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Sleep deprivation (SD) is suggested to be associated with reduced thermo-regulatory functions. This study aimed to quantify the effect of partial (PSD) and total (TSD) 24 h SD using a standard heat tolerance test (HTT). Eleven participants underwent HTT after well-rested state, PSD and TSD. No significant physiological differences were found between the exposures but subjective discomfort was higher after TSD. Evening chronotypes' temperature during HTT was higher after TSD compared with PSD (p = 0.017). After TSD, evening chronotypes compared to intermediate chronotypes' temperature was higher during the first hour of the HTT (p < 0.05), suggesting that thermo-regulatory function during exercise in the heat is influenced by chronotype.

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.

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.

Autonomic function during sleep and wakefulness has been extensively investigated, however information concerning autonomic changes during the wake to sleep transition is scarce. The objective of the present study was to non-invasively characterize autonomic function and additional physiologic changes during sleep onset in normal and abnormal sleep. The estimation of autonomic function was based on time-frequency analysis of the RR interval series, using the power components in the very-low-frequency range (0.005-0.04 Hz), low-frequency (0.04-0.15 Hz), and high-frequency range (0.15-0.5 Hz). The ratio of low to high frequency power represented the sympathovagal balance. Thirty-four subjects who underwent whole night polysomnography were divided into 3 groups according to their complaints and study results: normal subjects, apneic patients (OSAS), and subjects with various sleep disorders (VSD). The results indicated a significant increase in RR interval during sleep onset, although its variability decreased; respiratory rate did not change, yet respiration became more stable; EMG amplitude and its variability decreased with sleep onset. Very-low-frequency power started to decrease significantly 2 min before sleep onset in all groups; low-frequency power decreased and high-frequency power did not change significantly in all groups, accordingly their ratio decreased and reflected a shift towards parasympathetic predominance. Although autonomic function displayed similar behavior in all subjects, OSAS and VSD patients presented a higher sympathovagal balance reflecting enhanced sympathetic predominance in those groups compared to normal subjects, both before and after sleep onset. All parameters reached a nadir at a defined time point during the process of falling asleep. We conclude that the wake-sleep transition period represents a transitional process between two physiologically different states; this transition starts with a decrease in the very slow oscillations in heart rate that anticipates a step-change resetting of autonomic function, followed by a decrease in sympathovagal balance towards the end of the process.

This case study describes a 14-year-old male suffering from significant academic and personal difficulties, who has been diagnosed with depression, schizotypal personality disorder, and learning disabilities. Because of excessive sleepiness, assessment for a potential sleep disorder was performed. An overnight polysomnographic study revealed no primary sleep disorders. Wrist actigraphy revealed a non-24-hour sleep-wake pattern. Delay in temperature rhythm and dissociation with melatonin rhythms were also noted. Treatment with oral melatonin restored normal sleep-wake schedule. In a follow-up psychiatric evaluation, none of the above diagnoses were present. Greater awareness of sleep disorders may prevent psychiatric misdiagnosis of treatable sleep-wake schedule disorders.

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]

The last several decades have been characterized by the widespread usage of digital devices, especially smartphones. At the same time, there have been reports of both decline in sleep duration and quality and male fertility decline. The aim of this study was to assess the relationship between evening exposure to the light-emitting screens of digital media devices and measures of both sleep and sperm quality. Semen samples were obtained from 116 men undergoing fertility evaluation for the following sperm variables: volume (mL), pH, sperm concentration (million/mL), motility percentage (progressive% + non-progressive motility%), and total sperm count. Exposure to the screens of electronic devices and sleep habits was obtained by means of a questionnaire. Smartphone and tablet usage in the evening and after bedtime was negatively correlated with sperm motility (−0.392; −0.369; p <.05), sperm progressive motility (−0.322; −0.299; p <.05), and sperm concentration (−0.169; p <.05), and positively correlated with the percentage of immotile sperm (0.382; 0.344; p <.05). In addition, sleep duration was positively correlated with sperm total and progressive motility (0.249; 0.233; p <.05) and negatively correlated with semen pH (−0.349; p <.05). A significant negative correlation was observed between subjective sleepiness and total and progressive motility (−0.264; p <.05) as well as total motile sperm number (−0.173; p <.05). The results of this study support a link between evening and post-bedtime exposure to light-emitting digital media screens and sperm quality. Further research is required to establish the proposed causative link and may lead to the future development of relevant therapeutic and lifestyle interventions. [ABSTRACT FROM AUTHOR]

A patient who developed an irregular sleep-wake pattern following prolactin-secreting pituitary microadenoma is described. The patient reported difficulties in sleep onset and awakening at the desired time, which caused major dysfunction in his daily life activities. Despite these difficulties, the sleep-related complaints of the patient remained unrecognized for as long as three yrs. Statistical analyses of the patient's rest-activity patterns revealed that the disruption of the sleep-wake circadian rhythm originated from a disharmony between ultradian (semicircadian) and circadian components. The circadian component displayed shorter than 24 h periodicity most of the time, but the semicircadian component fluctuated between longer and shorter than 12 h periods. Additionally, desynchrony in terms of period length was found in the tentative analyses of the rest-activity pattern, salivary melatonin, and oral temperature. While the salivary melatonin time series data could be characterized by a best-fit cosine curve of 24 h, the time series data of oral temperature was more compatible with 28 h best-fit curve. The rest-activity cycle during the simultaneous measurements, however, was best approximated by a best-fit curve of 21h. The dysregulation of circadian rhythms occurred concomitantly, but not beforehand, with the onset of pituitary disease, thus suggesting an association between the two phenomena. This association may have interesting implications to the modeling of the circadian time-keeping system. This case also highlights the need to raise the awareness to circadian rhythm sleep disorders and to consider disruptions of sleep-wake cycle in patients with pituitary adenoma. [ABSTRACT FROM AUTHOR]

