Journal of Sleep Research

Published by Wiley
Online ISSN: 1365-2869
Print ISSN: 0962-1105
Publications
Arterial blood pressure is influenced by sleep-related breathing disorders. As cardiovascular consequences can be diagnosed by an accurate recording and analysis of blood pressure, new recording methodologies and an approach to analysis are presented here. Invasive continuous blood pressure recording is the common reference for all methodologies. As blood pressure varies rapidly in parallel with sleep-related breathing disorders it is indispensible to record blood pressure continuously. To introduce non-invasive methodology the Finapres system was used during sleep studies; a validation study showed severe limitations. This study was followed by the validation of an improved system called Portapres, which is portable, has two finger cuffs and a hydrostatic height compensation. Analysis of continuous blood pressure in patients with sleep apnoea is carried out to detect mechanisms which influence the cardiovascular risk. Spectrum analysis of systolic blood pressure showed two different major oscillations present in patients with obstructive sleep apnoea. One oscillation (<0.06 Hz) occurs in parallel with each apnoeic episode and the other oscillation (0.2-0.4 Hz) occurs in parallel with the obstructive efforts during each apnoea and in parallel with respiration during periods of snoring. These two oscillations were so specific that the use of non-invasive continuous blood pressure recording allowed an estimation of the extent of underlying breathing disorders, and assessment of cardiovascular risk in a patient with obstructive apnoea in terms of hypertension and on the basis of ambulatory monitoring.
 
Previous studies that have quantified fatigue-related cognitive impairment as blood alcohol concentration (BAC) equivalents have been limited by two issues: the effect of practice on tests of cognition and, more importantly, the statistic used to quantify change in cognitive performance. The current study addressed these issues by adopting an ABACA design, which allowed for the adequate control of practice effects, and by using effect size metrics, which enabled direct comparisons to be made in performance impairments as a result of fatigue (i.e. sustained wakefulness of 24 h) and alcohol (i.e. BAC of 0.05%). Cognitive performance under the fatigue and alcohol conditions required the use of the CogState battery. It was demonstrated that fatigue caused greater impairment than alcohol on the speed of continuous attention and memory and learning, and on the accuracy of complex matching. Alcohol was more detrimental than fatigue only on the accuracy of memory and learning. Performances on the remaining tasks were the same for both the fatigue and alcohol conditions. These differences and similarities in performance impairment are discussed emphasizing the deleterious cognitive effects of relatively short periods of sustained wakefulness.
 
Human leucocyte antigen (HLA) DQB1*0602 allele, a well-known genetic risk factor for narcolepsy, has been associated with sleep parameters in healthy subjects. We aimed to assess the association of this allele with daytime sleepiness and altered sleep electroencephalogram characteristics in the general population and in patients with obstructive sleep apnoea syndrome (OSAS). Eight hundred and ninety-four individuals from the Epidemiologic Study of Sleep were genotyped for the HLA DQB1*0602 allele. Full-night polysomnography was performed, and daytime sleepiness was analysed according to the Epworth Sleepiness Scale. HLA-DQB1*0602 allele-positive and -negative subjects in the general population, as well as in patients with OSAS, exhibited similar sleep parameters and levels of daytime sleepiness. However, spectral analysis showed that allele-positive individuals with OSAS exhibited higher theta power during sleep Stage 1 (P < 0.05) in occipital derivations, and lower delta power during sleep Stages 1 and 2 (P < 0.01) compared with individuals negative for the allele, even after correction for potential confounders as age, sex, body mass index and European ancestry. No significant differences in the electroencephalogram variables were found in individuals without OSAS. The data highlight the HLA-DQB1*0602 as a potential genetic factor influencing sleep physiology in individuals diagnosed with OSAS.
 
Demographic profile of ADHD cases 
Night-time sleep duration for ADHD cases and rest of cohort 
Bedtimes and wake-times of ADHD cases and rest of cohort 
Daytime sleep duration for ADHD cases and rest of cohort 
Total sleep duration for ADHD cases and rest of cohort 
Associations between sleep duration and disturbance in infancy and early childhood and attention deficit hyperactivity disorder diagnoses were investigated. Data from the Avon Longitudinal Study of Parents and Children, a population-based prospective longitudinal birth-cohort study of children born in 1991-1992 in South-West England, were employed. Eight thousand, one hundred and ninety-five children were assessed using the Development and Well-Being Assessment. One hundred and seventy-three cases (2.1%) met criteria for attention deficit hyperactivity disorder. Parental report at eight time points showed children with attention deficit hyperactivity disorder slept less than peers. Absolute differences were small and mainly restricted to night-time sleep, with no strong evidence of differences from controls, except at 69 months [5 years 9 months; 12 min (95% CI: 5-19), P = 0.001], at 81 months [6 years 9 months; 15 min (95% CI: 8-22), P < 0.001] and at 115 months [9 years 7 months; 11 min (95% CI: 4-18), P = 0.001]. The attention deficit hyperactivity disorder group had more night-waking at every age, significant from about 5 years. When tracking children's sleep along a normative centiles chart, a shift in sleep duration from one centile to a lower centile was a useful predictor of attention deficit hyperactivity disorder. Age-specific decreases of >1SD in sleep duration across adjacent time points was a significant predictor of attention deficit hyperactivity disorder at 3-5 years (P = 0.047). In children with attention deficit hyperactivity disorder, shorter sleep duration and sleep disturbances appear early and predate the usual age of clinical diagnosis. The rate of change of sleep duration relative to an individual, rather than absolute sleep duration at any stage, may prove beneficial in identifying increased risk of attention deficit hyperactivity disorder.
 
We investigated dopamine D1 receptors in the putamen and caudate nucleus with positron emission tomography in six patients with narcolepsy and five healthy controls using [11C]NNC 756 as ligand. The caudate-to-cerebellum and putamen-to-cerebellum ratios of [11C]NNC 756 were within normal limits in patients with narcolepsy. No evidence of increased D1 receptor binding in narcolepsy was found.
 
A few investigations have raised the question of a possible relationship between obstructive sleep apnoea syndrome (OSAS) and floppy eyelid syndrome (FES). FES is an easily inverted floppy eyelid with papillary conjunctivis, and is a subset of the general pathology, lax eyelid syndrome. The aim of the current study is to determine whether OSAS severity is associated with FES. One hundred and 27 consecutive subjects (aged 25-75 years) referred to the Strasbourg University Sleep Clinic with suspicion of OSAS were included. All patients underwent overnight ambulatory respiratory polygraphy, comprehensive ophthalmological examination and completed standard sleep questionnaires. OSAS severity was defined based on the patient's obstructive apnoea-hypopnoea index (AHI). As expected, age, body mass index (BMI) and the proportion of males increased with OSAS severity. FES was observed in 15.8% of the subjects without OSAS, 25.8% of the total OSAS population and the frequency was significantly increased (40%) in patients with severe OSAS (AHI > 30 h(-1)). A significant correlation between OSAS severity and FES was found after adjustment for age, sex and BMI, using a principal component analysis (PCA). The multivariate analysis included clinical, polygraphic and comorbidity data and was followed by logistic regressions for the main components extracted from the PCA. In summary, our findings show an association between OSAS severity and FES and suggest that severe OSAS might be an independent risk factor for FES. These two disorders may share common biological determinants, such as tissue elasticity. Finally, clinicians should be aware of this association so that underlying OSAS or FES can be detected.
 
