Our objective was to investigate the physiological mechanisms involved in the sleep restriction treatment of insomnia. A multiple baseline across subjects design was used. Sleep of five participants suffering from insomnia was assessed throughout the experimentation by sleep diaries and actigraphy. Ten nights of polysomnography were conducted over five occasions. The first two-night assessment served to screen for sleep disorders and to establish a baseline for dependent measures. Three assessments were undertaken across the treatment interval, with the fifth and last one coming at follow-up. Daily cortisol assays were obtained. Sleep restriction therapy was applied in-lab for the first two nights of treatment and was subsequently supervised weekly. Interrupted time series analyses were computed on sleep diary data and showed a significantly decreased wake time, increased sleep efficiency, and decreased total sleep time. Sleepiness at night seems positively related to sleep variables, polysomnography data suggest objective changes mainly for stage 2, and power spectral analysis shows a decrease in beta-1 and -2 powers for the second night of treatment. Cortisol levels seem to be lower during treatment. These preliminary results confirm part of the proposed physiological mechanisms and suggest that sleep restriction contributes to a rapid decrease in hyperarousal insomnia.
Sleep restriction therapy for insomnia was developed by Spielman et al. in 1987 [
Sleep restriction mechanisms are seen as involving physiological and psychological processes of sleep. Despite the effectiveness attributed to sleep restriction, little is known about how or why it improves sleep. From a physiological point of view, it is suggested that the prescribed total time spent in bed entrains the biological clock and produces a mild sleep-deprived state that increases daytime wakefulness and thus the sleep homeostatic drive [
Sleepiness has been seen as an inevitable part of treatment that appears in the first weeks of treatment [
A few studies have investigated cortical activity with PSG and power spectral analysis (PSA) before and after CBT-I [
Cortisol is another possible physiological marker of sleep restriction, as it is a marker of the hypothalamus-pituitary-adrenal axis activity [
In summary, although sleep restriction is currently recommended as a treatment of insomnia and frequently included in CBT-I, very few studies have evaluated sleep restriction therapy mechanisms, other than the seminal work by Spielman and colleagues [
Participants were recruited by physician referrals in the Greater Glasgow area. Inclusion criteria were as follows: (a) being between 18 and 65 years old; (b) presenting insomnia according to DSM-IV-TR [
Twenty-one eligible participants responded to the advertisement and underwent telephone screening. Sixteen were then excluded for the following reasons: sleep improved before the interview (
A single-case design called multiple baseline across subjects design [
Daily sleep efficiency course for each participant. Circled data correspond to PSG nights.
Daily total wake time course for each participant. Circled data correspond to PSG nights.
After the screening procedure, participants began a baseline with varying lengths before treatment. At baseline and throughout the experimentation, participants completed continuous assessments of their sleep, cortisol, sleepiness, and alertness. They also wore an actigraph from baseline until the end of treatment. Participants completed the Insomnia Severity Index at three assessment periods: baseline, posttreatment, and 3-month follow-up. At five occasions, they also spent two consecutive weekday nights of in-lab PSG, with the first two being at the first baseline week and for which the very first night served as a screening night for other sleep disorders. The following three occasions of PSG nights were scheduled during the treatment interval: (a) two nights at the first sleep restriction therapy session, (b) two nights when sleep was considered stabilized, and (c) two nights after three weeks of sleep stabilization. The remaining two PSG nights were at a 3-month follow-up.
Sleep was considered stabilized when sleep efficiency (SE) reached 85% or more, night-to-night variability was visually observed to have reduced relative to SE baseline, and a clinical judgment of progress was made. Night-to-night variability in sleep is an important feature of insomnia that is suggested to be an indicator of treatment responsiveness [
The sleep restriction administered in this study is outlined in a treatment manual [
Summary content of the sleep restriction therapy.
