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PubMed1979

Sleep onset and first cycle of sleep in human subjects: change with time of day.

The first cycle of sleep was studied in different situations: normal night sleep, naps, diurnal sleep after night shifts (3 x 8 shift workers). Results show two types of first cycle: some started with SWS (normal cycles), others with REM (sleep onset REM periods: SOREMPs). (1) Normal cycles: the length of SWS in the first cycle was positively correlated with prior wakefulness; conversely, the latency of SWS decreased as prior wakefulness increased; the decrease was due to the decrease in the length of the previous stage II or of the sleep onset latency (SOL). Length of sleep onset (SO) showed only few variations. The structure of the first cycle of shift workers' sleep probably reflects an important sleep loss. (2) SOREMPs occcurred during diurnal sleep. Some hypotheses about these cycles are discussed including REM 'pressures' (circadian, sleep loss) and inter-individual variations.

Adult↗
PubMed1995

Sleep, sleep deprivation and infectious disease: studies in animals.

Common perceptions that the desire for sleep is increased during mild infectious diseases like colds and 'the flu' have fostered beliefs that sleep promotes recovery from infectious disease and that lack of sleep increases susceptibility to infections. However, until recently, the relationship between infectious disease and vigilance received relatively little systematic study. At present, several model systems provide evidence that infectious disease is accompanied by alterations in sleep. Indeed, increased sleepiness, like fever and anorexia, may be viewed as a facet of the acute phase response to infectious challenge. Recent studies also suggest that sleep, sleep deprivation and infectious disease may be related via mechanisms of the immune system (Fig. 1). Data are now accumulating to address questions such as whether immune processes alter sleep, whether sleep or sleep deprivation influences immune competence, and whether sleep facilitates recovery from infectious disease.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2005

Heart rate responses to non-arousing trigeminal stimulation in infants: effects of sleep position, sleep state and postnatal age.

AIMS: The aim of this study was to examine the effects of maternal smoking, sleeping position, sleep state and postnatal age on heart rate changes following non-arousing trigeminal stimulation in infants. SUBJECTS: We studied healthy term infants, 13 of whom were born to mothers who did not smoke and 11 to mothers who smoked during pregnancy. Each infant was studied using daytime polysomnography on 3 occasions: (a) 2-3 weeks, (b) 2-3 months and (c) 5-6 months after birth. Nasal air-jet stimulation was presented in both active sleep (AS) and quiet sleep (QS) when infants slept both prone and supine. RESULTS: We found no difference between infants of smoking and non-smoking mothers in any of the parameters measured. Minimum HR (MinHR) following non-arousing trigeminal stimulation was significantly lower in the supine compared to the prone sleeping position at 2-3 weeks and 2-3 months of age (p<0.05) in AS, and at all 3 ages in QS (p<0.01). MinHR was significantly lower in QS compared to AS at 2-3 months when infants slept prone and at 5-6 months when sleeping supine (p<0.01). In QS, MinHR became lower with increasing postnatal age in both sleep positions (p<0.01). In AS, there was no maturational effect. The normalized bradycardia (DeltaHR%) was significantly greater in AS than in QS at 2-3 weeks of age (p<0.05) when infants slept supine. CONCLUSION: Our study has shown that there was a decrease in heart rate (MinHR) following trigeminal stimulation in infants up to 6 months of age and this was affected by sleep position and sleep state, being larger in the supine sleeping position and the QS state.

Age Factors↗
PubMed2005

A chronopharmacological preventive treatment for sleep-related migraine headaches and chronic morning headaches: Nitric oxide supersensitivity can cause sleep-related headaches in a subset of patients.