The aim of this study was to examine sleep architecture at high altitude and its relationship to periodic breathing during incremental increases in altitude. Nineteen normal, sea level-dwelling volunteers were studied at sea level and five altitudes in the Nepal Himalaya. Morning arterial blood gases and overnight polysomnography were performed in 14 subjects at altitudes: 0, 1400, 3500, 3900, 4200 and 5000 m above sea level. Subjects became progressively more hypoxic, hypocapnic and alkalinic with increasing altitude. As expected, sleep architecture was affected by increasing altitude. While time spent in Stage 1 non-rapid eye movement sleep increased at 3500 m and higher (P < 0.001), time spent in slow-wave sleep (SWS) decreased as altitude increased. Time spent in rapid eye movement (REM) sleep was well preserved. In subjects who developed periodic breathing during sleep at one or more altitudes (16 of 19), arousals because of periodic breathing predominated, contributing to an increase in the total arousal index. However, there were no differences in sleep architecture or sleeping oxyhaemoglobin saturation between subjects who developed periodic breathing and those who did not. As altitude increased, sleep architecture became progressively more disturbed, with Stage 1 and SWS being affected from 3500 m, while REM sleep was well preserved. Periodic breathing was commonplace at all altitudes, and while associated with increases in arousal indices, did not have any apparent effect on sleep architecture.
 
According to a recent hypothesis the therapeutic effects of antidepressants might be related to acute or cumulative suppression of NREM sleep intensity. This intensity has been proposed to be expressed in the EEG power density in NREM sleep. In the present study the relationship was examined between the changes of EEG power density in NREM sleep and the changes in clinical state in 16 depressed patients during treatment with citalopram, a highly specific serotonin uptake inhibitor. A one-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a one-week placebo period. In order to minimize systematic influences of sleep duration and NREM-REM sleep alterations, EEG power was measured over the longest common amount of NREM sleep stages 2, 3 and 4 (91.5 min). During the last treatment week and the week after withdrawal, a significant decrease of EEG power as compared to baseline was found in the 8-9 Hz frequency range. No clear-cut change, however, was observed in the EEG power of the delta frequency range (1-4 Hz), which is considered to be the principle manifestation of NREMS intensity. Furthermore, no relationship between changes in EEG power density and changes in clinical state could be demonstrated.
 
Responses to the eight-item Epworth Sleepiness Scale (ESS) obtained from 1560 World War II male veteran twin pairs [818 monozygotic (MZ), 742 dizygotic (DZ)] were analysed to determine the extent to which genetic influences are involved in self-reported daytime sleepiness in the elderly. Average ESS score (+/- SD) in this sample was 7.1 +/- 3.9, range 0--24. More than half of the twins (65%--67%) reported a moderate to high chance of falling asleep while lying down to rest; fewer than 3% admitted that this would occur while sitting and talking to someone or while stopped in traffic. Daytime sleepiness was not associated with age but was significantly and positively associated with obesity. The intraclass twin correlation on ESS scores was 0.39 in MZ pairs and 0.21 in DZ pairs (both P < 0.001). Structural equation modeling of the observed variance-covariance matrices for MZ and DZ twins estimated the heritability of ESS to be 38% (95% confidence interval 33%--44%). Environmental influences not shared by twin brothers accounted for the remaining variance in daytime sleepiness. A reasonable interpretation of the heritability of ESS in this healthy cohort of elderly male twins is a genetic susceptibility for disordered breathing during sleep.
 
To establish a dose-response relationship between the strength of electromagnetic fields (EMF) and previously reported effects on the brain, we investigated the influence of EMF exposure by varying the signal intensity in three experimental sessions. The head of 15 healthy male subjects was unilaterally exposed for 30 min prior to sleep to a pulse-modulated EMF (GSM handset like signal) with a 10 g-averaged peak spatial specific absorption rate of (1) 0.2 W kg(-1), (2) 5 W kg(-1), or (3) sham exposed in a double-blind, crossover design. During exposure, subjects performed two series of three computerized cognitive tasks, each presented in a fixed order [simple reaction time task, two-choice reaction time task (CRT), 1-, 2-, 3-back task]. Immediately after exposure, night-time sleep was polysomnographically recorded for 8 h. Sleep architecture was not affected by EMF exposure. Analysis of the sleep electroencephalogram (EEG) revealed a dose-dependent increase of power in the spindle frequency range in non-REM sleep. Reaction speed decelerated with increasing field intensity in the 1-back task, while accuracy in the CRT and N-back task were not affected in a dose-dependent manner. In summary, this study reveals first indications of a dose-response relationship between EMF field intensity and its effects on brain physiology as demonstrated by changes in the sleep EEG and in cognitive performance.
 
Prof Dr Isbrand van Diemerbroeck (1609–1674).
Hypnagogic and hypnopompic hallucinations are visual, tactile, auditory or other sensory events, usually brief but sometimes prolonged, that occur at the transition from wakefulness to sleep (hypnagogic) or from sleep to wakefulness (hypnopompic). Hypnagogic and hypnopompic hallucinations are often associated with sleep paralysis. Sleep paralysis occurs immediately prior to falling asleep (hypnagogic paralysis) or upon waking (hypnopompic paralysis). In 1664, the Dutch physician Isbrand Van Diemerbroeck (1609-1674) published a collection of case histories. One history with the title 'Of the Night-Mare' describes the nightly experiences of the 50-year-old woman. This case report is subject of this article. The experiences in this case could without doubt be diagnosed as sleep paralysis accompanied by hypnagogic hallucinations. This case from 1664 should be cited as the earliest detailed account of sleep paralysis associated with hypnagogic illusions and as the first observation that sleep paralysis and hypnagogic experiences occur more often in supine position of the body.
 
Subjective sleep quality and its related factors were investigated in 869 (530 F, 339 M) 17-year-old adolescents, who were selected from the pupils of state-run secondary schools in the city of Pavia in the north west of Italy. The study was conducted cross sectionally, and it consisted of a questionnaire based survey. One hundred and forty-two subjects (16.5% of the whole sample, 19% of the females and 11.7% of the males) met the criteria chosen for definition as poor sleepers (namely, a complaint of 'non restorative nocturnal sleep', 'often' or 'always' over the previous 12 mo). A significant association was found between chronic poor sleep and (1) gender (female) (2) emotional factors, such as worries, anxiety and depression (3) poor sleep hygiene (4) arousal related parasomnia. Only 4% of poor sleepers took sleep promoting drugs (including benzodiazepines, homeopathic products and other medications), generally without seeking medical advice.
 