Sleep restriction procedures | |
(i) Sleep diaries used to estimate total sleep time (TST) and sleep efficiency (SE) | |
(ii) Sleep window length = the average of the two last baseline weeks of TST | |
(iii) The minimum sleep window duration is five hours | |
(iv) Sleep window respected every night | |
(v) Alarm clock used to ensure arising | |
(vi) The sleep window | |
(a) is increased for 15–20 minutes if SE ≥ 85% | |
(b) is kept stable if SE is between 80% and 85% | |
(c) is decreased to correspond to the total sleep time estimated if SE < 80% | |
Session 1: sleep information and sleep restriction | |
Aim: to transmit information about normal sleep, sleep disorders, and their effects and to begin sleep restriction therapy | |
(i) Basic facts about sleep: sleep architecture, circadian rhythm and sleep homeostasis as regulators of sleep, and changes in sleep patterns over the life span | |
(ii) Nature and causes of insomnia | |
(iii) Introduction of sleep restriction therapy and determination of the first sleep window | |
Session 2: sleep restriction | |
Aim: to restructure sleep so that it meets individual needs and develops a stable pattern | |
(i) Review previous week | |
(ii) Continue sleep restriction | |
(iii) Teach participants to modify their own sleep window | |
(iv) Clarify the distinction between sleepiness and fatigue | |
Session 3 and following ones until sleep stabilization: sleep restriction, developing natural sleep patterns | |
Aim: same goal. In addition, teach participants to use sleep restriction | |
(i) Continue sleep restriction | |
(ii) Teach participants to modify their own sleep window | |
(iii) Encourage fidelity to the new sleep schedule | |
Last session: sleep restriction and therapeutic gain maintenance | |
Aim: same goal. In addition, focus on further improvement and therapeutic gain maintenance | |
(i) Continue sleep restriction | |
(ii) Teach participants to modify their own sleep window | |
(iii) Encourage fidelity to the new sleep schedule | |
(iv) Review the concept of homeostatic pressure and more generally of the sleep restriction rationale | |
(v) Maintain therapeutic gains and/or keep improving after treatment |
Sleep restriction therapy was introduced following each baseline period for four to six individual treatment sessions of 50 minutes. The first sessions are performed weekly until sleep is stabilized as previously described. Then, one more session is planned three weeks after sleep stabilization. Participants are instructed to increase their sleep window according to the same rules based on SE during weeks without a therapy session and at posttreatment after the supervised treatment periods. Also, they are invited to increase the sleep window by modifying their bedtimes to keep the lower limit constant throughout the treatment.
Initial screening included a 20-minute telephone interview to determine participant eligibility. Subsequently, a multimeasure pretreatment evaluation was conducted, comprised of a semistructured sleep history interview to diagnose insomnia and the SCID-IV [
Outcome measures (sleep-onset latency (SOL), wake after sleep onset (WASO), TST, and SE) were based on the average of baseline nights (BN1 and BN2: nights 1 and 2), first treatment nights (TR3 and TR4: nights 3 and 4), sleep stabilized nights (TR5 and TR6: nights 5 and 6), posttreatment nights (TR7 and TR8: nights 7 and 8), and follow-up nights (FUN9 and FUN10: nights 9 and 10).
A comparison between baseline and the introduction of treatment permits study of homeostatic processes occurring at the beginning of treatment. It is also possible that sleep recuperation occurs after the introduction of treatment. Clinical sleep data were derived from PSG night 2 (BN2), night 3 (TR3), and night 4 (TR4) only. PSA was computed for consecutive 4-second epochs, with a resolution of 0,25 Hz and an EEG segment length of 30 seconds. Data were cosine tapered, and fast Fourier transform windows were nonoverlapping. Frequencies were defined as follows: slow waves (0-1 Hz), delta (1–4 Hz), theta (4–7 Hz), alpha (7–11 Hz), sigma (11–14 Hz), beta-1 (14–20 Hz), beta-2 (20–35 Hz), gamma (35–60 Hz), omega (60–125 Hz), and total (0–125 Hz). Absolute power spectral values (
Salivary cortisol samples were drawn using a plastic tube. Each sample contained approximately 2 mL of saliva. Throughout the experimentation, samples were drawn 10 minutes before going to bed as well as 10 minutes after awakening. For home assessment, a kit of 14 plastic tubes was supplied weekly to each participant, who was instructed to collect salivary samples twice a day, not to eat or brush their teeth during the hour before collection, and to rinse their mouth with water 10 minutes before sampling. Then, they were instructed to put it in the appropriate plastic tube and to store it in their own refrigerator. Participants returned their 14 samples when they came to treatment sessions. In-lab and home salivary samples were stored at the Department of Biochemistry at the Glasgow Royal Infirmary and analyzed by an experienced biomedical technologist. When analyzed, samples were centrifuged (2500 rpm) for 10 minutes and the supernatant was frozen at −20c until assayed in the laboratory. These supernatants were radio immunoassayed using microencapsulated antibody and I-cortisol as a tracer. Cortisol level is expressed in nmol/mL.