Frequent and recurrent migraine headaches can, over time, pose the additional risks of stroke, brain damage, heart failure and attention deficit. This is why prevention should always be a part of the treatment. Nitric oxide supersensitivity is the hypothesis upon which this model is based. Its role in causing migraine headaches and chronic morning headaches can be triggered by both normal and abnormal characteristics of the sleep cycle and more specifically by the release of nitric oxide that occurs towards the end of the sleep cycle. Stress and the age-related loss of sleep continuity, together with the corresponding increase in cortisol levels, potentiate delta rebound. Delta rebound results in deeper sleep intensity. It is associated with increased nitric oxide production. Increased delta rebound then causes an increase in the amount and duration of nitric oxide release at night. Migraineurs are susceptible to migraine headaches because they are supersensitive to nitric oxide. The diurnal pattern of the incidence of sleep-related headaches in a subset of the general population is caused by the effect of nitric oxide supersensitivity during the sleep cycle. The proposed treatment is for both sleep-related migraine headaches and chronic morning headaches. It consists of melatonin and moclobemide taken during the night, close the end of the sleep cycle so as to achieve the maximum concentrations. Both melatonin and moclobemide affect three important aspects of sleep-related headaches: nitric oxide supersensitivity, stress system dysfunction and sleep pathology. Both melatonin and moclobemide have demonstrated effectiveness in preventing migraine headaches. Additionally, both melatonin and moclobemide are compatible with most of the other therapeutic agents used to prevent migraine headaches and with at least 1 therapeutic agent that is used to treat migraine headaches.

Antioxidants↗
PubMed2000

Acute effects of mirtazapine on sleep continuity and sleep architecture in depressed patients: a pilot study.

BACKGROUND: Mirtazapine, a clinically effective antidepressant, acts by antagonizing central alpha2-adrenergic and 5-HT2/5-HT3 receptors. No data are available regarding mirtazapine's effects on sleep architecture in patients with major depressive disorder. METHODS: Six patients meeting criteria for major depressive disorder and scoring > or =4 on the three Hamilton Depression Rating Scale sleep items were studied. Polysomnographic evaluations were performed at baseline and after 1 (15 mg at bedtime) and 2 weeks (30 mg at bedtime) of open-label mirtazapine treatment. RESULTS: Mirtazapine significantly decreased sleep latency and significantly increased total sleep time and sleep efficiency from baseline levels during week 1, with similar results observed after week 2. Mirtazapine did not significantly alter rapid eye movement sleep parameters. Clinically, Hamilton Depression Rating Scale and sleep disturbance ratings improved after treatment. CONCLUSIONS: Mirtazapine significantly improves sleep continuity in major depressive disorder patients with poor sleep quality at weeks 1 and 2 of treatment, while preserving sleep architecture.

Adolescent↗
PubMed2000

Behavioral sleep medicine. An emerging subspecialty in health psychology and sleep medicine.

As the knowledge base in sleep disorders medicine has broadened, a subspecialty that we will refer to as "behavioral sleep medicine" area is emerging. This article will define this subspecialty area, provide some historical context for its emergence, review issues related to specialty training and clinical practice, and suggest needs for future research.The term "behavioral sleep medicine" was selected because it clearly denoted the two fields from which our subspecialty emerged (health psychology/behavioral medicine and sleep disorders medicine). It suggests much about our approach to training, clinical practice, and research, and it appropriately implies that the field is open to PhD sleep specialists, MD sleep specialists, and other health care providers with the relevant training. Formally, behavioral sleep medicine refers to the branch of clinical sleep medicine and health psychology that: (1) focuses on the identification of the psychological (e.g. cognitive and/or behavioral) factors that contribute to the development and/or maintenance of sleep disorders and (2) specializes in developing and providing empirically validated cognitive, behavioral, and/or other nonpharmacologic interventions for the entire spectrum of sleep disorders.

Education↗
PubMed2002

Sleep and sleep habits from childhood to young adulthood over a 10-year period.