Reports of prolonged sleep periods in idiopathic central nervous system hypersomnia, as shown by ad libitum sleep recordings, are rare. A patient with idiopathic hypersomnia with extremely long sleep periods and sleep drunkenness after awakening is described. Polysomnographic recordings showed a spontaneous sleep period of 19.4 h and a normal Multiple Sleep Latency Test. These polysomnographic findings are clearly abnormal but essentially different form those of narcolepsy. Unlike narcolepsy, 'idiopathic hypersomnia' does not seem to be a distinct clinical entity but a category for different heterogenous subtypes.
 
A hypothesis concerning habitual sleep reduction and its adverse consequences among general population in modern societies has received wide publicity in the mass media, although scientific evidence supporting the hypothesis is scarce. Similarly, there is an extensively distributed belief, at least in Finland, that the prevalence of insomnia-related symptoms is increasing, but evidence for this is even sparser. These issues are important because of the known increased risk of mortality and health risks associated with sleep duration deviating from 7 to 8 h. To reveal possible trends in self-reported sleep duration and insomnia-related symptoms, we reanalyzed all available data from surveys carried out in Finland from 1972 to 2005. The main results were that a minor decrease of self-reported sleep duration has taken place in Finland, especially among working aged men. However, the size of the reduction (about 4%) was relatively small, approximately 5.5 min per each 10 years during the 33 years' time interval under study. The proportion of 7 h sleepers has increased and, correspondingly, the proportion of 8 h sleepers has decreased, but the extreme ends of the sleep duration distribution remained unchanged. Tentative evidence suggesting an increase in insomnia-related symptoms among working aged population during the last 10 years was found. In conclusion, the Finnish data during the past 33 years indicate a general decrease in self-reported sleep duration of about 18 min and an increase of sleep complaints, especially among the employed middle-aged population.
 
Successful psychological and physical adaptation in late life correlates with preservation of sleep quality and physiological integrity of nocturnal EEG sleep measures. Failure to adapt is associated with loss of sleep continuity, alterations in the temporal distribution of delta wave activity, and by either a relative increase in REM sleep (e.g. in mood disorders) or a decrease in REM sleep (e.g. neurodegenerative disorders). Maintenance of sleep (particularly REM sleep) into late life may not be just a correlate, but also possibly a mechanism, of successful aging and thus necessary to the long-term maintenance of vitality and engagement in life.
 
Obstructive sleep apnoea (OSA) is characterized by periods of upper airway collapse accompanied by repeated episodes of hypoxia. In experimental animals repeated bouts of hypoxia may evoke sustained augmentation of phrenic nerve activity, known as phrenic long-term facilitation (pLTF). This form of physiological compensation might contribute to stable breathing, minimizing the occurrence of apnoeas and/or hypopnoeas during sleep in patients with OSA. Serotonin (5-HT) has been shown to modulate respiratory neuronal activity, possibly via projections originating in the raphe nuclei. Our model focuses on the effects of 5-HT1A receptors blockade by selective antagonist WAY-100635 into the caudal raphe region on phrenic long-term facilitation after exposure to acute intermittent hypoxia (AIH) episodes. Adult, male, urethane-anaesthetized, vagotomized, paralyzed and mechanically ventilated Sprague-Dawley rats were exposed to AIH protocol. Experimental group received microinjection of WAY-100635 into the caudal raphe nucleus, whereas the control group received saline into the same site. Peak phrenic nerve activity and respiratory rhythm parameters were analysed during five hypoxic episodes, as well as at 15, 30 and 60 min after the end of hypoxias. In the control group, 1 h post-hypoxia pLTF was developed. Microinjections of selective 5-HT1A receptor antagonist WAY-100635 into the raphe nuclei prior to the AIH protocol prevented induction of pLTF. These results suggest that 5-HT1A receptor activation at supraspinal level is important for induction of pLTF, which is suggested to be an important respiratory neuroplasticity model in animal studies that possibly correlates with OSA in humans.
 
Disrupted sleep and stress are often linked to each other, and considered as predisposing factors for psychopathologies such as depression. The depressed brain is associated with reduced serotonergic and enhanced cholinergic neurotransmission. In an earlier study, we showed that chronic sleep restriction by forced locomotion caused a gradual decrease in postsynaptic serotonin-1A receptor sensitivity, whilst chronic forced activity alone, with sufficient sleep time, did not affect receptor sensitivity. The first aim of the present study was to examine whether the sleep loss-induced change in receptor sensitivity is mediated by adrenal stress hormones. The results show that the serotonin-1A receptor desensitization is independent of adrenal hormones as it still occurs in adrenalectomized rats. The second aim of the study was to establish the effects of sleep restriction on cholinergic muscarinic receptor sensitivity. While sleep restriction affected muscarinic receptor sensitivity only slightly, forced activity significantly hypersensitized the muscarinic receptors. This hypersensitization is because of the stressful nature of the forced activity protocol as it did not occur in adrenalectomized rats. Taken together, these data confirm that sleep restriction may desensitize the serotonin-1A receptor system. This is not a generalized effect as sleep restriction did not affect the sensitivity of the muscarinic cholinergic receptor system, but the latter was hypersensitized by stress. Thus, chronic stress and sleep loss may, partly via different pathways, change the brain into a direction as it is seen in mood disorders.
 
Hemoglobin A(1c) (HbA(1c)) is an indicator of long-term glycemic control. The purpose of this study was to determine whether habitual snoring is associated with increased HbA(1c) levels in non-obese and normoglycemic middle-aged men and women. A total of 6981 subjects (3362 men and 3619 women) aged 40-69 years from the Korean Health and Genome Study were examined for the study. Each participant received a comprehensive physical examination as well as a set of questions pertaining to demographic characteristics and snoring frequency. Habitual snoring was defined as a snoring frequency of > or = 4 days week(-1). After adjusting for age, abdominal obesity, and other confounding covariates, male habitual snorers showed a 1.69-fold excess [95% confidence interval (CI) 1.30-2.19] odds of having a high HbA(1c) level. Similarly, premenopausal women with habitual snoring had a 2.31 times (95% CI 1.22-4.39) significantly higher odds of having elevated HbA(1c)levels compared with non-snorers. This association was not found in postmenopausal women. Multivariate analysis revealed that male habitual snorers aged 40-50 had a 2.08-fold excess (95% CI 1.40-3.09) risk of having an elevated HbA(1c) level. In male habitual snores over 50, the strength of association was attenuated. Our findings based on cross-sectional data support a hypothesis that habitual snoring is associated with impaired glucose tolerance even in non-obese and normoglycemic men and premenopausal women. However, as waist circumference as an index of abdominal obesity (visceral adiposity) in the present study may only partially represent the effect of visceral fat, there may be a residual confounding from visceral obesity in our result. Longitudinal follow-up studies are necessary to confirm the association between sleep-disordered breathing and impaired glucose tolerance and to examine the causal relationship in a healthy population without obesity and diabetes.
 