Insomnia Serverity Index (ISI) [
Adherence to treatment protocol was evaluated with sleep diaries and actigraphy. A daily percentage of adherences to the prescribed time to go to bed as well as to arising time were computed separately for each participant and assessment device. Going to bed more than 15 minutes earlier and getting out of bed more than 15 minutes later than the prescribed sleep window was considered as nonadherence to the respective element of the sleep restriction procedure. A daily average in minutes of nonadherence time was also computed for each participant and assessment device.
Clinical judgments of treatment response were made according to the following criteria: (a) having a marked decreased in ISI score from baseline to posttreatment, (b) having sleep stabilized during treatment, and (c) presenting a significant increase in SE during treatment. Participants’ responses were recorded as responder (meeting three of the above criteria), moderate responder (two criteria), or minimal responder (one criterion).
Sleep diary data for four dependent variables (i.e., SOL, TWT, TST, and SE) were divided into consecutive series according to each period (i.e., baseline, treatment, and posttreatment) for each participant. An interrupted time series analysis (ITSA) [
To study the physiological mechanisms of sleep restriction, statistical analyses were chosen as a function of (a) the objective, that is, to document the effect of sleep restriction on objective sleep, on subjective sleepiness and alertness, and on morning and evening cortisol levels, and (b) the nature of available data for each participant. For example, few data points are available for PSG, given the limited number of nights that each participant spent in the lab, while series of daily data are available from sleep diaries.
Descriptive statistics were computed and visually inspected for PSG data for each two-night period spent in the laboratory except for the baseline nights where data were taken only for the second night because of a possible first night effect. For the PSA, statistical analyses were performed separately for participants who responded to treatment and for those who did not. Considering the small sample sizes, nonparametric statistics were used. The Friedman test evaluated potential statistical differences between the second baseline night (BN2) and the two first treatment nights (TR3 and TR4) for power spectral analysis variables of responders. In case of a significant Friedman test, post hoc analyses were performed using the Wilcoxon signed-rank test and a Bonferroni correction was applied, which resulted in a significance level of
To study the longitudinal association between alertness, sleepiness, and sleep, Spearman correlations were calculated between subjective levels of alertness and sleepiness in the morning and the previous night’s sleep variables (SOL, WASO, TWT, TST, and SE). Similar correlations were calculated between sleepiness at night and sleep variables. Finally, daily morning and evening cortisol levels were measured to ensure the reliability of these data, and z-scores were derived to facilitate comparisons between participants. Weekly means of standard scores were computed. Given the small sample size, no inferential analysis was performed.
Figures
Results for the nature and direction of change for each sleep variable and participant are presented in Table
Nature and direction of change between baseline, treatment, and post-treatment for each sleep variable and participant.
Sleep variables/participants | DFE |
|
Treatment | Posttreatment | AR | AO | |||
---|---|---|---|---|---|---|---|---|---|
Time | Level | Slope | Level | Slope | |||||
Sleep-onset latency | |||||||||
1 | 64 | 91.04 | −0.56ns | −34.28*** | 0.30ns | 7.27ns | 1.52ns | 1, 11 | 2 |
2 | 70 | 93.89 | −0.65** | 3.07ns | 0.46ns | 4.99ns | 0.10ns | 7 | 4 |
3 | 74 | 56.90 | 2.09ns | −69.77* | −2.72ns | 37.23ns | −2.22ns | 1 | 3 |
