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Delayed sleep phase disorder (DSPD) is a circadian rhythm sleep disorder characterized by a substantial delay in the major sleep period, resulting in difficulties falling asleep and awakening at a socially desirable time in the morning. This study is the first to investigate the NEO-Personality Inventory-Revised profile of young adults with DSPD. The study includes 40 patients diagnosed with DSPD (mean age = 20.7) and 21 healthy controls (mean age = 21.1). Results showed that young adults with DSPD scored higher on Neuroticism, lower on Extroversion, and much lower on Conscientiousness than the control group. Assessing the personality profile of young adults with DSPD before initiating treatment might provide useful clinical guidance regarding the individual needs for follow up during treatment.

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Delayed sleep phase disorder is characterized by a delay in the timing of the major sleep period relative to conventional norms. The sleep period itself has traditionally been described as normal. Nevertheless, it is possible that sleep regulatory mechanism disturbances associated with the disorder may affect sleep duration and/or architecture. Polysomnographic data that may shed light on the issue are scarce. Hence, the aim of this study was to examine polysomnographic measures of sleep in adolescents and young adults with delayed sleep phase disorder, and to compare findings to that of healthy controls. A second aim was to estimate dim light melatonin onset as a marker of circadian rhythm and to investigate the phase angle relationship (time interval) between dim light melatonin onset and the sleep period. Data from 54 adolescents and young adults were analysed, 35 diagnosed with delayed sleep phase disorder and 19 healthy controls. Results show delayed timing of sleep in participants with delayed sleep phase disorder, but once sleep was initiated no group differences in sleep parameters were observed. Dim light melatonin onset was delayed in participants with delayed sleep phase disorder, but no difference in phase angle was observed between the groups. In conclusion, both sleep and dim light melatonin onset were delayed in participants with delayed sleep phase disorder. The sleep period appeared to occur at the same circadian phase in both groups, and once sleep was initiated no differences in sleep parameters were observed.

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The aim of the present study was to investigate the prevalence of "behaviorally induced insufficient sleep syndrome (BIISS)" which is a newly defined hypersomnia, among adolescents. BIISS is characterized by excessive daytime sleepiness, short habitual sleep duration and sleeping considerably longer than usual during weekend/vacations. The study was conducted in the Hordaland County, Norway using a cluster sampling procedure. In all, 1285 high school students (aged 16-19 years) participated by completing self-report questionnaires on a computer. The estimated prevalence of BIISS was 10.4%. The results from logistic regression analyses showed that use of alcohol and living in an urban area were positively related to BIISS, whereas a high level of education in mothers was negatively related to BIISS. BIISS was associated with poor grades and symptoms of anxiety and depression.

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BACKGROUND: Pediatric sleep is a rapidly developing area, and understanding of sleep disorders in children and adolescents is improving. The article aims to present new knowledge to Norwegian physicians. MATERIAL AND METHODS: The article is based on review articles and clinical guidelines identified through non-systematic searches in PubMed, limited to the period 2007-2009. RESULTS: Primary and secondary sleep disorders in children and adolescents are common, but underdiagnosed. Sleep disorders may occur as early as infancy and the clinical presentation often differs from that in adults. These disorders may have serious consequences in the short and long run. Information about sleep and circadian rhythm, positive routines and good sleep hygiene may prevent sleep disorders and form natural constituents of treatment of all such disorders in youngsters. A non-pharmacological approach with cognitive behavioural interventions is the most important treatment of insomnia. Randomized studies and guidelines for pharmacological therapy are needed. INTERPRETATION: Sleep disorders in children and adolescents demand special knowledge and attention. Norway needs an increase in capacity and competent experts to evaluate sleep disorders in children and adolescents.

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One of the most established hypotheses of depression focuses on alteration of the serotonergic (5-HT) function. Recent evidence suggests that serotonergic involvement in depression may be modulated by the action of gamma-hydroxybutyric acid (GABA). Furthermore, altered GABAergic function is also evident in depressed patients and in animal models of depression. Disturbed sleep is characteristic of patients with mood disorders. The most pronounced changes of the 5-HT firing activity occur during sleep. Hence, the present paper reports a study on simultaneously measurement of hippocampal levels of serotonin and GABA during waking and sleep in the chronic mild stress (CMS) animal model of depression. The neurotransmitter findings are accompanied by depression-like symptoms (e.g. sleep alterations and reduced sucrose intake, a putative indicator of anhedonia in rodents). Our results show that animals exposed to CMS had lower hippocampal GABA levels compared to controls. In addition, after CMS there was a lack of 5-HT stage-dependency. A subgroup (five out of eight animals) showed a consistent increase in 5-HT levels in slow wave sleep and REM sleep. We also observed that this increase occurred in those animals regarded as most anhedonic (lowest intake of sucrose solution). Moreover, REM sleep was positively correlated with anhedonia. No interaction between 5-HT and GABA was found in the hippocampus. The data suggest that both GABAergic and serotonergic systems may be simultaneously but independently involved in depression. The alteration in 5-HT function may represent a link between depression-like behaviour and sleep abnormalities found in depressed patients.

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Many symptoms of human depressive disorders are also observed in animals after exposure to unpredictable stressors. The chronic mild stress (CMS) paradigm was developed in order to better model the human situation by using chronic mild stressors over a longer period. It is claimed that the model induces anhedonia in the animals, a core symptom of depression in humans. Despite the fact that the CMS model has a high degree of face validity, there are a number of laboratories in which the establishment of the model is less reliably observed. We have examined behavior (sexual activity and open field activity) together with hedonic measures (sucrose and saccharine intake) after exposure to CMS. CMS decreased male sexual activity (e.g. reduced capability to ejaculate) and increased activity in an open field test. The hedonic measures showed diverging results after CMS in our laboratory. Sucrose consumption was reduced, while saccharine consumption did not show a comparable change. It is concluded that CMS induces comparable alterations to some depression-like symptoms in humans. Saccharine consumption is not a reliable indicator of the hedonic responsiveness to CMS.

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Depression in humans is associated with sleep abnormalities of three types: altered rapid eye movement (REM) sleep, fragmented sleep, and reduced delta sleep. In an animal model of depression, chronic exposure to mild stressors (CMS, e.g. periods of soiled cage, reversed light/dark cycle, grouped housing, food and/or water deprivation) causes behavioral and hormonal changes which, in humans, often are associated with depression. In the CMS model, a reduced sucrose intake has been defined as one of the core symptoms of depression, anhedonia, although this finding is not consistent among various laboratories. In the present study, we investigated if the CMS procedure, in our laboratory, would cause decreased sucrose intake and, also, give sleep changes similar to what is found in depressed patients. Exposure to CMS decreased sucrose intake in our rats. The largest effect was obtained after 2 weeks of the stress protocol. CMS rats spent more time in REM sleep and showed more fragmented sleep compared to their baseline recording, while there were no changes in the control rats. Increased sleep fragmentation in CMS rats was particularly evident by increased number of arousals, and increased REM sleep and slow-wave-sleep-1 (SWS-1) episodes. The duration of sleep stage episodes was decreased. The amount of slow-wave-sleep-2 (SWS-2) was not decreased, however SWS-2 in percent of total SWS was reduced. Correlation analysis showed that animals that had less consumption of sucrose spent more time in REM sleep and had increased number of REM sleep episodes. In this study, CMS appears to be a model of depression.

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