The aim of this study was to evaluate the effects of a 200-mg administration of caffeine on polysomnographic sleep variables and quantitative sleep electroencephalography (EEG) in 12 young (20-30 years) and 12 middle-aged (40-60 years) moderate caffeine consumers (one to three cups of coffee per day). All subjects were submitted to both a caffeine (200 mg) and placebo (lactose) condition in a double-blind cross-over design. The conditions were separated by 1 week. Compared with the placebo condition, the evening ingestion of caffeine lengthened sleep latency, reduced sleep efficiency, and decreased sleep duration and amount of stage 2 sleep in both age groups. Caffeine also reduced spectral power in delta frequencies in frontal, central and parietal brain areas, but not in prefrontal (PF) and occipital regions. Moreover, caffeine increased spectral power in beta frequencies in frontal and central brain areas in both age groups. A suppression of spectral power in the PF area in low delta frequencies (0.5-1.00 Hz) and a rise in spectral power in the parietal region in high alpha (10.00-12.00 Hz) and beta frequencies (17.00-21.00, 23.00-25.00, 27.00-29.00 Hz) occurred solely in middle-aged subjects. No such changes were noticeable in young subjects. Generally, caffeine produced similar effects in young and middle-aged subjects. Only a few frequency bins showed more effects of caffeine in middle-aged subjects compared with young subjects. Furthermore, sleep EEG results do not entirely support the hypothesis that caffeine fully mimics the effects of a reduction of homeostatic sleep propensity when following a normal sleep-wake cycle.
 
Sleep problems and sleep restriction are popular topics of discussion, but few representative data are available. We document Britain's sleep based on a nationally representative sample of 1997, 16-93 year olds, who participated in face-to-face interviews. Fifty-eight per cent of respondents reported sleep problems on one or more nights the previous week and 18% reported that the sleep they obtained was insufficient on the majority of nights. Sleep durations were longest in the youngest participants (16-24 years), who slept on average 1 h longer than the 7.04 (SD 1.55) sample average. Sleep duration showed no appreciable change beyond middle age. Men and women reported sleeping similar amounts but women reported more sleep problems. Men reported sleeping less when there were more children in their household. Workers (i.e. employees) reported sleeping less on workdays than on non-workdays, but those based at home and those not employed did not. Inability to switch off from work was related to sleep duration on non-workdays. Across all participants average sleep duration exhibited a non-monotonic association with quality of life (i.e. contribution of sleep to energy, satisfaction and success in work, home and leisure activities). Quality of life was positively associated with sleep duration, for durations up to 9 h, but negatively associated with quality of life beyond this. Comparison of our data with the US national sleep poll revealed that Britain sleeps as little or less, whereas a comparison with data reported 40 years ago revealed no statistically reliable reductions. Although we may not sleep less than four decades ago, when we report sleeping less we also tend to associate that lack of sleep with poor performance and quality of life.
 
A prominent media publicity cluster during 2007-2008 in Australia linked the common hypnotic zolpidem to adverse drug reaction reports of parasomnias, amnesia, hallucinations and suicidality. The collection of adverse drug reaction data through spontaneous reporting systems is a mainstay of drug safety monitoring, but a stimulated reporting event such as this often renders such data uninterpretable. As such, we aimed to investigate whether these associations were present before the media cluster and then to quantify the effect of stimulated reporting on those four specific outcomes. Using disproportionality analyses we compared zolpidem to all other drugs in the database, and then separately to each of all hypnotics, then all benzodiazepines, and then temazepam alone, and did so in every year from 2001 to 2008. Year-by-year analyses of Reporting odds ratios for zolpidem exposure and adverse events of interest, adjusted for a number of covariates, revealed an association between zolpidem exposure and parasomnias, amnesia and hallucination both before and after the cluster of media publicity beginning in early 2007. The odds ratios increased significantly after the media publicity for only parasomnias and amnesia. Suicidality was increased in some analyses, but limited data make this outcome difficult to interpret. We conclude that zolpidem adverse drug reaction reports have higher odds for parasomnia, amnesia, hallucination and perhaps suicidality compared to either all other drugs or hypnotics, even before the media publicity cluster. However, the extant literature and the limitations of these spontaneously reported adverse drug reaction data do not allow us to conclude that these events are related causally to zolpidem.
 
In a recent review, Frank and Heller (2003) provided support for their 'presleep theory' of sleep development. According to this theory, rapid eye movement (REM) and non-rapid eye movement (Non-REM) sleep in rats emerge from a common 'dissociated' state only when the neocortical EEG differentiates at 12 days of age (P12). Among the assumptions and inferences associated with this theory is that sleep before EEG differentiation is only 'sleep-like' and can only be characterized using behavioral measures; that the neural mechanisms governing presleep are distinct from those governing REM and Non-REM sleep; and that the presleep theory is the only theory that can account for developmental periods when REM and Non-REM sleep components appear to overlap. Evidence from our laboratory and others, however, refutes or casts doubt on these and other assertions. For example, infant sleep in rats is not 'sleep-like' in that it satisfies nearly every criterion used to characterize sleep across species. In addition, beginning as early as P2 in rats, myoclonic twitching occurs only against a background of muscle atonia, indicating that infant sleep is not dissociated and that electrographic measures are available for sleep characterization. Finally, improved techniques are leading to new insights concerning the neural substrates of sleep during early infancy. Thus, while many important developmental questions remain, the presleep theory, at least in its present form, does not accurately reflect the phenomenology of infant sleep.
 
Chronic sleep deprivation is common among workers, and has been associated with negative work outcomes, including absenteeism and occupational accidents. The objective of the present study is to characterize reciprocal relationships between sleep and work. Specifically, we examined how sleep impacts work performance and how work affects sleep in individuals not at-risk for a sleep disorder; assessed work performance outcomes for individuals at-risk for sleep disorders, including insomnia, obstructive sleep apnea (OSA) and restless legs syndrome (RLS); and characterized work performance impairments in shift workers (SW) at-risk for shift work sleep disorders relative to SW and day workers. One-thousand Americans who work 30 h per week or more were asked questions about employment, work performance and sleep in the National Sleep Foundation's 2008 Sleep in America telephone poll. Long work hours were associated with shorter sleep times, and shorter sleep times were associated with more work impairments. Thirty-seven percent of respondents were classified as at-risk for any sleep disorder. These individuals had more negative work outcomes as compared with those not at-risk for a sleep disorder. Presenteeism was a significant problem for individuals with insomnia symptoms, OSA and RLS as compared with respondents not at-risk. These results suggest that long work hours may contribute to chronic sleep loss, which may in turn result in work impairment. Risk for sleep disorders substantially increases the likelihood of negative work outcomes, including occupational accidents, absenteeism and presenteeism.
 
