 1987). The questionnaire was only introduced
half way through the study, and was thus administered to only
nine participants. The Stanford Sleepiness Scale (SSS) was
administered prior to each trial over the treatment procedure
as a measure of current subjective sleepiness (Hoddes et al.,1973). This is a frequently used measure of sleepiness,consisting of a choice from a range of descriptives from
1 = !Feeling active and vital; alert; wide awake" to 7 = !Lost
struggle to remain awake".
Actigraphy
Participants wore an ActiTrac activity monitor (IM Systems,
Baltimore, MD, USA) on their non-dominant wrist duringassessment periods. Activity counts were averaged for each 30s epoch, recorded and downloaded for analysis. Actigraphy
sleep onset time was estimated as the start of the first period ofat least 15 consecutive minutes of no wrist activity after lights
out time (Jean-Louis et al., 1996). Amount of WASO wasestimated from an algorithm using the number of epochs withmovement from initial sleep onset to final wake up time (asindicated by the subject"s movement, corroborated by sleep
diary). Automatic analyses were utilized to produce scores for
TST across the period in bed, determined from the time ofestimated sleep onset to the time of final wake up, minus
WASO. Sleep Efficiency was calculated by dividing the TST by
the time in bed, multiplying it by 100. Actigraphic sleep
estimates have been demonstrated to be moderately related topolysomnography measures of sleep in insomnia sufferers, andas such it has been suggested that actigraphy can be a reliableindicator of objective changes in sleep over time within
participants with insomnia undergoing behavioural therapy,
with the advantage of inexpensively providing data acrossmultiple nights (Ancoli-Israel et al., 2003).
Polysomnography
Participants were monitored throughout the ISR sleep latency
treatment trials utilising electroencephalography (EEG; CZOZ bipolar placement) and electro-oculography (EOG). EEG
was used to determine sleep onset during treatment using
labview5 (a modified version of the Laboratory Virtual
Instrument Engineering Workbench; National Instruments
Corporation, Texas, USA), a computer software program used
to graphically quantify raw EEG power within different
frequency bandwidths. This method has been validated against
standard raw EEG defined SOL on the Multiple Sleep Latency
Test (r = +0.90; Lack et al., 2003). Sleep onset was determined in accordance with conventional criteria as described in
Rechtschaffen and Kales (1968). Sleep onset was deemed tooccur when the alpha power reduced to less than one half of
the average relaxed wakefulness baseline for three consecutive
epochs. This three consecutive epoch criterion is thought to! 2007 European Sleep Research Society, J. Sleep Res., 16, 276–284

Intensive Sleep Retraining treatment for chronic primary insomnia

Procedure
Pretreatment
After a full explanation of the study and a tour of the Sleep
Laboratory, participants completed the DASS questionnaire.
After this final screening questionnaire and familiarisation
with the Sleep Laboratory, participants completed a 2-weekbaseline assessment period using sleep ⁄ wake diaries andactigraphy.
Treatment
Participants arrived at the Sleep Laboratory at 18:00 hours,
allowing time for EEG and EOG placement, equipment
calibrations and participant settling time (approximately
30 min). Participants were required to spend the treatment
period in bed, with the exception of bathroom visits. The
treatment, scheduled to begin at approximately 2 h prior tohabitual bedtime (range: 19:30–21:00 hours), involved a series
of !sleep trials". Subjective sleepiness was monitored immediately prior to each trial by the SSS. For each sleep trial
participants were provided instructions to !lie down, relax andlet yourself fall asleep". Lights were then extinguished, thebedroom door was closed, and the experimenter retired to an
adjoining monitoring room. Participants were then monitored
via EEG for sleep onset, then being allowed to sleep for at least
1.5 min, up to 4 min (Average: 3.1 min, SD = 1.2). The
duration of sleep allowed in each trial was limited in order tomaintain homeostatic sleep drive and short sleep latencies. If
sleep was not achieved in 25 min the trial was terminated. The
following trial began 30 min following the initiation of theprevious trial. Thus, sleep onset trials were conducted at eachhalf hour time point throughout the treatment period. Eachparticipant completed a minimum of 50 sleep onset trials
during the therapy period (range: 50–56). Treatment ceased
with sufficient time to travel home prior to habitual bedtime.
In between trials, participants remained in semi-supine orsupine position in bed, awake and engaging in minimal activity

