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Recently, addiction to regular doses of hypnotics has become a problem. While many patients report a desire to reduce their dosage, many do not agree with their physicians’ suggestions for reduction. In this study, we created an online short video targeting patient motivation to reduce hypnotics usage and examined its efficacy and factors associated with the intention to reduce medication. We created a 10 min video that included “sleep education,” “guidance for reducing the use of hypnotics,” and “systematic motivation for reducing the use of hypnotics” and posted it on our website. For 1 year, we conducted a questionnaire survey to determine the effectiveness of the video and factors associated with the intention to reduce hypnotics use. Of 4548 viewers, 609 (13.4%) completed the questionnaire, 369 (67.9%) of whom used hypnotics. Most respondents were older adults. The intention to reduce medication use was significantly strengthened after watching the video in 37.7% of medication users (effect size 0.404). In the group that was not inclined toward medication reduction before viewing, 85.2% of patients had stronger intentions to reduce medication use after watching the video (effect size 0.818). “Memorable content about side effects” was extracted as a factor related to reinforcement of the intention to reduce medication use, suggesting that prescribing physicians’ descriptions of current insomnia treatment is inadequate in explaining side effects to patients. A short informational video can have beneficial effects on patients’ motivation for dose reduction or cessation of hypnotics.

Escitalopram has been shown to be effective for treating major depression (MDD); however, research is lacking regarding its effect on treating MDD-related sleep impairments. The purpose of this study was to assess the efficacy of escitalopram monotherapy and investigate changes in insomnia, depressive symptoms, and quality of life (QOL). Participants were 14 patients with MDD who enrolled in a clinical trial at Jikei University Katsushika Medical Center. Escitalopram monotherapy was used, and hypnotics were administered three times per week for individuals suffering from sleep impairments. The following variables were assessed: (1) sleep quality [Pittsburgh sleep quality index (PSQI)], (2) depression [Zung self-rating depression scale (ZSRDS)], and (3) quality of life (QOL) as determined by the Sheehan disability scale (SDISS) and short form (36) health survey (SF-36). These assessments were conducted prior to any treatment (pre-test) and again 8–12 weeks after treatment (post-test). Monotherapy (E = escitalopram alone; n = 6) and combination therapy (E+ = escitalopram + zolpidem; n = 8) groups were compared. All participants completed the full protocol (average 9.4 ± 1.8 weeks). Regardless of treatment group, participants improved on all assessments (including sleep impairment). However, groups did not differ in their level of improvement. A two-factor ANOVA revealed that the E+ group showed particular improvements in QOL. In treating MDD and associated sleep impairments, zolpidem did not confer additional benefits. Thus, clinicians should consider E monotherapy for patients with MDD-related sleep impairments before prescribing combination therapies.

The authors evaluated the effects of brief group cognitive behavioral therapy for insomnia (G-CBT-I) in outpatients with psychophysiological insomnia (PPI). This brief G-CBT-I was designed to yield results in a shorter period of time, because its strategy was intended to lower the dropout rate and enhance the cost performance. And also, it was intended to be easy to make use of CBT-I for both therapists and patients. This process consists of four components and only two sessions weekly, and a total therapy time is approximately 3 h. Thirty-three participants (including 17 women) with PPI received G-CBT-I therapy. The short-term outcome (4 weeks after G-CBT-I) was measured using sleep logs, actigraphy, the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J), and the Japanese version of the Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-J). The long-term outcome was evaluated by checking medical records at 6 months after G-CBT-I. At 4 weeks after G-CBT-I, subjective sleep onset latency decreased by 32.1%, and objective sleep efficiency increased to approximately 90%. The dissociation between subjective and objective evaluations of sleep decreased. The total score of the PSQI-J and the scores on the DBAS-J (“consequences of insomnia”, “control and predictability of sleep”, and “sleep-promoting practice”) were decreased. At the long-term follow-up, the amount of hypnotics needed by each participant decreased by 0.6 mg (1 being equivalent to 1 mg of flunitrazepam) (33% reduction). These findings suggested that patients with PPI could derive significant benefit from brief G-CBT-I therapy.