The 24-h rhythm of growth hormone (GH) is thought to be controlled primarily by sleep processes with a weak circadian component. This concept has been recently questioned in sleep-deprived persons. To test the notion of a high sleep-dependency of GH release, we established simultaneous 24-h rhythms of GH and melatonin, a circadian marker, in night workers who form a model for challenging sleep and circadian processes. Ten day-active subjects and 11 night workers were studied during their usual sleep-wake schedule, with sleep from 23:00 to 07:00 hours and 07:00 to 15:00 hours, respectively. Experiments were conducted in sleep rooms under continuous nutrition, bed rest, and dim light. Melatonin and GH were measured every 10 min over 24 h. In day-active subjects, melatonin and GH showed the well-known 24-h profiles, with a major sleep-related GH pulse accounting for 52.8 +/- 3.5% of the 24-h GH production and the onset of the melatonin surge occurring at 21:53 hours +/- 18 min. In night workers, melatonin showed variable circadian adaptation, with the onset of secretion varying between 21:45 and 05:05 hours. The sleep-related GH pulse was lowered, but the reduction was compensated for by the emergence of large individual pulses occurring unpredictably during waking periods, so that the total amount of GH secreted during the 24 h was constant. One cannot predict the degree of GH adaptation from the highly variable melatonin shift. These results argue against the concept that sleep processes exert a predominant influence on GH release whatever the conditions. When sleep and circadian processes are misaligned, the blunting of the sleep-related GH pulse is counteracted, as in sleep-deprived persons, by a compensatory mechanism promoting GH pulses during wakefulness.
 
Insomniacs report daytime functioning problems, but studies of neurobehavioral functioning in insomniacs have shown little objective evidence of impairment. In addition, very little is known about the influence of the circadian clock on performance in chronic insomniacs. In the present study, we investigated whether chronic insomnia is associated with an overall performance deficit, and what the effect is of circadian rhythmicity, under strictly controlled laboratory conditions. A 24-h experiment was carried out under constant routine conditions. Psychomotor performance, body temperature, and subjective functioning of 11 insomniacs and 13 healthy subjects were assessed. The insomniacs showed significant overall performance impairments in vigilance, working memory, and motor control. In addition, body temperature, performance and subjective functioning showed a circadian pattern similar to healthy subjects, with trough values in the late night/early morning and peak values in the early evening. Self-reported functioning among the insomniacs indicated mood disturbances, concentration problems, elevated fatigue and elevated sleepiness. The results indicated that chronic insomnia is associated with a substantial lowering of the 24-h level of performance and subjective functioning, irrespective of the type of task and/or the particular parameter, and without differential effects of circadian rhythmicity. Apparently, chronic insomnia has a negative impact upon performance as measured under strictly controlled, unmasked conditions.
 
Periodic Leg Movements (PLM) in sleep occur in a wide variety of sleep/wake disorders but their relationship with sleep disturbance, and notably with the concomitant existence of a 'restless legs' syndrome (RLS) remains unclear. We performed 24-h ambulatory polygraphy in a population of 54 consecutive, unselected patients with PLMs (Coleman's index greater than 5/h) who complained of different sleep disorders. A Principal Component Analysis (PCA) was conducted on seven variables from the sample, namely PLM index, patient's age, sleep stage changes per hour, sleep depth index (SWS+PS/TST), diurnal sleep time, number of awakenings exceeding 2 min and presence of a RLS. PCA yielded four independent factors. The PLM index and the changes of sleep stage clustered in a single factor, linking therefore sleep fragmentation to the frequency of PLMs. The second factor appeared to reflect a circadian sleep/wake disorder, combining diurnal sleep time with the number of long night awakenings. The third factor was mainly loaded by the patients' age and the sleep depth index, thus reflecting a well known relationship. Finally, the variable reflecting the existence of a RLS appeared isolated in a single factor, independent from the three previously described. These results confirm and extend the link between PLMs and sleep fragmentation, as well as the recently described dissociation between PLMs and diurnal somnolence. On the other hand, our analysis suggests that in PLM patients the concomitant existence of a RLS is not related to the frequency of occurrence of PLMs, at least when these latter are quantified independently of their arousal index.
 
The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function, primarily in the thalamus, a subcortical structure involved in alertness and attention, and in the prefrontal cortex, a region subserving alertness, attention, and higher-order cognitive processes. To test this hypothesis, 17 normal subjects were scanned for quantifiable brain activity changes during 85 h of sleep deprivation using positron emission tomography (PET) and (18)Fluorine-2-deoxyglucose ((18)FDG), a marker for regional cerebral metabolic rate for glucose (CMRglu) and neuronal synaptic activity. Subjects were scanned prior to and at 24-h intervals during the sleep deprivation period, for a total of four scans per subject. During each 30 min (18)FDG uptake, subjects performed a sleep deprivation-sensitive Serial Addition/Subtraction task. Polysomnographic monitoring confirmed that subjects were awake. Twenty-four hours of sleep deprivation, reported here, resulted in a significant decrease in global CMRglu, and significant decreases in absolute regional CMRglu in several cortical and subcortical structures. No areas of the brain evidenced a significant increase in absolute regional CMRglu. Significant decreases in relative regional CMRglu, reflecting regional brain reductions greater than the global decrease, occurred predominantly in the thalamus and prefrontal and posterior parietal cortices. Alertness and cognitive performance declined in association with these brain deactivations. This study provides evidence that short-term sleep deprivation produces global decreases in brain activity, with larger reductions in activity in the distributed cortico-thalamic network mediating attention and higher-order cognitive processes, and is complementary to studies demonstrating deactivation of these cortical regions during NREM and REM sleep.
 
The present study examined the impact of mild (24 h) sleep deprivation and of the circadian rhythm on auditory temporal resolution, measured by dichotic temporal order judgment (TOJ). The rationale for the present study was based on several areas of research. First, the 'sleep-based neuropsychological perspective' hypothesis posits that sleep reduction initially impacts the functions associated with intact prefrontal cortical activity, e.g. language tasks. Secondly, recent studies indicate the importance of the role of auditory temporal resolution in speech comprehension. Thirdly, there is accumulating evidence of the involvement of prefrontal cortical structures in auditory temporal resolution. We hypothesized that mild to moderate sleep deprivation would affect dichotic TOJ negatively. The results showed that: (1) 24 h of sleep deprivation significantly reduced the overall level of accuracy in dichotic TOJ and increased dichotic TOJ threshold from 57.61 ms to 73.93 ms, a reduction in temporal resolution of 28.3%; (2) dichotic TOJ was subject to a small, but significant diurnal rhythm having a nadir in early to mid afternoon. As auditory temporal resolution of speech and non-speech sounds seems to be dependent on intact functioning of the left inferior and left dorso-lateral prefrontal cortex (PFC), these data strengthen the argument that even mild to moderate sleep deprivation can impact negatively on PFC-dependent functions. Furthermore, based on these findings, we suggest that the deficit in auditory temporal resolution in individuals suffering from sleep loss may also affect language comprehension. http://www.ariel.ac.il/research/apl/publications
 
A novel animal-analog of the human psychomotor vigilance task (PVT) was validated by subjecting rats to 24 h of sleep deprivation (SD) and examining the effect on performance in the rat-PVT (rPVT), and a rat multiple sleep latency test (rMSLT). During a three-phase (separate cohorts) crossover design, vigilance performance in the rPVT was compared with 24 h SD-induced changes in sleepiness assessed by polysomnographic evaluation and the rMSLT. Twenty-four hours of SD was produced by brief rotation of activity wheels at regular intervals in which the animals resided throughout the experiment. In the rPVT experiment, exercise controls (EC) experienced the same overall amount of locomotor activity as during SD, but allowed long periods of undisturbed sleep. After 24 h SD response latencies slowed, and lapses increased significantly during rPVT performance when compared with baseline and EC conditions. During the first 3 h of the recovery period following 24 h SD, polysomnographic measures indicated sleepiness. Latency to fall asleep after 24 h SD was assessed six times during the first 3 h after SD. Rats fell asleep significantly faster immediately after SD, than after non-SD baseline sessions. In conclusion, 24 h of SD in rats increased sleepiness, as indicated by polysomnography and the rMSLT, and impaired vigilance as measured by the rPVT. The rPVT closely resembles the human PVT test widely used in human sleep research and will assist investigation of the neurobiologic mechanisms that produce vigilance impairments after sleep disruption.
 