such as reading or watching video films. If a participant
appeared to have difficulty maintaining wakefulness during theinter-trial wake periods, quiet conversations initiated by theexperimenter avoided inadvertent sleep onsets. No time cues
were provided during the routine, and no feedback wasprovided as to whether the participants met criteria for sleep
onset during the trials. The ambient temperature was kept
constant at 22 "C and room illumination was 50 lux, measured
at the head of the bed. Small portions of food were provided
every 2 h to satiate hunger, but to avoid the soporific effects oflarge meals on sleepiness. Following the therapy procedure,
participants were allowed to return home to obtain a recovery
sleep (with an allotted bed period maximum of 8 h), beginningat a time as close as possible to the participants" habitual
bedtimes.
Post-treatment
The 2-week post-treatment monitoring was initiated following
two nights of recovery sleep after the treatment routine,
implemented to exclude effects of acute sleep deprivation on
sleep variables (Bonnet, 1985). A further 2-week follow-up
period was undertaken beginning at 6 weeks after treatment.
Questionnaires were completed at the end of every 2-weekassessment period. Following the final assessment, participants
were paid a nominal reimbursement fee to contribute towards
accumulated travel costs.
RESULTS
Treatment protocol
Figure 1 illustrates the mean SOL for participants, averaged ateach half hourly time point over the treatment period. As
participants started treatment approximately 2 h prior tohabitual bedtime, some initial and final trial times include
fewer than 17 participants. The maximum of 17 participants
were included from 21:00 hours on night 1 until 21:00 hours onnight 2 of treatment. The sleep onset criteria were satisfied in
93% of the sleep trials, indicating the success of the treatment
protocol in allowing the repetitive experience of falling asleep.
The mean SOL for all trials was 6.9 min (SD = 3.6). The

Figure 1. Mean Sleep Onset Latency andStanford Sleepiness Scale scores at each sleep
trial time throughout the treatment
procedure.

Sleep onset latency (SOL:min)

25.00

5.00
4.50

20.00

4.00
3.50

15.00

3.00
2.50

10.00

2.00
1.50

5.00

1.00

SOL
0.00
19:30 21:30 23:30! 2007 European Sleep Research Society, J. Sleep Res., 16, 276–284

1:30

3:30

5:30

7:30

9:30

SSS

11:30 13:30 15:30 17:30 19:30 21:30

Sleep trial time

0.50
0.00

Stanford sleepiness scale (SSS) score

identify unequivocal sleep, and is advocated for experimentaluse (Carskadon, 1986).

279

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J. Harris et al.
utilised. Post hoc analyses examined the significance of thedifference between pretreatment and both post-treatment and6-week follow up.

average TST within nap opportunities was 3.1 min (SD = 1.2).
Those few trials that were terminated after 25 min withoutachieving sleep onset were almost entirely restricted to the first
few hours of the treatment period. The figure also demonstrates
the usefulness of the routine in providing a large number of
rapid sleep onsets. On average, 32.0 trials per participant
contained a SOL value of <5 min in length.
The figure demonstrates that the mean SSS for each trial
increased over the procedure, indicating a subjective increasein sleepiness, in addition to the increased objective sleepiness(decreased sleep onset latencies).

Sleep Onset Latency
There was a significant change over time in mean subjective SOL(see Fig. 2). Mean SOL decreased significantly by 30.4 min fromthe pretreatment mean value of 69.9 to 39.5 min post-treatment.
At the 6-week follow up the improvement in SOL remained
significant. Objective mean SOL decreased with marginal
statistical significance over time, from 47.8 min pretreatment
to 34.6 min at post-treatment. Post hoc analyses indicated thatthe mean objective SOL value at follow up (38.1 min) was nolonger significantly different from baseline (Table 1).

Treatment response
Response to treatment in subjective (sleep diary) and objective(actigraphic) estimates of sleep parameters, and questionnairevariables was determined by examining the change frombaseline (pretreatment) values (see Table 1) using repeatedmeasures anovas. The assumptions of anova were largely met,with Q-Q plots confirming the normality of the residuals foreach variable. For those variables that violated sphericity
assumptions, a Greenhouse-Geisser adjustment has been

Wake Time after Sleep Onset
A significant change over time was also demonstrated insubjective WASO figures (see Table 1). The mean subjective
WASO was significantly reduced by 28 min at post-treatment,
and 34.5 min at follow up. Although actigraphy measured

Table 1 anova and post hoc analyses for treatment-related changes on sleep parameters

MeasureSleep Onset Latency(min)
SOL (sleep diary)
SOL (actigraph)
Total Sleep Time(min)
TST (sleep diary)
TST (actigraph)
Wake After Sleep
Onset (min)WASO (sleep diary)
WASO (actigraph)
Sleep Efficiency(%)
SE (sleep diary)
SE (actigraph)

Pretreatment

Post-treatment

Follow up

Mean

SD

Mean

SD

Mean

SD

F

d.f.