4 | 67 | 83.01 | −0.18ns | −31.35*** | 0.38ns | −71.90** | 33.30*** | 9 | 5 |
5 | 74 | 72.97 | −0.28ns | −18.93* | 0.34ns | −15.86ns | 0.43ns | 6, 10, 11 | 5 |
| |||||||||
Mean | n/a | 79.56 | 0.08 | −30.25 | −0.25 | −7.65 | 6.63 | n/a | n/a |
| |||||||||
Total wake time | |||||||||
1 | 63 | 89.99 | −0.71ns | −46.30*** | 0.52ns | 21.22ns | −0.43ns | 4 | 5 |
2 | 73 | 73.08 | 0.75ns | −155.94*** | −0.38ns | 8.22ns | −3.15ns | 14 | 5 |
3 | 72 | 59.70 | 1.89ns | −87.79** | −1.94ns | 43.12ns | −3.46ns | 3, 9 | 4 |
4 | 72 | 59.34 | −1.04ns | −140.16*** | 1.35ns | 60.47ns | −6.89ns | 8 | 0 |
5 | 79 | 47.73 | −0.58ns | −50.56* | 0.30ns | −37.65ns | 5.17ns | 9, 13 | 1 |
| |||||||||
Mean | n/a | 69.97 | 0.06 | −96.15 | −0.03 | 19.08 | −1.75 | n/a | n/a |
| |||||||||
Total sleep time | |||||||||
1 | 62 | 77.54 | 0.77ns | −65.55** | 0.48ns | −41.98ns | 14.89* | 14 | 5 |
2 | 71 | 61.44 | −4.57ns | −0.31ns | 6.19* | −109.06* | 9.09ns | 1, 10, 11 | 3 |
3 | 72 | 57.33 | −0.44ns | −134.33*** | 2.41ns | −63.32ns | 5.14ns | 1 | 5 |
4 | 71 | 24.79 | 1.15ns | −60.08* | −1.43ns | −41.27ns | 10.94ns | 6, 12 | 0 |
5 | 79 | 30.95 | 0.43ns | −17.26ns | −0.39ns | 35.12ns | 5.41ns | 5 | 2 |
| |||||||||
Mean | n/a | 50.41 | −0.53 | −55.51 | 1.45 | −44.10 | 9.09 | n/a | n/a |
| |||||||||
Sleep efficiency | |||||||||
1 | 61 | 89.89 | 0.20ns | 7.10** | −0.13ns | −3.83ns | 0.18ns | 0 | 5 |
2 | 71 | 71.57 | −0.28ns | 36.08*** | 0.13ns | −6.46ns | 1.03ns | 1, 10 | 4 |
3 | 72 | 50.96 | −0.30ns | 10.49ns | 0.37ns | −9.83ns | 0.80ns | 1, 9 | 4 |
4 | 68 | 51.79 | 0.06ns | 18.60** | −0.10ns | −20.02ns | 2.55ns | 12, 14 | 3 |
5 | 79 | 35.47 | 0.12ns | 7.19ns | −0.05ns | 8.02ns | −0.61ns | 1, 9, 13 | 0 |
| |||||||||
Mean | n/a | 59.94 | −0.04 | 15.89 | 0.04 | −6.42 | 0.79 | n/a | n/a |
DFE: degree of freedom; AR: autocorrelation; AO: number of outliers; ns: not significant.
Data presented in Table
Descriptive information of participants and treatment course.
ISI | Sleep window | Respect to time off bed (min) | Respect to arising time (min) | ||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Age | Insomnia duration | Sleep stabilisation |
Actigraph |
Sleep diary |
Actigraph |
Sleep diary | |||||||
B | Post | Fu3 | Duration of the 1st | Modification | |||||||||
(Years) | |||||||||||||
P1 | 22 | 17 | 11 | 6 | 7 | 6:30 | Weekly ↑ by 15 min | 6 | 16.4 (16.7) | 18.3 (34.5) | −8.9 (17.7) | 0.9 (28.4) | |
P2 | 36 | 6 | 18 | 10 | 10 | 5:00 | Weekly ↑ by 15 min until week 6 | 9 | 4.4 (11.4) | −0.6 (14.1) | 7.7 (11.1) | 13.6 (15.7) | |
P3 | 62 | 5 | 17 | 13 | 8 | 6:40 | ↑ by 15 min at weeks 3, 5, and 6 | 16 | 24.1 (24.2) | −1.6 (2.7) | 23.8 (19.8) | 13.4 (11.8) | |
P4 | 36 | 15 | 15 | 0 | 0 | 6:00 | ↑ by 15 min at weeks 3 and 4 | n/a | −21.2 (0.0) | −9.5 (19.2) | 72.2 (0.0) | 5.38 (18.6) | |
P5 | 53 | 20 | 11 | 6 | 7 | 6:15 | Weekly |
25 | −1.98 (17.9) | 13.5 (11.8) | 46.0 (25.0) | 29.0 (15.8) |
ISI: Insomnia Severity Index; B: baseline; Post: posttreatment; Fu3: 3-month follow-up; ↑: increase;
Sleep restriction was adapted as a function of individual response to treatment. Accordingly, the first sleep window length and its modification during treatment varied for each participant (see Table
Percentages of adherence varied greatly across individuals and weeks. Moreover, the adherence rate was lower when assessed using the actigraph than using the sleep diary. Deviations from the sleep window were different for each participant. The data show that four participants modified their sleep window during the week (see Table
Based on the clinical criteria described in the Data Analysis section, three participants responded to treatment (participants 1, 2, and 3), one had a minimal treatment response (participant 5), and one dropped out of treatment (participant 4). Therefore, participants 1, 2, and 3 were considered as being treatment responders and participants 4 and 5 as nonresponders.