The aim of this epidemiological study was to utilise a cross-sectional as well as a longitudinal approach to examine sleep habits and how they develop in young people in Iceland. The 668 subjects (1-20 years) who responded to a postal survey in 1985 were followed up 5 and 10 years later. The majority of the variance in bedtime and sleep duration was explained by age, but also to a considerable degree by other factors such as residence, season, and year of survey or interaction of these factors. Natural phenomena, such as the diminution of total sleep duration in the first years of life and the tendency for longer sleep on weekends compared to weekdays were confirmed. The lengthening of sleep on weekends was first significant at the age of 9 and was greater among adolescents than young adults. The incidence of daytime sleepiness increased in adolescence, as did napping, at which time their nocturnal sleep time significantly decreased. Over a period of 10 years, a significant shift to earlier wake-up times occurred in children up to 15 years of age, which resulted in a shortened total sleep time. The idea that individual sleep duration is an inherent parameter is supported by the high positive correlation of total sleep time across a 10-year period (r=.73). The present data confirm that Icelandic adolescents (aged 11, 13, and 15) have delayed bedtimes and shorter nocturnal sleep compared to European peers.

Adolescent↗
PubMed2005

Essentials of sleep recordings in Drosophila: moving beyond sleep time.

The power of Drosophila genetics can be used to facilitate the molecular dissection of sleep regulatory mechanisms. While evaluating total sleep time and homeostatic processes provides valuable information, other variables, such as sleep latency, sleep bout duration, sleep cycle length, and the time of day when the longest sleep bout is initiated, should also be used to explore the nature of a genetic lesion on sleep regulatory processes. Each of these variables requires that the recording interval used to identify periods of sleep and waking be determined accurately and empirically. This article describes the procedures for recording sleep in Drosophila and associated methodological constraints. In addition, it provides results from a normative data set of 1037 Canton-S female flies and 639 male flies to illustrate the nature and variability of sleep variables that one can extract from 24 h of data collection in Drosophila.

Animals↗
PubMed2002

REM sleep latency and wakefulness in the first sleep cycle as markers of major depression: a controlled study vs. schizophrenia and normal controls.

INTRODUCTION: REM sleep latency is a clinically significant sleep variable that is found to be decreased in several psychiatric disorders. However, it is not known whether alteration of REM sleep latency is similar across disorders. In order to test whether incorporation of wakefulness in the first sleep cycle has a different outcome on REM sleep latency in different clinical groups, the authors have investigated correlation between sleep variables in the first sleep cycle in 25 patients with major depression, 24 patients with chronic schizophrenia, and in 10 healthy subjects. RESULTS: REM sleep latency correlates with the duration of wakefulness in the first cycle in patients suffering from chronic schizophrenia and in healthy subjects. This correlation does not hold true in patients suffering from major depression. CONCLUSION: Wakefulness incorporated in the first cycle influences REM sleep latency in healthy subjects and in patients suffering from chronic schizophrenia but not in patients suffering from major depression. This finding further supports the evidence that reduced REM sleep latency is a nonflexible marker of depression.

Adult↗
PubMed2000

Brain site-specificity of extracellular adenosine concentration changes during sleep deprivation and spontaneous sleep: an in vivo microdialysis study.

Previous data suggested that increases in extracellular adenosine in the basal forebrain mediated the sleep-inducing effects of prolonged wakefulness. The present study sought to determine if the state-related changes found in basal forebrain adenosine levels occurred uniformly throughout the brain. In vivo microdialysis sample collection coupled to microbore high-performance liquid chromatography measured extracellular adenosine levels in six brain regions of the cat: basal forebrain, cerebral cortex, thalamus, preoptic area of hypothalamus, dorsal raphe nucleus and pedunculopontine tegmental nucleus. In all these brain regions extracellular adenosine levels showed a similar decline of 15 to 20% during episodes of spontaneous sleep relative to wakefulness. Adenosine levels during non-rapid eye movement sleep did not differ from rapid eye movement sleep. In the course of 6h of sleep deprivation, adenosine levels increased significantly in the cholinergic region of the basal forebrain (to 140% of baseline) and, to a lesser extent in the cortex, but not in the other regions. Following sleep deprivation, basal forebrain adenosine levels declined very slowly, remaining significantly elevated throughout a 3-h period of recovery sleep, but elsewhere levels were either similar to, or lower than, baseline. The site-specific accumulation of adenosine during sleep deprivation suggests a differential regulation of adenosine levels by as yet unidentified mechanisms. Moreover, the unique pattern of sleep-related changes in basal forebrain adenosine level lends strong support to the hypothesis that the sleep-promoting effects of adenosine, as well as the sleepiness associated with prolonged wakefulness, are both mediated by adenosinergic inhibition of a cortically projecting basal forebrain arousal system.

