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1/4. Therapeutic progress of two sibling cases exhibiting sleep-wake rhythm disorder.

    In this study, two females, siblings who exhibited a non-24 h sleep-wake rhythm (non-24 h) at home were observed. However, they showed a delayed sleep phase syndrome (DSPS) immediately after admission to Kurume University Hospital. melatonin (3 mg) was commenced following chronotherapy and this improved their sleep-wake rhythm. polysomnography (PSG) showed decreased sleep latency and increased sleep stage. In these cases, the involvement of environmental factors was strongly suggested for the sleep-wake rhythm abnormalities as well as familial factors.
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2/4. Case of a non-24 h sleep-wake syndrome patient improved by phototherapy.

    polysomnography (PSG) and body temperature were examined in a patient with non-24 h sleep-wake syndrome who responded to phototherapy. The patient was a 17-year-old male who had been suffering from a free-running sleep-wake rhythm for 2 months. phototherapy was administered to the patient while he was admitted to our hospital. This treatment immediately changed the free-running sleep-wake and body temperature rhythm of the patient to the environmental 24-h rhythm. On a polysomnography, total sleep time and stages 1 and 2 and REM sleep were decreased, and percentage stage 3 4 was increased by phototherapy. The time of minimum body temperature (mBT) was located at the latter half of the sleep phase through the clinical course of the patient.
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3/4. association between delayed sleep phase and hypernyctohemeral syndromes: a case study.

    STUDY OBJECTIVE: We investigated whether the hypernyctohemeral syndrome (non-24-hour sleep-wake syndrome) may show a clinical association with the delayed sleep phase syndrome (DSPS) in a 39-year-old woman who developed sleep disturbances following a traumatic brain injury. MEASUREMENTS AND RESULTS: sleep-wake log documentation and wrist-activity recordings for more than 6 consecutive months confirmed the patient's tendency to live on longer-than-24-hour "days." Episodes of relative coordination to the 24-hour day were also noted, suggesting that the patient was transiently in and out of phase with environmental synchronizers too weak to fully entrain her to the geophysical environment. Interestingly, we noted a tendency to initiate sleep between 3:00 am and 5:00 am and wake up from sleep between noon and 1:00 pm. CONCLUSIONS: These results support an association between the hypernyctohemeral syndrome and the DSPS. This association may carry implications for the treatment of circadian rhythms disorders.
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4/4. Working under daylight intensity lamp: an occupational risk for developing circadian rhythm sleep disorder?

    A 47-yr-old male was admitted to the Institute for fatigue and sleep medicine complaining of severe fatigue and daytime sleepiness. His medical history included diagnosis of depression and chronic fatigue syndrome. Antidepressant drugs failed to improve his condition. He described a gradual evolvement of an irregular sleep-wake pattern within the past 20 yrs, causing marked distress and severe impairment of daily functioning. He had to change to a part-time position 7 yrs ago, because he was unable to maintain a regular full-time job schedule. A 10-day actigraphic record revealed an irregular sleep-wake pattern with extensive day-to-day variability in sleep onset time and sleep duration, and a 36 h sampling of both melatonin level and oral temperature (12 samples, once every 3 h) showed abnormal patterns, with the melatonin peak around noon and oral temperature peak around dawn. Thus, the patient was diagnosed as suffering from irregular sleep-wake pattern. Treatment with melatonin (5 mg, 2 h before bedtime) did not improve his condition. A further investigation of the patient's daily habits and environmental conditions revealed two important facts. First, his occupation required work under a daylight intensity lamp (professional diamond-grading equipment of more than 8000 lux), and second, since the patient tended to work late, the exposure to bright light occurred mostly at night. To recover his circadian rhythmicity and stabilize his sleep-wake pattern, we recommended combined treatment consisting of evening melatonin ingestion combined with morning (09:00 h) bright light therapy (0800 lux for 1 h) plus the avoidance of bright light in the evening. Another 10-day actigraphic study done only 1 wk after initiating the combined treatment protocol revealed stabilization of the sleep-wake pattern with advancement of sleep phase. In addition, the patient reported profound improvement in maintaining wakefulness during the day. This case study shows that chronic exposure to bright light at the wrong biological time, during the nighttime, may have serious effects on the circadian sleep-wake patterns and circadian time structure. Therefore, night bright light exposure must be considered to be a risk factor of previously unrecognized occupational diseases of altered circadian time structure manifested as irregularity of the 24 h sleep-wake cycle and melancholy.
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