Means and standard deviations for PSG variables are presented in Table
Means (M) and standard deviations (SD) of polysomnographic data.
Sleep variables | Evaluation periods | ||||
---|---|---|---|---|---|
Baseline |
Treatment |
Posttreatment |
Follow-up | ||
1st nights |
Sleep stabilized | ||||
Treatment responders ( |
|||||
SOL (min) | 51.8 (69.9) | 13.0 (15.5) | 7.7 (7.6) | 14.8 (11.1) | 46.0 (65.0) |
WASO (min) | 55.1 (25.9) | 26.2 (14.3) | 17.5 (17.5) | 42.0 (56.9) | 32.5 (29.9) |
TST (min) | 330.1 (80.5) | 306.7 (32.6) | 348.5 (18.6) | 350.9 (37.3) | 371.5 (29.4) |
SE (%) | 74.8 (16.3) | 88.2 (4.4) | 92.5 (4.6) | 86.3 (11.6) | 85.2 (14.5) |
% stage 2 | 52.1 (6.4) | 49.9 (6.9) | 46.5 (4.9) | 55.3 (6.8) | 54.7 (8.1) |
% stages 3-4 | 21.9 (5.1) | 23.7 (7.5) | 24.6 (3.9) | 14.0 (19.8) | 15.6 (8.1) |
% REM | 17.8 (5.0) | 22.7 (5.5) | 25.2 (2.8) | 27.5 (4.2) | 26.1 (2.4) |
| |||||
Nonresponders ( |
|||||
SOL (min) | 17.1 (13.0) | 18.0 (7.7) | 6.3 (6.7) | 5.3 (0.4) | 28.0 (24.5) |
WASO (min) | 115.5 (73.6) | 26.3 (8.5) | 64.3 (27.9) | 55.8 (2.5) | 64.8 (15.2) |
TST (min) | 302.4 (85.1) | 289.1 (39.2) | 285.0 (25.5) | 312.8 (1.1) | 385.8 (40.7) |
SE (%) | 68.8 (14.9) | 86 (3.5) | 79.5 (6.4) | 83.0 (0.0) | 80.0 (8.5) |
% stage 2 | 56.0 (5.3) | 54.8 (8.7) | 70.1 (1.6) | 56.0 (4.9) | 63.0 (1.8) |
% stages 3-4 | 15.8 (4.4) | 18.7 (10.2) | 2.0 (1.7) | 10.5 (3.6) | 6.2 (5.1) |
% REM | 21.9 (8.0) | 21.2 (5.3) | 24.9 (0.3) | 32.2 (2.0) | 27.7 (6.9) |
BN2: baseline night 2; TR3: the third night in lab and the first of treatment; TR4: the fourth night in lab and the second of treatment; SOL: sleep-onset latency; WASO: wake time after sleep-onset; TST: total sleep time; SE: sleep efficiency; REM: rapid eye movement; min: minutes.
Results for sleep stages indicate that the percentage of stage 2 sleep decreased slightly while the percentage of time asleep in stages 3 and 4 seemed to increase slightly between baseline and the first two nights of sleep restriction. REM sleep seemed to show the most marked increase at that time. These changes seemed to remain stable when sleep became stabilized. At posttreatment, percentage of time spent asleep in stage 2 appeared to return to baseline level while percentage of stages 3 and 4 decreased beneath the baseline level. For minimal responders, sleep stage changes were similar during the first night of in-lab treatment. Afterwards, stage 2 increased and stages 3-4 decreased drastically. Moreover, the proportion of REM sleep increased to 32% of the night for one participant.
Median power values for band frequencies from the second baseline night (BN2) and the two first treatment nights (TR3 and TR4) are presented in Table
Median (range) power values for responders for beta-1 and beta-2 band frequencies.