P-value

69.94
47.80

(35.38)(31.33)39.46****
34.60*(18.71)(25.47)47.05**
38.06(26.36)(32.06)

14.84
4.15

1.4
10

0.000
0.049

317.20356.08(80.19)(70.46)381.76****384.00*(68.90)(55.11)359.82**361.78(93.11)(64.15)

16.46
2.92

15
10

0.000
0.100

87.49
104.43(63.03)(75.15)59.46**
102.67(53.88)(68.36)53.02**
90.58*(56.02)(61.89)

6.18
3.5

15
10

0.011
0.073

62.44
69.85

(15.85)(14.71)75.71****
72.81*(13.64)(15.57)73.70****
74.57***(14.95)(13.51)

22.66
10.50

15
10

0.000
0.003

180
160
140
120
100
80
60
40
20
0

430
SOL

TST

400
370
340
310
280

1

2

3

4

5

6

7

8

9 10 11 12 13 14 0

Pre-treatment

00

T R1 R2

1

2

3

4

5

6

7

8

9 10 11 12 13 14250

Total sleep time (min)Sleep onset latency (min)Asterisks indicate post hoc significant changes from pretreatment: *P < 0.05, **P £ 0.01, ***P £ 0.001, ****P < 0.0001.

Post-treatment

Figure 2. Mean daily Sleep Onset Latency and Total Sleep Time immediately prior to, and following T (treatment), R1 (recovery night 1) and R2(recovery night 2).
! 2007 European Sleep Research Society, J. Sleep Res., 16, 276–284

Intensive Sleep Retraining treatment for chronic primary insomnia
WASO showed a reduction by the follow-up period (seeTable 1) it was of minimal clinical importance (13.8 min).

281

Profile of Mood States
Analyses indicated that the POMS Fatigue subscale scores
reduced following treatment, with only the immediate posttreatment change being significantly reduced from baseline (seeTable 2). Marginally significant changes in the POMS Vigour
subscale scores indicated that vigour increased following
treatment and was maintained at follow up.

Total Sleep Time
Subjective TST showed a statistically significant change overtime (see Fig. 2). Mean TST significantly increased from a
pretreatment mean value of 5 h, 17 min to a post-treatment
value of 6 h and 21 min, an average increase of 65 min. This
improvement from baseline was maintained at follow up, withan average increased TST by 42.6 min. The 28-min increase in
TST as indicated by actigraphy at post-treatment, was nolonger significantly different from baseline by follow up.

Sleep Anticipatory Anxiety
The overall change in the total SAAQ score was only
approaching statistical significance (see Table 2). However,as previous research has indicated that cognitive factors often
seem more important in insomnia than somatic factors(Nicassio et al., 1985), the somatic and cognitive items were
evaluated separately. Although the somatic items in this scale
did not significantly change over time, significant reductions
were seen in cognitive sleep anticipatory anxiety from pretreatment to post-treatment and follow up.

Sleep Efficiency
A significant improvement over time was observed for subjective SE, improving by 13% to post-treatment, with an improvement from baseline of 11% maintained at follow up (seeTable 1). Objective SE improved only slightly from pretreatment by a mean of only 2.9% to post-treatment, and 4.7% tofollow up. No significant changes over time were found in either
the objective or subjective time in bed component of SE.

Dysfunctional Beliefs and Attitudes About Sleep
Although no overall significant main effects for time were
found in the DBAS variable, post hoc analyses indicated trends
for improvement following treatment.

Immediate treatment response
In order to assess and highlight the immediacy of response
following treatment, Fig. 2 shows average daily SOL and TST
variables both before treatment and immediately following therecovery nights. The graph indicates that an immediate change
in sleep variables following treatment is maintained throughout this post-treatment assessment period.

Sleep Self Efficacy Scale
The SES measure showed a significant increase in sleep selfefficacy scores over time, indicating improved self-efficacy forsleep following treatment (see Table 2).