The purpose of this study was to compare the efficacy of individual and group cognitive behavioral therapy for insomnia (CBT-I) in outpatients with primary insomnia diagnosed by DSM-IV-TR. The participants were 20 individually treated (I-CBT-I) and 25 treated in a group therapy format (three to five patients per group) (G-CBT-I), which showed no significant difference regarding demographic variables between groups. The same components of CBT-I stimulus control therapy, sleep restriction therapy, cognitive therapy, and sleep hygiene education were applied on both groups. The short-term outcome (4 weeks after treatment) was measured by sleep logs, actigraphy, the Pittsburgh Sleep Quality Index (PSQI), and the Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS), and was compared between I-CBT-I and G-CBT-I. The results indicated that CBT-I was effective in improving subjective and objective sleep parameters and subjective sleep evaluations for both individual and group treatment. However, I-CBT-I resulted in significantly better improvements over G-CBT-I, in (i) objective and subjective sleep onset latency time, (ii) objective sleep efficacy and moving time during sleeping, (iii) overall sleep quality and duration of actual sleep time in PSQI, (iv) consequences of insomnia, control and predictability of sleep, sleep requirement expectation, and sleep-promoting practices in DBAS. The present study suggested the superiority of I-CBT-I over G-CBT-I in clinical settings, and further evaluations are necessary.

Aim: Twenty patients (14 of them women) suffering from psychophysiological insomnia (PPI) were enrolled for cognitive behavior therapy (CBT). The mean age of the patients was 56.9 years, and the mean duration of insomnia morbidity was 8.9 years. Each received individual combined CBT treatments consisting of stimulus control, sleep reduction, cognitive therapy and sleep hygiene education over a period of 1 month. Methods: Just before the CBT and after its completion, sleep measurements were conducted that involved (i) sleep logs, Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS), and the Pittsburgh Sleep Quality Index (PSQI); (ii) actigraphy measurement; (iii) dissociation between subjective and objective evaluation of sleep calculated from sleep logs and actigraphy results; and (iv) correlation between DBAS and the aforementioned sleep parameters. Because the intention was to focus on patients' incorrect cognition about sleep, the definition ‘changes in dissociation between the sleep log and actigraphically measured sleep’ was used as the primary outcome and ‘changes in DBAS score’ as the secondary outcome. Results: After the CBT the following was found: (i) underestimation by PPI patients of the objective evaluation of sleep; (ii) a decrease in the dissociation between the subjective and objective evaluation of sleep; (iii) improvement of the DBAS; and (iv) improvement of sleep logs and actigraphy measurements. Moreover, there was a correlation between the improvement of PSQI, sleep logs and DBAS. Conclusion: CBT for insomnia is able to redress incorrect cognition about sleep, leading to improvement of the disorder.

In human volunteers who have been continuously experiencing unsatisfactory sleep, effects of glycine ingestion (3 g) before bedtime on subjective sleep quality were investigated, and changes in polysomnography (PSG) during sleep were analyzed. Effects on daytime sleepiness and daytime cognitive function were also evaluated. Glycine improved subjective sleep quality and sleep efficacy (sleep time/in-bed time), and shortened PSG latency both to sleep onset and to slow wave sleep without changes in the sleep architecture. Glycine lessened daytime sleepiness and improved performance of memory recognition tasks. Thus, a bolus ingestion of glycine before bedtime seems to produce subjective and objective improvement of the sleep quality in a different way than traditional hypnotic drugs such as benzodiazepines.

To estimate the process of re-entrainment we measured the melatonin rhythm on an eastward flight. After the baseline study, 24-hour blood sampling of six male subjects was done on the first and fifth days. During the daytime the subjects were exposed to natural zeitgeber outdoors every day except the blood sampling day. They were analyzed with an illuminometer when under the bright light condition. Four of the six subjects showed orthodromic re-entrainment, another subject showed antidromic re-entrainment, and the other subject kept the baseline pattern of plasma melatonin. The rate of re-entrainment in orthodromic re-entrainment was about 55 min per day. Measuring the circadian rhythm of plasma melatonin has clarified the inter-individual re-entrainment difference.