SUMMARY Our objective was to investigate whether sleep-like states occur in the cockroach, Blaberus giganteus by applying the methods formerly used for another cockroach species, Leucophaea maderae and the scorpions, Heterometrus and Pandinus. The behaviour of isolated animals (n= 10) kept under LD 12:12 h was recorded by time-lapse video for three consecutive 24-h periods. Nine behavioural states were scored for 1-min real-time epochs. Rest was subdivided into 4 sub-states on the basis of body posture and the position of the antennae. The cockroaches showed a nocturnal behaviour exhibiting a bout of locomotion at dark onset which lasted several hours, and a preference for rest in the light period. Immobility with both the body and the antennae touching the substrate (state 1) was the predominating state in the light period. In order to establish whether the sub-states of rest represented different levels of vigilance the arousal threshold was measured by determining the latency of a behavioural response to a vibration stimulus. The levels of arousal differed significantly in four behavioural states in the light period but not in the dark period. In state 1 the animals exhibited the lowest arousal whereas in the activity states arousal was the highest. The state with the highest arousal threshold occurred in the beginning of the light period. Thereafter, arousal progressively increased and remained relatively high during the dark period. The effect of 6-h deprivation of rest by the gentle shaking of the cages whenever the animals were immobile, resulted in a reduced latency to state 1, a small increase of state 1 and a more prominent initial increase of activity during recovery. In conclusion, this study provides evidence for the existence of a 24-h variation of vigilance in the cockroach. It further indicates that a ‘rest deficit’ gives rise to a compensatory response. The data support the notion that sleep-like states are present in these insects.
 
Polycythaemia, peripheral oedema formation and hypertension have classically been described in association with obstructive sleep apnoea (OSA). However, there is very limited information about blood volume in OSA and how it changes during long-term treatment with nasal continuous positive airway pressure (nCPAP). Plasma (PV) and red-cell volumes (RCV), 24-h ambulatory blood pressure (BP), 24-h natriuresis and morning plasma aldosterone, renin activity and atrial natriuretic peptide in 11 men with a mean age of 47 y (range 37-55), apnoea index (AI) of 55 (22-106), body mass index of 36 (30-43) and seated BP of > or = 140/90 mmHg without any medication were measured. BP-measurements were repeated after 3 weeks and all measurements after 3 mo of nCPAP treatment. Aldosterone and 24-h mean heart rates decreased during treatment. Twenty-four-h BP decreased after 3 weeks but that decrease did not persist after 3 mo of treatment. There was a relationship between changes in night-time mean BP and PV and aldosterone. The haematocrit declined in every patient. No significant changes were found in the mean PV or RCV. They were in all instances lower than has earlier been described for normal, non-obese subjects. These data also suggest that OSA causes divergent individual disturbances in blood volume homeostasis which can be corrected by nCPAP.
 
Obstructive sleep apnoea (OSA) is common in patients with resistant hypertension, but understanding of the pathogenic mechanisms linking both conditions is limited. This study assessed the prevalence of OSA and the relationships between OSA and 24-h blood pressure (BP) in 62 consecutive patients with resistant hypertension, defined as clinic BP values ≥ 140/90 despite the prescription of at least three drugs at adequate doses, including a diuretic. In order to exclude a 'white coat effect', only patients with ambulatory 24-h BP values ≥ 125/80 were recruited. Patients underwent polysomnography, 24-h ambulatory BP monitoring and completed the Epworth sleepiness scale (ESS). OSA was defined as an apnoea-hypopnoea index (AHI) ≥ 5 and excessive daytime sleepiness (EDS) by an ESS ≥ 10. A multiple linear regression analysis was used to assess the association of anthropometric data, OSA severity measures and ESS with 24-h systolic and diastolic BP. Mean 24-h BP values were 139.14/80.98 mmHg. Ninety per cent of patients had an AHI ≥ 5 and 70% had an AHI ≥ 30. Only the ESS was associated with 24-h diastolic BP [slope 0.775, 95% confidence interval (CI) 0.120-1.390, P < 0.02); age was associated negatively with 24-h diastolic BP (slope -0.64, 95% CI -0.874 to -0.411, P < 0.001). Compared with those without EDS, patients with EDS showed a significantly higher frequency of diastolic non-dipping pattern (69.2% versus 34.7%, P < 0.032). Our results demonstrate a high prevalence of severe OSA in patients with resistant hypertension and suggest that EDS could be a marker of a pathogenetic mechanism linking OSA and hypertension.
 
This paper describes several different methods for the analysis of blood pressure and heart rate variability over the 24 hours, both in the time and in the frequency domain. The mechanisms possibly involved in the genesis of the variations in blood pressure and heart rate which occur over a 24-hour period are also discussed. Finally, new approaches to the dynamic evaluation of the sensitivity of baroreflex control of heart rate and of its changes over the 24 hours in daily life conditions, based on computer analysis of the interaction between fluctuations in blood pressure and heart rate, are described. Data obtained by applying these methods in different clinical conditions (normotensive vs. hypertensive subjects, young vs. elderly individuals and pure autonomic failure patients) are presented.
 
Brain imaging studies demonstrate that sleep deprivation reduces glucose metabolism and blood flow in the prefrontal cortex, and such reductions are associated with impairments in cognitive functioning. Although some of the greatest metabolic declines occur within the orbitofrontal cortex, little is known about the effects of sleep loss on the types of processes mediated by this region, including emotion, motivation, feeding, and olfaction. The present study tested odor identification accuracy when individuals were well rested and again following 24 h of wakefulness. Relative to rested baseline performance, sleep-deprived individuals demonstrated a significant decline in the ability to identify specific odors on the Smell Identification Test. This decrement in olfactory functioning occurred concomitantly with slowed psychomotor speed and increased ratings of self-reported sleepiness. Performance on a task that required complex mental set shifting did not change significantly following sleep deprivation, suggesting that the decrements in odor identification could not be attributed to task difficulty. Finally, while there was no relationship between subjective sleepiness and odor identification at rested baseline, greater subjective sleepiness was associated with better odor identification ability following 24 h of sleep loss. Possible implications of these findings are discussed.
 
