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The well-known Two-Process Model of Sleep Regulation describes the integration of the circadian rhythm of arousal and sleep – Process C, and the homeostatic pressure to sleep – Process S. Presently, the known biological markers for Process C are melatonin and core body temperature; whereas, for Process S, there is no biological marker except that of aspects of the electroencephalogram (EEG). Endozepines are a class of endogenous compounds that act like benzodiazepines (BZ), i.e., serving as ligands for the BZ binding sites on GABAA receptors. Not much is known about the role of endozepines, in particular non-peptide endozepines, in the sleep field except very few reports about high concentrations observed in endozepine stupor, a rare phenomenon of idiopathic recurring stupor. We focused on hypoxanthine and thromboxane A2, which are considered to have endozepine function. This study aimed to examine the effect of 24 h of acute sleep deprivation on blood levels of hypoxanthine and thromboxane A2 of healthy subjects without sleep problems or disorders. The results showed a significant decrease of both compounds in the morning after sleep deprivation in comparison to the unrestricted normal sleep condition, thereby suggesting that these endozepines are secreted regularly while asleep, and, thus, are necessary for the sleep process. This study is the first to suggest a connection between specific biological markers – endozepines and Process S – in the Two-Process Model of Sleep Regulation and, furthermore, it sheds light on the possible role of endozepines in sleepiness and fatigue. [ABSTRACT FROM AUTHOR]

Two behavioral phenomena characterize human motor memory consolidation: diminishing susceptibility to interference by a subsequent experience and the emergence of delayed, offline gains in performance. A recent model proposes that the sleep-independent reduction in interference is followed by the sleep-dependent expression of offline gains. Here, using the finger-opposition sequence–learning task, we show that an interference experienced at 2 h, but not 8 h, following the initial training prevented the expression of delayed gains at 24 h post-training. However, a 90-min nap, immediately post-training, markedly reduced the susceptibility to interference, with robust delayed gains expressed overnight, despite interference at 2 h post-training. With no interference, a nap resulted in much earlier expression of delayed gains, within 8 h post-training. These results suggest that the evolution of robustness to interference and the evolution of delayed gains can coincide immediately post-training and that both effects reflect sleep-sensitive processes. [ABSTRACT FROM AUTHOR]

This retrospective study describes the effects of long-term treatment with melatonin in 33 adolescents (age range, 10-18 years) with delayed sleep phase syndrome (DSPS). Patients were treated with oral melatonin, 3 to 5 mg/day for an average period of 6 months. During the treatment, sleep onset was advanced and sleep duration was longer. Treatment was also associated with a decrease in the proportion of patients reporting school difficulties. No adverse effects of melatonin were noted. This study indicates that long-term treatment with melatonin can be beneficial for adolescents with DSPS in terms of sleep-wake schedule and school performance. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

We evaluated 32 nonmedicated male adolescents diagnosed with attention-deficit/hyperactivity disorder (ADHD) in childhood, 35 male adolescents similarly diagnosed who were receiving methylphenidate (MPH), and 77 control boys. Both ADHD groups completed self-report questionnaires assessing sleep disturbances; weekday and holiday sleep duration; and symptoms of ADHD, anxiety, and depression. Parents and teachers rated the severity of the participants' ADHD. The control group completed self-report questionnaires assessing sleep disturbances. We found that nonmedicated participants and controls did not differ in the severity of sleep disturbance. In contrast, the medicated participants demonstrated a significantly greater severity of sleep disturbance compared with the nonmedicated participants and reported elevated levels of symptoms of ADHD, anxiety, and depression. Specific analyses showed that depressive symptoms contributed significantly to the degree of sleep disturbance when controlling for ADHD diagnosis and MPH treatment. These findings suggest that among adolescents with ADHD symptoms, the severity of symptoms of depression may contribute to the degree of sleep disturbance in addition to the effect of their primary disorder and MPH treatment. [ABSTRACT FROM AUTHOR]

Abstract: Arousals are considered one of the main causes of daytime sleepiness. They impede the proper flow of sleep cycles and cause weariness. Manual scoring of arousals is time-consuming, requires expert knowledge, and has high inter-scorer variability. A major difficulty in detecting arousals automatically is the existing variance across patients. Based on data mining techniques, we present a different approach to the automatic detection of arousals that overcomes the hurdle of differences in signal characteristics across patients. Offline we used a training-set of adult patients to define a set of general rules to detect arousals (termed meta-rules). This was done by analyzing the correlations between occurrences of arousals and the EEG, EMG, pulse and SaO2 signals as follows: (1) each signal was mathematically projected into several spaces (termed projected-signals); (2) from each such projected-signal, the algorithm extracted time points that indicated meaningful changes (termed critical-points); (3) data mining techniques were applied to all the critical-points to discover patterns of repeating behavior; (4) classes of patterns which were highly correlated with manually scored arousals were formalized as meta-rules. Online we used a test-set of adult patients from two other different sleep laboratories. Using the meta-rules, the algorithm extracted individual rules for each patient (termed actual-rules), and used them to automatically detect the patients’ arousals. These arousals were significantly correlated (R =0.88, p <0.0001; sensitivity=75.2%, positive predictive value=76.5%) with those detected manually by experts. Since the total number of arousals is a measure of sleep quality, this algorithm constitutes a novel approach to automatically estimate sleep quality. [Copyright &y& Elsevier]

Background: Studies on the prevalence of sleep disorders have found great variability due to different data collection methods and case definitions. We aimed at assessing the prevalence of sleep disorders in a large, unselected population using validated clinical patient records. To the best of our knowledge, this is the first large clinically based study on sleep disorders.Methods: This retrospective study used the computerized data of 2.3 million members of Maccabi Healthcare Services (MHS) public mandated health provider. Among enrolled MHS members alive in June 2018, electronic medical records were searched from January 2010 for sleep disorders using diagnosis codes, sleep medications, and recorded sleep studies.Results: A total of 195,201 patients (9% of the total MHS population) were identified. Patients were 48.3% men and the average age at diagnosis was 50.4 years (SD = 20.9). Prevalence increased with age; 3.2% in children under 10 years, 5.2% in young adults, and 22.3% among seniors aged 75 or older. The two most prevalent disorders were insomnia (7.4%), and sleep-related breathing disorders (2%). Less prevalent disorders included central disorders of hypersomnolence (100 per 100,000), circadian rhythm sleep-wake disorders (49 per 100,000), parasomnias (140 per 100,000), and sleep-related movement disorders (20 per 100,000).Conclusions: The overall prevalence of sleep disorders including insomnia and sleep related breathing disorders in Israel were similar to other western countries despite stressful life events of ongoing war and terrorism. The large sample size allowed us to calculate the prevalence of more rare sleep disorders, which have been generally less known. [ABSTRACT FROM AUTHOR]