Adenosine↗
PubMed2003

Sleep microstructure around sleep onset differentiates major depressive insomnia from primary insomnia.

In the present study we investigate whether alterations of sleep propensity or of wake propensity are implicated in sleep initiation disturbances encountered in major depressive insomnia and in primary insomnia. For this purpose, the time course of electroencephalogram (EEG) power density during the period preceding sleep onset and during the first non-rapid eye movement (REM) period was examined in three age and gender matched groups of 10 women and 11 men (healthy controls, primary insomniacs and depressive insomniacs). In contrast to healthy controls and depressive insomniacs, patients with primary insomnia did not experience a gradual decrease of their alpha and beta1 power during the sleep onset period and had a lower delta activity in the 5 min preceding sleep onset. Compared with the two other groups, depressive patients exhibit less dynamic changes in slow wave activity during the first non-REM period. The present results suggest that hyperarousal (high 'Process W') may mainly be implicated in the sleep initiation difficulties of primary insomniacs whereas the homeostatic sleep regulation process seems to be partially maintained. In our major depressed patients, the sleep initiation disturbances appeared to relate to a lower sleep pressure (low 'Process S') rather than to hyperarousal. This study supports the idea that different mechanisms are implicated in sleep disturbances experienced by primary insomniacs and major depressive insomniacs.

Adult↗
PubMed1997

Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: Changes under nCPAP treatment.

Nocturnal arousals are the essential cause of disturbed sleep structure in patients with obstructive sleep apnoea syndrome (OSAS). The aim of this study was to analyse the relationship between sleep stages, respiratory (type-R) and movement (type-M) related EEG arousals. Furthermore, the value of these arousals as a criterion for the efficiency of nCPAP treatment was estimated. We examined 38 male patients aged between 30 and 71 (49.1 +/- 20.9 SD) y. All patients suffered from OSAS. The mean respiratory disturbance index (RDI) was 47.3 +/- 27.8 per h. Polysomnographic monitoring was carried out on 4 subsequent nights: baseline night, 2 nights of nCPAP titration and nCPAP control night. Sleep was visually scored and EEG arousals were classified into type R and M, depending on whether changes of respiration or movement caused the arousal. The RDI, the R index (type-R/h), the M index (type-M/h) and the R and M indices in different sleep stages were calculated. During the baseline night a deficit of slow wave sleep (SWS) and REM sleep was found. Furthermore there were more type-R than type-M arousals registered (17.4 h-1 [3.6-43.6] vs. 5.9 h-1 [1.6-11.8]) (P < 0.01). They occurred during stages NREM 1, NREM 2 and REM (P < 0.01). An SWS sleep rebound and a reduction of the SWS and REM latencies were already found during the first CPAP night. The R index was reduced during the first CPAP night in all sleep stages (P < 0.01) and remained approximately the same in the following 2 nights (3. CPAP night: 1.1 h-1 [0.3-5.0]). Type M arousals occurred more in stages 1 and 2 (P < 0.01), and remained unchanged under nCPAP. We concluded that differentiation of nocturnal arousals may provide more detailed information regarding the influence of breathing disturbances on sleep. Respiratory related, not movement related, arousals may be a useful additional tool in judging the efficiency of OSAS.

Adult↗
PubMed1998

6-Sulfatoxymelatonin excretion and self-reported sleep in good sleeping controls and 55-80-year-old insomniacs.