In a retrospective cohort study undertaken in 12 European countries, 249 female narcoleptic patients with cataplexy (n = 216) and without cataplexy (n = 33) completed a self-administrated questionnaire regarding pregnancy and childbirth. The cohort was divided further into patients whose symptoms of narcolepsy started before or during pregnancy (308 pregnancies) and those in whom the first symptoms of narcolepsy appeared after delivery (106 pregnancies). Patients with narcolepsy during pregnancy were older during their first pregnancy (P < 0.001) and had a higher body mass index (BMI) prior to pregnancy (P < 0.01). Weight gain during pregnancy was higher in narcoleptic patients with cataplexy (P < 0.01). More patients with narcolepsy-cataplexy during pregnancy had impaired glucose metabolism and anaemia. Three patients experienced cataplexy during delivery. The rate of caesarean sections was higher in the narcolepsy-cataplexy group compared to the narcolepsy group (P < 0.05). The mean birth weight and gestational age of neonates were within the normal range and did not differ across groups. Neonatal care was affected adversely by symptoms of narcolepsy in 60.1% of those with narcolepsy during pregnancy. This study reports more obstetric complications in patients with narcolepsy-cataplexy during pregnancy; however, these were not severe. This group also had a higher BMI and higher incidence of impaired glucose metabolism during pregnancy. Caesarian section was conducted more frequently in narcolepsy-cataplexy patients, despite cataplexy being a rare event during delivery. Furthermore, symptoms of narcolepsy may render care of the infant more difficult.
 
The present study systematically compared the effects of fatigue and alcohol intoxication on a range of neurobehavioural tasks. By doing so, it was possible to quantify the performance impairment associated with fatigue and express it as a blood alcohol impairment equivalent. Twenty-two healthy subjects aged 19-26 years participated in three counterbalanced conditions. In the sustained wakefulness condition, subjects were kept awake for 28 h. In the alcohol and placebo conditions, subjects consumed either an alcoholic or non-alcoholic beverage at 30 min intervals, until their blood alcohol concentration reached 0.10%. In each session, performance was measured at hourly intervals using four tasks from a standardised computer-based test battery. Analysis indicated that the placebo beverage did not significantly effect mean relative performance. In contrast, as blood alcohol concentration increased performance on all the tasks, except for one, significantly decreased. Similarly, as hours of wakefulness increased performance levels for four of the six parameters significantly decreased. More importantly, equating the performance impairment in the two conditions indicated that, depending on the task measured, approximately 20-25 h of wakefulness produced performance decrements equivalent to those observed at a blood alcohol concentration (BAC) of 0.10%. Overall, these results suggest that moderate levels of fatigue produce performance equivalent to or greater than those observed at levels of alcohol intoxication deemed unacceptable when driving, working and/or operating dangerous equipment.
 
The objective of the present study was to further elucidate the mechanisms involved in the wake-promoting effects of psychomotor-stimulants. Many previous studies have tightly linked the effects of stimulants to dopamine neurotransmission, and some studies indicate that serotonin 2A receptors modulate these effects. However, the role of dopamine in arousal is controversial, most notably because dopamine neurons do not change firing rates across arousal states. In the present study, we examined the wake-promoting effects of the dopamine-releaser amphetamine using non-invasive telemetric monitoring. These effects were evaluated in rhesus monkeys as a laboratory animal model with high translational relevance for human disorders of sleep and arousal. To evaluate the role of dopamine in the wake-promoting effects of amphetamine, we used in vivo microdialysis targeting the caudate nucleus, as this approach provides clearly interpretable measures of presynaptic dopamine release. This is beneficial in the present context because some of the inconsistencies between previous studies examining the role of dopamine in arousal may be related to differences between postsynaptic dopamine receptors. We found that amphetamine significantly and dose-dependently increased arousal at doses that engendered higher extracellular dopamine levels. Moreover, antagonism of serotonin 2A receptors attenuated the effects of amphetamine on both wakefulness and dopamine overflow. These findings further elucidate the role of dopamine and serotonin 2A receptors in arousal, and they suggest that increased dopamine neurotransmission may be necessary for the wake-promoting effects of amphetamine, and possibly other stimulants.
 
We studied the effect of sleep excess on the sleep-wakefulness pattern of rats. Subarachnoid infusion of prostaglandin D2 or the adenosine A2a receptor agonist CGS21680 effectively induced slow wave sleep (SWS) for the first 12 h of the night-time period, whereas they did not induce sleep during the following 24 h of infusion. An increase in the amount of wakefulness was seen during the last 12 h of prostaglandin D2 infusion. The amounts of wakefulness strongly increased during the following 36-h recovery period. Rebound wakefulness was extraordinarily strong after the cessation of CGS21680 infusion, reaching almost complete insomnia during the night-time. Treatment of animals with prostaglandin D2 overnight, following by treatment with CGS21680 on the next night, resulted in the strongest induction of wakefulness rebound. During the rebound period, the amount of wakefulness reached up to 50 min per hour in the daytime. Rebound of wakefulness depended on the amounts of preceding SWS induced by infusion of prostaglandin D2 for 6 or 12 h and of CGS21680 for 12 h. The larger the amount of SWS, the larger the amount of the following rebound of wakefulness. Rebounds of wakefulness occurred as a result of decrease in SWS amounts, whereas paradoxical sleep amounts did not change. Desensitization of adenosine A2a receptors and accumulation of prostaglandin E2 may be involved in the production of strong wakefulness rebound following relatively long treatments (more than 12 h) with prostaglandin D2 or CGS21680.
 
Mutations in clock genes are associated with abnormal circadian parameters, including sleep. An association has been reported previously between a polymorphism (3111C), situated in the 3'-untranslated region (3'-UTR) of the circadian gene Clock and evening preference. In the present study, this polymorphism was assessed in: (1) 105 control subjects with defined diurnal preference, (2) 26 blind subjects with free-running circadian rhythms and characterized with regard to circadian period (tau) and (3) 16 delayed sleep phase syndrome patients. The control group was chosen from a larger population (n = 484) by Horne-Ostberg questionnaire analysis, from which three subgroups were selected (evening, intermediate and morning preference). Data from sleep diaries completed by 90% of these subjects showed a strong correlation between preferred and estimated timings of sleep and wake. The mean timings of activities for the evening group were at least 2 h later than the morning group. Genetic analysis showed that, in contrast with the previously published finding, there was no association between 3111C and eveningness. Neither was there an association between 3111C and tau, nor a significant difference in 3111C frequency between the normal and delayed sleep phase syndrome groups. To assess the effect of this polymorphism on messenger RNA (mRNA) translatability, luciferase reporter gene constructs containing the two Clock polymorphic variants in their 3'-UTR were transfected into COS-1 cells and luciferase activity measured. No significant difference was observed between the two variants. These results do not support Clock 3111C as a marker for diurnal preference, tau, or delayed sleep phase syndrome in humans.
 
