Search

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.

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 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 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.