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1/11. 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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2/11. 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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3/11. Effects of phototherapy on the phase relationship between sleep and body temperature rhythm in a delayed sleep phase syndrome case.

    We examined polysomnography (PSG) and body temperature of a patient with delayed sleep phase syndrome (DSPS) who was successfully treated with only phototherapy. This case showed a possible improvement of the phase relationship between sleep and body temperature rhythm given that the time of minimum body temperature (mBT) shifted to the latter portion of the sleep phase after constant phototherapy.
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4/11. A pedigree of one family with delayed sleep phase syndrome.

    The prevalence of delayed sleep phase syndrome (DSPS) has been estimated to be quite low. Although no genetic inheritance pattern has been described, it has been reported that close to 50% of DSPS patients have biological relatives with similar symptoms. A pedigree of one extended family with symptoms suggestive of DSPS has been identified. Morningness-eveningness questionnaires were administered to all first- and second-degree relatives of a proband identified with DSPS. A total of 51 (86%) questionnaires were returned, and 6 adult biological relatives of 27 (22%) showed a preference for eveningness, which is much higher than reported in the general population. Both the paternal and maternal branches contained affected individuals, suggesting the possibility of a bilineal mode of inheritance. While the trait did not obey simple Mendelian inheritance, the vertical patterns of transmission were consistent with either an autosomal dominant mode of inheritance with incomplete penetrance or a multifactorial mode of inheritance. These data provide some preliminary support to the notion that eveningness, and thus DSPS, may have a genetic component. The prevalence of symptoms suggestive of DSPS is higher in this family than reported in the general population. case reports such as this support the utility of larger, more systematic studies. It is unclear whether this degree of familiarity is representative of that in the general population.
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5/11. Physical symptoms under forced-phase advance treatment in a patient with delayed sleep phase syndrome: a case report.

    The physical symptoms that are observed with forced waking in patients with delayed sleep phase syndrome (DSPS) often prevent the successful treatment of patients. Better understanding of these symptoms will assist in providing appropriate treatment in such patients. Herein, a 19-year-old female patient with DSPS is described, in whom headache, fatigue, and dizziness were observed under forced-phase advance treatment. Statistical analysis showed that her headache was dependent on the therapeutic week, and her fatigue was dependent on the period of the day. There was no association between dizziness and either factor. Experience with this patient indicates that the fatigue observed with forced waking is related to the circadian system. This relationship should be explored for other physical symptoms as well.
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6/11. Low, but not high, doses of melatonin entrained a free-running blind person with a long circadian period.

    In a previous report, we were unable to entrain one out of seven totally blind people with free-running endogenous melatonin rhythms to 10 mg of exogenous melatonin. This person had the longest circadian period (24.9 h) of the group. We now find that this person can be entrained to 0.5 mg of melatonin, but not to 20 mg. These results are consistent with the idea that too much melatonin may spill over onto the wrong zone of the melatonin phase-response curve.
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7/11. Case study of circadian rhythm sleep disorder following haloperidol treatment: reversal by risperidone and melatonin.

    A patient with Gilles de la tourette syndrome treated with haloperidol, ingested once daily after awakening from sleep, exhibited an irregular sleep-wake pattern with a free-running component of approximately 48 h. Transfer to risperidone, ingested once daily after awakening from sleep, was beneficial resulting in a sleep-wake cycle more synchronized at the appropriate phase to the external zeitgebers, and fewer nocturnal disturbances. The circadian sleep-wake schedule was fully synchronized when the patient had been subsequently treated with melatonin at 21:00h, before intended nocturnal sleep, in addition to risperidone in the morning. Restoration of the sleep-wake circadian pattern was accompanied by the patient's subjective report of significant improvement in his quality of life, social interactions, and occupational status. This observation suggests that circadian rhythm sleep disorders can be related to the typical neuroleptic haloperidol and restored by the atypical neuroleptic risperidone. Similar findings reported in patients suffering from other disorders support the hypothesis that the described disruption of the sleep-wake schedule is medication rather than illness-related. Therefore, it is very important to realize that circadian rhythm sleep disorders may be a side effect of neuroleptics.
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8/11. Non-24-hour sleep-wake syndrome following a car accident.

    The authors report the case of a 39-year-old sighted woman who displayed non-24-hour sleep-wake cycles following a car accident. The phase relationship between endogenous circadian markers such as plasma melatonin and 6-sulfatoxymelatonin rhythms and self-selected sleep times was abnormal. A laboratory investigation indicated that she was sensitive to bright light as a circadian synchronizer. MRI and brain CT scans were normal, but microscopic brain damage in the vicinity of the suprachiasmatic nucleus or its output pathways is plausible.
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9/11. 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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10/11. Reevaluating spells initially identified as cataplexy.

    BACKGROUND AND PURPOSE: cataplexy, transient episodes of bilateral muscle weakness with areflexia provoked by emotions, is a state highly specific to narcolepsy. cataplexy is diagnosed based on clinical interview. Two screening tools have been developed recently but their usefulness has been limited because of length or current lack of psychometric data. Used effectively even these screening tests require the interpreting physician to have an understanding of the typical features of cataplexy. Most physicians encounter patients with cataplexy fairly infrequently, making it difficult to gain proficiency in detecting cataplexy based on clinical interview alone. Relatively little attention has been given to the differential diagnosis of cataplexy, which increases the likelihood of unnecessary sleep testing or false positive diagnosis. patients AND methods: This case series describes six cases where cataplexy was initially diagnosed. In all cases the weakness spells were eventually not attributed to cataplexy. The presentation and characteristics of these cases will be presented as a means to discuss the differential diagnosis of cataplexy. RESULTS: These cases represent a diverse set of medical disorders including bradycardia, migraine, delayed sleep phase syndrome, conversion disorder, malingering and a chronic psychotic disorder. CONCLUSIONS: A more in-depth understanding of the classic features of cataplexy should improve recognition of this fascinating state. Improved cataplexy recognition will enhance the appropriate usage of sleep tests and eventually increase the timeliness and accuracy of the diagnosis of narcolepsy with cataplexy.
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