Table 2 anova and post hoc analyses for treatment-related changes on questionnaire measures
Pretreatment
Questionnaire

MeanProfile of Mood
States (POMS)
Fatigue subscale
14.40
Vigour subscale
12.067
Sleep Anticipatory
Anxiety (SAA)
SAA total score
14.81
SAA cognitive score
10.13
SAA somatic score
5.25
Dysfunctional Beliefs andAttitudes about Sleep (DBAS)
DBAS total score
79.19
Sleep Self Efficacy (SES)SES total score
20.2
Depression, Anxiety,Stress Scale (DASS)
Depression
8.38
Anxiety
4.13
Stress15.5

Post-treatment

Follow up

SD

Mean

SD

Mean

SD

F

d.f.

P-value(6.86)(6.76)

8.17**
17.50*(6.28)(6.65)

10.87
16.87*(7.84)(6.82)

6.457
3.796

13
13

0.011
0.05

(4.94)(3.56)(2.08)

12.13
7.81**
4.31(5.00)(2.68)(2.80)

11.56
7.13***
4.31(5.55)(3.16)(2.98)

3.76
10.78
0.711

1.35
1.45
14

0.056
0.001
0.508

(16.09)72.44*(15.41)

72.09(16.78)

3.09

1.36

0.083

(4.93)

28.2**(5.77)

26.95**(4.87)

8.128

8

0.012

(8.33)(3.22)(11.33)

5.44
2.63
10.88

(8.25)(3.07)(5.21)

5.38
3.38
11.63

(9.00)(4.99)(7.01)

0.924
1.516
2.21

14
14
1.26

0.420
0.254
0.15

Asterisks indicate post hoc significant changes from pretreatment: *P £ 0.05, **P £ 0.01, ***P £ 0.001, ****P < 0.0001.
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J. Harris et al.

Depression, Anxiety Stress Scales
Although all of the subscales (depression, anxiety and stress)of the DASS-21 showed mean decreases over time, the changes
were not statistically reliable in this study.
DISCUSSION
The current study was designed to investigate a novel
behavioural therapy for primary insomnia, ISR. The treatment
protocol was successfully applied, resulting in a large numberof rapid sleep onsets over the treatment period.
Following this single laboratory treatment session, there
were significant improvements in objective and subjective sleep
parameters, and some daytime functioning and psychologicalvariables. The improvements of sleep shown in this study werevery similar to those in an earlier pilot study (N = 4) using the
ISR treatment protocol. The subjective sleep variables
demonstrated the greatest improvement in sleep, with sleep
latency reducing by 30 min, TST increasing by over an hour,
and wake time overnight reducing by almost 30 min immediately after the treatment. For the most part, these improvements were maintained up to 2 months following treatment.
This degree of improvement was comparable, at least in the
short-term, to that obtained from non-drug therapies in theliterature. For instance, meta-analyses indicate that diary
reported SOL decreases from an average of 60–65 min to
35 min following treatment (Morin et al., 1994, 1999a; Murtagh and Greenwood, 1995). Improvements in subjective TST
in response to ISR even exceeded improvements following
other therapies, which research indicates tends to be in therange of 30 min (Morin et al., 1999a).
There are a number of advantages to the provision of nondrug insomnia treatment in a rapid manner. The ISR protocol
allows treatment implementation in a single sitting, which thencounters issues regarding the length and potential difficulty ofpresent non-drug therapies. Although some clinical research
trials of SCT have demonstrated an early improvement in SOL
for some clients (Turner and Ascher, 1979; Espie et al., 1989),
the rapid treatment response in the present study indicatedimprovement in all sleep variables immediately after treatment
without concomitant reductions in bed period. In that respect
it is comparable with pharmacotherapy in terms of rapidity of
response. The ISR procedure, involving increased sleepinessand frequent awakenings from sleep during treatment,
although procedurally onerous, was associated with only
occasional reports of side effects (e.g. headache and irritability). The procedure was reasonably well tolerated by participants, and all were able to complete the protocol, indicating
the potential for a low drop-out rate from treatment completion. Future systematic reporting of side effects in a larger
study would, however, be useful.
Nevertheless, despite immediate improvements of a significant magnitude, it must be noted that post-treatment values,
on average, leave room for improvement. The implementationof the ISR therapy, in isolation of any other treatment,