BN2 | TR3 | TR4 | |||||
---|---|---|---|---|---|---|---|
Sleep stages | Median | Range | Median | Range | Median | Range | |
Beta-1 | |||||||
Cycle 1 | NRem | 2.41 | 1.62–12.14 | 2.09 | 1.92–9.06 | 1.48 | 1.13–2.98 |
Rem | 1.83 | 0.78–5.93 | 1.88 | 0.89–6.37 | 2.45 | 0.58–3.11 | |
1 | 3.01 | 1.06–7.54 | 2.93 | 2.93-2.93 | 1.80 | 1.14–2.45 | |
2* | 4.27 | 2.99–13.88 | 3.29 | 2.22–11.89 | 3.15 | 1.31–5.13 | |
3* | 2.30 | 2.10–9.09 | 1.91 | 1.59–6.97 | 1.34 | 1.29–3.95 | |
4 | 1.53 | 1.40–7.45 | 1.62 | 1.48–5.09 | 3.02 | 2.90–4.64 | |
Cycle 2 | NRem* | 3.86 | 1.72–11.04 | 3.44 | 1.33–4.75 | 1.81 | 1.14–2.55 |
Rem | 1.65 | 0.73–5.28 | 1.11 | 0.98–6.34 | 1.33 | 0.66–2.86 | |
1 | 1.40 | 1.40-1.40 | 1.55 | 1.55-1.55 | 1.88 | 1.40–2.36 | |
2 | 8.45 | 2.31–14.80 | 3.44 | 2.31–6.78 | 2.79 | 1.67–5.13 | |
3 | 2.02 | 1.42–8.16 | 5.10 | 1.15–9.04 | 1.75 | 1.28–3.83 | |
4 | 3.37 | 1.27–5.47 | 2.44 | 0.95–3.92 | 1.44 | 0.76–1.56 | |
All cycles | NRem* | 3.21 | 1.76–11.99 | 2.77 | 1.69–7.43 | 2.38 | 1.19–4.22 |
Rem | 1.57 | 0.77–5.78 | 1.52 | 1.02–6.36 | 1.67 | 0.61–3.04 | |
1 | 3.46 | 1.14–7.05 | 2.71 | 1.33–7.25 | 2.39 | 0.95–3.19 | |
2* | 3.53 | 2.23–14.64 | 3.30 | 2.18–10.10 | 3.19 | 1.51–5.77 | |
3* | 2.09 | 1.51–8.47 | 1.91 | 1.34–6.79 | 1.57 | 1.33–3.87 | |
4 | 1.53 | 1.37–5.96 | 1.62 | 1.22–4.14 | 1.38 | 0.92–1.62 | |
| |||||||
Beta-2 | |||||||
Cycle 1 | NRem | 0.75 | 0.56–3.27 | 1.01 | 0.92–4.08 | 0.51 | 0.51–1.10 |
Rem | 1.13 | 0.86–4.01 | 1.04 | 0.89–5.29 | 0.98 | 0.60–1.64 | |
1 | 1.43 | 0.87–5.64 | 1.08 | 1.08-1.08 | 1.16 | 0.93–1.38 | |
2 | 1.25 | 0.89–3.13 | 1.39 | 1.31–5.82 | 1.19 | 0.66–2.09 | |
3 | 0.67 | 0.63–2.25 | 0.80 | 0.58–2.46 | 0.48 | 0.47–1.15 | |
4 | 0.56 | 0.50–2.17 | 0.84 | 0.59–2.48 | 1.18 | 0.96–1.61 | |
Cycle 2 | NRem* | 1.78 | 0.67–2.51 | 1.00 | 0.47–1.89 | 0.67 | 0.42–0.93 |
Rem | 1.11 | 0.79–3.24 | 0.95 | 0.84–5.70 | 0.86 | 0.53–1.55 | |
1 | 1.43 | 1.43-1.43 | 1.35 | 1.35-1.35 | 1.00 | 0.92–1.07 | |
2 | 3.01 | 0.75–4.51 | 1.00 | 0.78–5.43 | 0.70 | 0.55–1.41 | |
3 | 0.68 | 0.53–2.18 | 1.49 | 0.48–2.50 | 0.60 | 0.45–1.14 | |
4* | 1.09 | 0.47–1.71 | 1.04 | 0.49–1.59 | 0.53 | 0.32–0.75 | |
All cycles | NRem | 1.14 | 0.77–3.01 | 0.96 | 0.90–2.76 | 0.75 | 0.52–1.36 |
Rem | 1.11 | 0.82–3.59 | 1.00 | 0.88–5.72 | 0.92 | 0.58–1.80 | |
1 | 1.39 | 1.25–5.09 | 1.27 | 1.15–9.01 | 1.06 | 1.03–2.78 | |
2* | 1.10 | 0.75–3.07 | 1.29 | 1.18–3.73 | 0.85 | 0.58–1.64 | |
3 | 0.66 | 0.54–2.20 | 0.80 | 0.52–2.35 | 0.55 | 0.47–1.14 | |
4 | 0.56 | 0.49–1.82 | 0.84 | 0.54–1.75 | 0.51 | 0.35–0.77 |
BN2: baseline night 2; TR3: the third night in lab and the first of treatment; TR4: the fourth night in lab and the second of treatment; NREM: nonrapid eye movement; REM: rapid eye movement. *Significant results at
Overall, a variable representing the mean power value of all the cycles was computed for each band frequency and sleep stage. As documented in Table
For minimal responders, BN2 data were missing for all the variables for the cycles from 1 to 5. Therefore, statistical analyses were performed only on TR3 and TR4. Results for the first 2 cycles and all cycles combined are shown in Table
Longitudinal associations between sleepiness and alertness in the morning, sleepiness at night, and sleep variables were assessed with correlational analyses. Table
Correlation coefficients between subjective sleepiness, alertness, and sleep variables for each participant during treatment.