Objective.—A controlled objective and subjective evaluation of sleep in a consecutive series of persons who had had a whiplash injury, shortly following the injury and 3 to 5 months later. Methods.—In whiplash-injured subjects and healthy controls, sleep characteristics were monitored objectively throughout the night by means of an actigraph. The following morning, participants in both groups filled out a prestructured “sleep log” that conveyed their subjective impressions as to how they had slept. The correlation between objectively measured sleep characteristics and the symptoms and physical findings, respectively, resulting from whiplash injury were also examined. Results.—Actigraphic monitoring did not reveal a significant group difference between whiplash-injured subjects and controls with respect to any of the sleep characteristics recorded. In self-maintained “sleep logs,” however, the whiplash-injured subjects reported a significantly prolonged sleep latency and significantly impaired sleep quality compared with controls (P<.001 and P<.04, respectively). In whiplash-injured subjects, the number of arousals was positively correlated with the number of symptoms and with the number of physical signs of whiplash injury (P<.01 and P<.001, respectively). Sleep efficiency was inversely correlated with the number of injury-related findings on physical examination (P<.009). Conclusion.—Sleep, as monitored by actigraph in whiplash-injured subjects, was not adversely affected by whiplash injury. The subjective impressions of the subjects, as recorded in “sleep logs,” suggest the opposite conclusion. A significant correlation exists between certain symptoms and signs of whiplash injury and abnormalities in given sleep characteristics as detected by actigraph. [ABSTRACT FROM AUTHOR]

Summary Obstructive sleep apnea is a prevalent sleep‐disordered breathing condition characterized by repetitive reduction in breathing during sleep. The current care standard for obstructive sleep apnea is continuous positive air pressure devices, often suffering from low tolerance due to limited adherence. Capitalizing on the unique neurocircuitry of olfactory perception and its retained function during sleep, we conducted a pilot study to test transient, respiration‐based olfactory stimulation as a treatment for obstructive sleep apnea markers. Thirty‐two patients with obstructive sleep apnea (apnea–hypopnea index ≥ 15 events per hr) underwent two polysomnography sessions, “Odour” and “Control”, in random order. In “Odour” nights, patients were presented with transient respiratory‐based olfactory stimulation delivered via a computer‐controlled commercial olfactometer (Scentific). The olfactometer, equipped with a wireless monitoring, analysed respiratory patterns and presented odour upon detection of respiratory events. No odours were presented in “Control” nights. Following exclusions, 17 patients entered the analysis (four women, 47.4 (10.5) years, body mass index: 29.4 (6.3) kg m−2). We observed that olfactory stimulation during sleep reduced the apnea–hypopnea index (“Odour”: 17.2 (20.9), “Control”: 28.2 (18.6), z = −3.337, p = 0.000846, BF10 [Bayesian Factor 10]= 57.9), reflecting an average decrease of 31.3% in the number of events. Relatedly, stimulation reduced the oxygen desaturation index by 26.9% (“Odour”: 12.5 (15.8), “Control”: 25.7 (25.9), z = −3.337, p = 0.000846, BF10 = 9.522). This effect was not linked to the severity of baseline obstructive sleep apnea markers (ρ = −0.042, p = 0.87). Olfactory stimulation did not arouse from sleep or affect sleep structure, measured as time per sleep stage (F1,16 = 0.088, p = 0.77). In conclusion, olfactory stimulation during sleep was effective in reducing the severity of obstructive sleep apnea markers without inducing arousals, and may provide a novel treatment for obstructive sleep apnea, prompting continued research. [ABSTRACT FROM AUTHOR]

Background: In this study we examined the effects of caffeine on sleep quality and melatonin secretion. Melatonin is the principal hormone responsible for synchronization of sleep. Melatonin secretion is controlled by neurotransmitters that can be affected by caffeine.Methods: In the first part of the study, six volunteers drank either decaffeinated or regular coffee in a double-blind fashion on one day, and the alternate beverage 7 days later. Sleep parameters were assessed by actigraphy. In the second part of the study, the subjects again drank either decaffeinated or regular coffee, and they then collected urine every 3 h for quantitation of 6-sulphoxymelatonin (6-SMT), the main metabolite of melatonin in the urine.Results: We found that drinking regular caffeinated coffee, compared to decaffeinated coffee, caused a decrease in the total amount of sleep and quality of sleep, and an increase in the length of time of sleep induction. Caffeinated coffee caused a decrease in 6-SMT excretion throughout the following night.Conclusions: The results of our study confirm the widely held belief that coffee consumption interferes with sleep quantity and quality. In addition, we found that the consumption of caffeine decreases 6-SMT excretion. Individuals who suffer from sleep abnormalities should avoid caffeinated coffee during the evening hours. [Copyright &y& Elsevier]