There is only scant information on sleep characteristics and long-term follow-up in patients with Kleine-Levin syndrome (KLS). This study describes the clinical course, results of polysomnography and long-term follow-up in a relatively large group of patients with KLS. During the years 1982-97, we encountered 34 patients (26 males and eight females) with KLS. We were able to obtain the original polysomnographs from 28 males and four females. In 25 patients, data regarding their present state of health were obtained. Fourteen agreed to be present at a detailed interview and examination while 11 gave the information by phone. The mean age at onset was 15.8 +/- 2.8 years and the mean diagnostic delay, 3.8 +/- 4.2 years. The mean duration of a single hypersomnolent attack was 11.5 +/- 6.6 days. The main abnormal findings extracted out of 35 polysomnographs obtained from 32 patients during and/or in-between attacks included: decreased sleep efficiency, and frequent awakenings from sleep stage 2. All 25 patients reported present perfect health, with no evidence of behavioral or endocrine dysfunction. In adolescents with periodic hypersomnia, the diagnosis of KLS should be explored. Sleep recordings during a hypersomnolent period will often show frequent awakenings from sleep stage 2. The long-term prognosis is excellent.
 
Although it is well known that sleep loss results in poor judgement and decisions, little is known about the influence of social context in these processes. Sixteen healthy young adults underwent three games involving bargaining ('Ultimatum' and 'Dictator') and trust, following total sleep deprivation (TSD) and during rested wakefulness (RW), in a repeated-measures, counterbalanced design. To control for repeatability, a second group (n = 16) was tested twice under RW conditions. Paired anonymously with another individual, participants made their simple social interaction decisions facing real monetary incentives. For bargaining, following TSD participants were more likely to reject unequal-split offers made by their partner, despite the rejection resulting in a zero monetary payoff for both participants. For the trust game, participants were less likely to place full trust in their anonymous partner. Overall, we provide novel evidence that following TSD, the conflict between personal financial gain and payoff equality is focused upon avoidance of unfavourable inequality (i.e. unfairness). This results in the rejection of unfair offers at personal monetary cost, and the lack of full trust which would expose one to being exploited in the interaction. As such, we suggest that within a social domain decisions may be more influenced by emotion following TSD, which has fundamental consequences for real-world decision-making involving social exchange.
 
Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers' emotion expression. Ten healthy children (seven females; 30-36 months old) followed a strict sleep schedule (≥12.5 h time in bed per 24-h) for 5 days, before each of two randomly assigned afternoon emotion assessments following Nap and No-Nap conditions (resulting in an 11-day protocol). Children viewed emotion-eliciting pictures (five positive, three neutral, three negative) and completed puzzles (one solvable, one unsolvable). Children's faces were video-recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently 'taxes' young children's emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems.
 
The objectives of this study were to test the sensitivity of the short form 36 health survey questionnaire (SF 36) to sleep disruption in patients with obstructive sleep apnoea (OSA) and assess its use as an outcome measure for treatment with nasal continuous positive airway pressure (CPAP). Two hundred and twenty-three subjects under investigation for snoring and/or daytime somnolence completed the questionnaire at presentation and again after a six month period. Subjects with OSA requiring treatment scored lower on all dimensions of the SF 36 (P < 0.05) than normative scores for the general population. The largest differences were for vitality (24%) and social functioning (27.9%). After six months of treatment with CPAP there was an improvement in all scores and the score for vitality was no longer significantly different from that of the general population. The SF 36 is sensitive to the effects of sleep disruption in subjects with obstructive sleep apnoea, is a useful outcome measure for treatment with CPAP and its value in other sleep disorders should be assessed.
 
Modafinil is an alerting substance which has been used successfully to treat narcolepsy. Nothing is known about its effect on hormone secretions. For this purpose, eight healthy young men were enrolled in a double blind trial to test the effects of modafinil on daily plasma melatonin, cortisol and growth hormone (GH) rhythms. Blood was sampled for hormone assays, every hour during the daytime and every 30 min during the nighttime. In addition, rectal temperature and mental performances were determined during the study which comprised 3 sessions, two weeks apart: a 24 h control session including a night with sleep (S1) and two 48 h sessions S2 and S3 with a sleep-deprived night (N1) followed by a recovery night (N2). Modafinil (300 mg x 2) or placebo were randomly attributed during N1 at 22 h and 8 h. As expected, performance was improved after modafinil administration and body temperature was maintained or increased. Plasma melatonin and cortisol profiles were similar after modafinil and placebo administration. The levels observed during the recovery and the control nights (N2) displayed no difference. For GH, during both sleep deprived nights, secretion was dramatically reduced compared with the control one, although the number of secretory episodes was unchanged. These data show that the alerting property of modafinil is not related to an alteration of hormone profiles and suggest that the acute modafinil administration is devoid of short-term side-effects.
 
Increased sleep need following traumatic brain injury, referred to in this study as post-traumatic pleiosomnia, is common, but so far its clinical impact and therapeutic implications have not been characterized. We present a case-control study of 36 patients with post-traumatic pleiosomnia, defined by an increased sleep need of at least 2 h per 24 h after traumatic brain injury, compared to 36 controls. We assessed detailed history, sleep-activity patterns with sleep logs and actigraphy, nocturnal sleep with polysomnography and daytime sleep propensity with multiple sleep latency tests. Actigraphy recordings revealed that traumatic brain injury (TBI) patients had longer estimated sleep durations than controls (10.8 h per 24 h, compared to 7.3 h). When using sleep logs, TBI patients underestimated their sleep need. During nocturnal sleep, patients had higher amounts of slow-wave sleep than controls (20 versus 13.8%). Multiple sleep latency tests revealed excessive daytime sleepiness in 15 patients (42%), and 10 of them had signs of chronic sleep deprivation. We conclude that post-traumatic pleiosomnia may be even more frequent than reported previously, because affected patients often underestimate their actual sleep need. Furthermore, these patients exhibit an increase in slow-wave sleep which may reflect recovery mechanisms, intrinsic consequences of diffuse brain damage or relative sleep deprivation.
 
Sleepwalkers have been shown to have an unusually high number of arousals from slow wave sleep and lower slow wave activity (SWA) power during the night than controls. Because sleep deprivation increases the frequency of slow wave sleep (SWS) arousals in sleepwalkers, it may also affect the expression of the homeostatic process to a greater extent than shown previously. We thus investigated SWA power as well as slow wave oscillation (SWO) density in 10 sleepwalkers and nine controls at baseline and following 38 h of sleep deprivation. There was a significant increase in SWA during participants' recovery sleep, especially during their second non-rapid eye movement (NREM) period. SWO density was similarly increased during recovery sleep's first two NREM periods. A fronto-central gradient in SWA and SWO was also present on both nights. However, no group differences were noted on any of the 2 nights on SWA or SWO. This unexpected result may be related to the heterogeneity of sleepwalkers as a population, as well as our small sample size. SWA pressure after extended sleep deprivation may also result in a ceiling effect in both sleepwalkers and controls.
 
Top-cited authors
Dieter Riemann
  • University Medical Center Freiburg
Damien Leger
  • Université Paris Descartes - Sorbonne Paris Cité; APHP
Torbjörn Åkerstedt
  • Karolinska Institutet
Christoph Nissen
  • University Psychiatric Services Bern
Kai Spiegelhalder
  • University Medical Center Freiburg