resulted in a SE improvement of 11% from baseline, up to
74% 2 months after treatment. Although clinically significant
improvement has been defined in research as a SE ‡80–85%(Morin et al., 1999a), the lower final SE values may reflect theseverity of insomnia symptoms in this group. Absolute
improvement compares with the response to multifaceted
psychological intervention (e.g. 12.3%; Morin et al., 1994).
Suboptimal treatment response from this protocol may havebeen a result of not providing any recommendations regarding
sleep hygiene (Morin et al., 1999a), or further treatment
instructions to follow upon completion of the ISR. It is
possible that behaviours that had previously precipitatedand ⁄ or maintained the insomnia were still present after
therapy, thereby predisposing to a relapse of poor sleep.
However, this design was desired to determine the impact of
this rapid conditioning treatment in isolation from the impactof other treatment. Further research may provide data on
whether the rapid response seen after a single treatment period
can be further enhanced by therapy instructions, such as
adjunctive SCT after the implementation of ISR.
The aspects of the treatment protocol that may contribute to
the post-treatment improvements are a matter of speculation.
The treatment was designed to decondition the insomnia
arousal response to the sleep onset attempt that is typicallyobserved in primary insomnia, or correspondingly, to recondition positive cues for sleep onset. This process is presumed tobe similar to that hypothesized for SCT or Sleep Restriction
Therapy. In SCT, sleep restriction typically occurs in the firstweeks of the therapy and increases homeostatic sleep drive,
gradually facilitating reduced sleep latencies. This behaviouralinsomnia treatment typically takes a few weeks to produce atreatment response. The conditioning cues for sleep onset may
be such factors as the bedroom environment, temporal andsleepiness cues, and attempts to initiate sleep, including lights
being turned off, and closing the eyes. Some of these cues arealso present in the Sleep Laboratory environment. Thereby, an
expectation of a generalization of the ISR treatment responseto the home environment is, perhaps, reasonable. However,
future research may be aimed towards providing this kind of
rapid treatment within the home environment, allowing agreater specificity in conditioning, as well as a reduced cost oftreatment.
Improvements may have been facilitated by perceptions of
having fallen asleep at the termination of sleep trials. The
average nap length of 3.1 min was greater than the 1.5 minallowed in the original pilot study. Following the nap, theparticipants may perceive an awakening from sleep thus
confirming they had, in fact, fallen asleep. This alone, may
be therapeutic. If the degree to which the procedure istherapeutic is dependent upon perception of having fallen
asleep, this will have important implications for the conditioning model. For example, if there is no therapeutic benefit
for participants who did not perceive sleep onsets despite rapid
sleep attainment, the purely behavioural conditioning theoretical basis for treatment may be challenged. Although theperception of sleep was not formally assessed, nor was! 2007 European Sleep Research Society, J. Sleep Res., 16, 276–284

Intensive Sleep Retraining treatment for chronic primary insomnia
confirmatory feedback of sleep onset given, this may be aworthwhile avenue of future research. Further research withlarger sample sizes may also attempt to determine the relative
therapeutic importance of the number of trials in which sleep isattained, and the rapidity of those sleep onsets.
The near-total sleep deprivation occurring during thetreatment also needs consideration for its potential therapeutic
benefit. Although this degree of sleep deprivation would be
expected to improve sleep for one or two nights, this effectshould be temporary. The inclusion of two nights of recovery
sleep before the start of the post-treatment assessment shouldhave eliminated the acutely heightened homeostatic sleep drive
as a contributor to improved sleep during the 2-week posttreatment assessment period (Bonnet, 1985; Lorenzo et al.,1995). There may also be a key component of treatment
arising from the experience of sleep deprivation. The sleep
deprivation and sleepiness experienced during the treatment
period may have been less adverse than participants expected,
resulting in a decreased fear of sleeplessness. Future research
may examine the potential for improved sleep following total
sleep deprivation, without the use of sleep onset trials, thereby
testing the specific efficacy of the sleep trials in promoting
improved sleep.
The potential for improvement to be due to a placebo effectis unable to be ruled out in the current study. Likewise, thesmall sample size in this investigation, and the limited length offollow up, restricts the conclusions that can be drawn from theresults. Future research should evaluate this treatment withgreater participant numbers, utilizing a randomised placebocontrolled design to further explore the utility of ISR.
Further investigation of ISR therapy is warranted. Immediate improvements in sleep and daytime functioning, comparable to other non-drug treatments, were observed after the
25–28 h treatment regime. Indeed, the rapidity of response
seen in this study improves upon the speed of response that is
generally seen with behavioural therapies. Further research
may compare ISR to other individual behavioural therapies, aswell as ISR in combination with other behavioural therapies.
ACKNOWLEDGEMENTS
The authors would like to thank Paul Douglas and Leon Snigg
for their technical assistance.
Financial support: nil
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