The effects of glycine on sleep quality were examined in a randomized double-blinded cross-over trial. The volunteers, with complaints about the quality of their sleep, ingested either glycine (3 g) or placebo before bedtime, and their subjective feeling in the following morning was evaluated with the St. Mary’s Hospital Sleep Questionnaire and Space-Aeromedicine Fatigue Checklist. The glycine ingestion significantly improved the following elements: “fatigue”, “liveliness and peppiness”, and “clear-headedness”. These results suggest that glycine produced a good subjective feeling after awakening from sleep.

The author's goal was to investigate the effects of surgical treatment on psychophysiological measurements in 17 patients with obstructive sleep apnea syndrome (OSAS) and also to clarify the improvement process of each evaluation. Given the changes in respiratory disturbance and sleep architecture, it was obvious that surgical treatment had therapeutic effects on OSAS patients a few months after the surgery. In that process, a dissociation between objective and subjective sleepiness was observed. The improvement in objective sleepiness [multiple sleep latency test (MSLT)] was more delayed than the improvement in subjective sleepiness (Stanford Sleepiness Scale, Spaceaeromedicine fatigue checklist). The improvement of MSLT was associated with an improvement in sleep fragmentation. This finding suggests that the disruption of sleep continuity accompanied by respiratory disturbance might be responsible for the occurrence of objective sleepiness. It can be concluded that the effective management of OSAS needs to address the full range of psychophysiological manifestations, especially objective measurement of daytime sleepiness.

The effect of 3 mg of melatonin on the rate of re-entrainment of plasma melatonin rhythm after an 11-h eastward flight was assessed. Eight subjects participated in the study, and underwent 24-h blood samplings once before the flight and twice after the flight. Subjects were exposed to natural zeitgeber outdoors and took 3 mg of malatonin at 20:00 h local time on the days when no blood sampling was done. Antidromic re-entrainment was dominant whereby melatonin administration in the evening promoted re-entrainment. Melatonin accelerated the rate of re-entrainment by 15 min per day and alleviated the jet lag symptoms.

The purpose of this study was to clarify the changes in psycho-physiological functions after anaesthesia with propofol (PF). The subjects were seven healthy male volunteers and the duration of the anaesthesia was 1 h (14:00–15:00 h). The plasma concentration of PF immediately decreased after the anaesthesia. The subjective sleepiness and VAS (visual liner analogue scale) scores (i.e. effort to do something) increased significantly at 20 min after the anaesthesia. However, these changes were improved at 80 min after the anaesthesia. The sleep latency at the nocturnal sleep 8 h after the anaesthesia was prolonged significantly, but the other parameters including the distributions of stage 3 + 4 and the rapid eye movement ‘REM’ stage were not changed.

In order to assess the effect of melatonin on jet lag a field study was undertaken. The process of re-entrainment of circadian melatonin rhythm was investigated in six subjects. Except during 24-h blood sampling, the subjects were exposed to natural zeitgeber (time giver) outdoors and given 3 mg melatonin at 23:00 h. The subjects were exposed to bright sunlight from 3000 to 12 000 lx. All of them showed orthodromic re-entrainment with taking melatonin, while two out of the six did not show orthodromic re-entrainment without taking melatonin. Melatonin accelerated the rate of the re-entrainment of the circadian melatonin rhythm. Melatonin was useful to jet travel from Tokyo to Los Angeles.