Participants/alertness and sleepiness | Sleep variables | ||||
---|---|---|---|---|---|
SOL | WASO | TWT | TST | SE | |
Participant 1 | |||||
Alertness | −0.30* | 0.13 | −0.07 | 0.19 | 0.12 |
Sleepiness | 0.51*** | 0.01 | 0.35** | −0.37** | −0.42 |
Sleepy at night | −0.39** | −0.29* | −0.39** | −0.02 | 0.32 |
Participant 2 | |||||
Alertness | −0.41** | −0.28* | −0.32* | 0.53*** | 0.35** |
Sleepiness | −0.01 | 0.26 | 0.28* | −0.17 | −0.28* |
Sleepy at night | −0.29* | −0.07 | −0.07 | −0.07 | 0.01 |
Participant 3 | |||||
Alertness | −0.02 | −0.28 | −0.22 | 0.25 | 0.21 |
Sleepiness | −0.02 | 0.32* | −0.02 | −0.16 | 0.01 |
Sleepy at night | −0.16 | 0.31* | 0.05 | −0.08 | −0.04 |
Participant 4 | |||||
Alertness | 0.01 | −0.27 | 0.08 | 0.29 | 0.03 |
Sleepiness | 0.13 | 0.55*** | 0.17 | −0.52*** | −0.28 |
Sleepy at night | −0.30 | −0.16 | −0.05 | 0.18 | 0.09 |
Participant 5 | |||||
Alertness | −0.13 | −0.44** | −0.28 | 0.29 | 0.31* |
Sleepiness | −0.07 | 0.39** | 0.17 | −0.17 | −0.19 |
Sleepy at night | −0.25 | −0.27 | −0.38** | 0.24 | 0.36* |
SOL: sleep-onset latency; WASO: wake after sleep-onset; TWT: total wake time including SOL, WASO, and early morning awakening; TST: total sleep time.
*
The mean morning cortisol level for the participants was 22.4 nmol/mL (SD = 11.4) and the evening level was 4.3 (SD = 5.1), which are within the normal range for these times of day. Overall, 69 of 262 evening saliva samples and 62 of 262 morning saliva samples were missing or unessayable, with saliva being contaminated before reaching the lab. Most of the missing saliva samples are from participant 4 who did not complete the experiment. Higher cortisol levels are associated with higher wake times. Figure
Evening and morning cortisol levels compared to their respective average for participants 1, 2, and 3. 0 as z-score means participant’s average of cortisol levels. A negative z-score means a cortisol level lower than participant’s average while a positive z-score means a cortisol level higher than participant’s average of cortisol levels.
Our study illustrates that physiological mechanisms of sleep restriction therapy could be evaluated using an appropriate methodological strategy. By beginning measurements on the first night of treatment, it was revealed that sleep restriction might have a rapid impact on subjective sleep and on the physiological markers of sleep. First, the results showed that sleep restriction decreased total wake time sleep-onset latency and increased sleep efficiency. Second, these results showed that the subjective total sleep time is decreased by about one hour during the first week of treatment. Visual inspection of PSG data suggests that stage 2 decreases when introducing the treatment, while stage 3 seems to increase. An increase in REM sleep can also be observed. PSA indicated a change in beta-1 and -2 beginning with the second treatment night. Third, the results illustrated a potential action of sleep restriction on cortisol levels as both morning and evening cortisol levels seem to decrease during treatment. Fourth, with respect to sleepiness, the results show that greater sleepiness at night is associated with higher sleep efficiency and shorter wake time during the night. They also suggest that alertness in the morning is associated with previous sleep time. Finally, the results on sleepiness indicate that these associations were not present before treatment, suggesting that they are induced by sleep restriction.