The clinical data of 86 cases of primary circadian rhythm sleep disorder (primary CRSD) were retrospectively examined and compared to 40 cases of secondary circadian rhythm sleep disorder (secondary CRSD), who had presented with some kind of psychiatric or medical disorder, and had exhibited sleep-wake rhythm disorders that were judged to be secondary CRSD based on sleep logs. The comparison of cases found that: (i) the mean age at first presentation to the clinic was significantly younger for primary CRSD compared to secondary CRSD; (ii) more secondary CRSD cases were unemployed than were Primary CRSD cases; (iii) more cases in the secondary CRSD group had a clear trigger for sleep-wake rhythm disorder onset than cases in the primary CRSD group; and (iv) the types of sleep-wake rhythm disorders in the primary CRSD group consisted of delayed sleep phase syndrome (DSPS), 72 (83.7%), non-24 pattern, 11 (12.8%), and irregular, 3 (3.5%). In the secondary CRSD group there were 25 (62.5%) cases of DSPS pattern, 1 (2.5%) of non-24 pattern and 14 (35.0%) with irregular pattern. The 56 (65.1%) cases with primary CRSD showed good response to vitamin B12 and bright light therapy; however, 28 (70.0%) cases with secondary CRSD did not respond to such therapies.

We estimated the re-entrainment of plasma melatonin rhythm after an eastward flight to New York in 2000 and after a westward flight to London in 2001. Blood samples were taken at 1.5 h intervals for 24-h from eight subjects once before the flight and twice after the flight. They were exposed to natural zeitgeber outdoors. The symptoms of six subjects were moderate in London. All subjects showed the orthodromic re-entrainment, and the phase shift was small (46.3 min/day) in the westward flight. It seemed that the direction of flight was as important for jet lag symptoms as was sunlight exposure.

The dissociation and correlation between objective (actigraph) and subjective (sleep diary, sleep questionnaire) evaluation about one’s own sleep in nine psychophysiological insomnia outpatients was investigated. We found that objective TST (total sleep time) and MT (nocturnal moving time) in actigraph correlated with subjective depth of sleep, number of awakening, physical and mood condition on waking, and total point of questionnaire, while objective sleep latency did not correlate with any subjective measurements. For longer TST and lesser MT, a better subjective sleep evaluation was induced. Subjective sleep latency did not correlate with objective sleep latency but it did with objective sleep onset time. Moreover, the number of subjective awakenings did not correlate with the number of objective awakenings, but with it did with objective TST and MT.

This preliminary study intended to investigate the effects of a selective serotonin re-uptake inhibitor (SSRI) on obstructive sleep apnea syndrome (OSAS). The patient was diagnosed polysomnographically as having a moderate OSAS. He was administered 50 mg of fluvoxamine (FLV) for 1 week. After the drug administration, the changes in breathing and sleep parameters, and Epworth Sleepiness Scale (ESS) scores were examined. There was a pronounced improvement in the apnea-hypopnea index (AHI), mean and the lowest arterial oxygen saturation (SaO2), per cent of desaturation under 90%, and in the ESS scores. Therefore, we expected that SSRI may become a choice of treatment for patients with OSAS.

We investigated the re-entrainment of melatonin rhythm in an 11-h eastward-bound flight. Eight male subjects participated in the present study. Blood sampling was carried out once before the flight and twice after the flight. During the daytime the subjects were exposed to natural zeitgeber outdoors on the day except the blood sampling. Seven of eight subjects showed antidromic re-entrainment, and the other subject showed orthodromic re-entrainment. The intensity of natural day light in New York amounted to 20 000 lx. As for the direction of the re-entrainment in New York the antidromic re-entrainment is naturally dominant.

The sleep architectures of obstructive sleep apnea syndrome (OSAS) in the young child (child-OSAS, n = 17; mean age: 5.9+/-2.7 years; male:female 14:3) were compared with that of OSAS in the adult (n = 19; mean age: 44.7+/-10.7 years; male:female 18:1) and that of primary snoring in the child (n = 5; mean age: 7.0+/-2.4 years; male:female 5:0). Child-OSAS and OSAS in the adult had the same severity in oxygen desaturation. Child-OSAS showed lower Apnea-Hypopnea Index compared with OSAS in the adult. Sleep continuity in child-OSAS was not impaired compared with OSAS in the adult. Sleep fragmentation in child-OSAS was not so remarkable. The quantity of slow wave sleep in child-OSAS was similar to that of primary snoring in the child. Both profiles of sleep architectures showed nearly the same pattern.