Objective sleep data obtained in the present study present similarities and divergences with results from other studies. They are similar to Cervena and colleagues [
Our results reporting an increase in REM sleep are similar to those of other studies reporting PSG data after treatment [
Contrary to expectations, PSA do not indicate increase in SWS during sleep restriction therapy. This surprising result diverges from other studies [
The cortisol results seem congruent with an improvement in sleep during our sleep restriction treatment. Indeed, cortisol levels (evening and morning) are lower during treatment than at baseline for participants who had a treatment response. Moreover and most importantly, the decrease in cortisol levels can be detected very early in treatment. Cortisol levels are known to be higher for people with insomnia than for good sleepers [
In addition to the physiological sleep restriction therapy mechanisms, the findings highlight the rapid change observed in subjective sleep. Indeed, sleep restriction provides a rapid and marked decrease in wake time that is sustained during treatment. The findings also confirm a previously observed decrease in TST, quantifying that decrease at about an hour. Interestingly, these benefits in sleep were observed in spite of variations in the compliance data. It seems that individuals cope differently with difficulties encountered during treatment; some delayed their sleep window while some others shortened or changed the timing of the sleep window. Therefore, it appears that sleep restriction can be effective without a full application by the participant of the sleep restriction procedure.
Taken together, the data on PSG, sleepiness, and cortisol provide indications that sleep restriction decreases hyperarousal and cortical activity while increasing sleepiness to facilitate sleep. It is not clear, however, if these involve an increase of the homeostatic drive for all participants. The decrease in beta powers and in cortisol levels during treatment might reflect a decrease in hyperarousal. Contrary to both expectations and visual inspection of PSG, no increase in powers of lower frequency bands (slow or delta) indicative of greater homeostatic pressure was observed across nights. This, along with an increase in REM sleep, could reflect a malfunction of the homeostatic drive, implying that a decrease in wake time and sleep time will not generate the expected homeostatic sleep drive effect as previously suggested [
These preliminary results possess some methodological limitations, although they are promising as a further step toward understanding sleep restriction mechanisms. A first limit concerns the small sample size that precludes obtaining strong statistical evidence of the mechanisms. Second, the procedure of daily assessing several variables during 10 to 12 weeks could have rendered the participants’ tasks onerous, thus affecting data reliability. For this reason, sleep diary data were analyzed using ITSA. Third, cortisol data itself has several limitations: the trend for cortisol levels to decrease during baseline precludes definitive statements. The weekly adjustment of the sleep window might also have affected the evening cortisol level. However, although the time of going to bed differed for participants, the results followed a similar pattern. Moreover, both evening and morning cortisol levels were within the normal range for the time of day and the saliva methodology replicated that used in another study [
This research evaluated the impact of sleep restriction on physiological markers of sleep, thus allowing a description of the putative physiological mechanisms for this treatment. The PSG and PSA results of the present study are innovative. They illustrate how a more in-depth investigation of the physiological variables related to sleep restriction could enlighten the knowledge on how sleep restriction works and on cortical activity in insomnia. The methodology used should be taken as a guideline for future studies. These findings illustrated the relevance of dismantling CBT-I to understand each component of treatment mechanism and enhance treatment efficacy. Future studies should investigate if the REM sleep increase observed with sleep restriction contributes to the improvement of sleep perception in insomnia. Circadian timing of sleep restriction and of other CBT-I components should also be further investigated in other studies. In addition, the sleepiness results, along with results obtained for TST, suggest that more attention should be given to the relationship between these two variables over the course of sleep restriction to evaluate a potential acute negative effect of sleep restriction. Finally, future studies should focus on empirically identifying sleep restriction mechanisms of action in order to increase efficacy and make relevant clinical recommendations concerning this promising form of therapy.
This research was supported by a studentship from the Canadian Institutes of Health Research awarded to the first author and by grants from The Welcome Trust, Chief Scientist Office (Section Government Hewett Department), and the Dr. Mortimer and Theresa Sackler Foundation awarded to the second author. The authors wish to thank Dr. Maria Gardani for her work during the experimentation, Dr. Simon Kyle for his helpful comments on the paper, and Dr. James Everett for English revision.