The pineal hormone melatonin is thought to play a role in sleep initiation and maintenance. This was examined in a large sample of good sleeping controls (n = 52) and sleep maintenance insomniacs (n = 56), aged 55-80 y. Subjects collected 5 d of self-reported sleep diary measures, and 12-h urine samples (08.00-20.00 and 20.00-08.00 h) for analysis of the urinary melatonin metabolite, 6-sulphatoxymelatonin (aMT.6S). Insomniacs reported a significantly greater amount of wake after sleep onset, less sleep in total, less efficient sleep and poorer quality sleep compared to controls. However, no significant differences in melatonin excretion were observed between controls and insomniacs, with both groups showing similar mean (SEM) 12-h night-time [30.9 (2.9) vs. 30.6 (3.3) nmoles, respectively] as well as 24-h total [38.7 (3.4) vs. 36.7 (3.8)] aMT.6S excretion levels. No significant correlations were observed with any sleep parameters nor any effects of medication (anti-inflammatory agents, hormone replacement therapy, and an undifferentiated group of medications). The present results do not support a simple relationship between total melatonin production and self-reported sleep quality and duration in the aged.

Age Factors↗
PubMed1998

Behavioural treatment for sleep problems in children with severe learning disabilities and challenging daytime behaviour: effect on sleep patterns of mother and child.

Children with sleep problems present serious management problems to their parents. Such children are also more likely to have additional problems, behavioural disturbance being particularly common. This randomized controlled trial of behavioural interventions for the children's sleep problems was conducted to explore the efficacy and mechanisms of treatment in children with the most extreme forms of problems: severe learning disabilities, severe sleep problems and severe daytime challenging behaviour. Fifteen index families received behavioural advice for the child's sleep problem and compared with 15 matched controls who received no such advice. Repeat assessments of the children's and mothers' sleep were made by parental report as well as actometry. Objective changes in the children's sleep quality and quantity were not seen after treatment. However, mothers in the treatment group reported improvements in the children's sleep problems and had an increased sleeping time themselves following treatment. The results indicate that sleep problems can be successfully treated in this group of children, although the mechanisms of treatment may not be as direct as supposed. This has implications for understanding of sleep problems in children with learning disabilities and also for clinical practice, when considering ways of offering help to these highly 'challenged' families.

Analysis of Variance↗
PubMed2001

Association between polysomnographic sleep measures and health-related quality of life in obstructive sleep apnea.

Many facets of health-related quality of life are diminished in obstructive sleep apnea (OSA) as they are in other chronic medical conditions. We speculated that impairment in health-related quality of life (HRQoL) might result from the fatigue and daytime somnolence associated with the sleep disorder, as an indirect result from the fragmentation of night-time sleep in OSA. Our hypothesis was that sleep fragmentation measures would correlate with poorer HRQoL measured by medical outcomes study (MOS) subscales. Thirty-nine patients with polysomnographically-confirmed OSA participated in this study. Pearson's correlations were performed with the following sleep architecture variables: wake after sleep onset, the total number of brief arousals, the number of respiratory-related arousals, the rate of respiratory events per hour, and total sleep time. To our surprise, although the total number of arousals was associated with health distress (r=-0.481, P < 0.005), it did not correlate with any other subscales indicating poorer physical and mental health. The relatively insensitive measure of total sleep time (TST) correlated in the expected direction with most subscales. However, after controlling for age and gender, respiratory disturbance indices (RDI) and/or number of arousals emerged as significantly associated with mobility, cognitive functioning, social functioning, energy and fatigue, and health distress. Our findings suggest that polysomnographic indicators of sleep quality and sleep continuity may be an important influence determining many aspects of HRQoL in OSA patients.

Adult↗
PubMed1999

Correlation between the circadian sleep propensity rhythm and hormonal rhythms under ultra-short sleep-wake cycle.

The aim of this study was to clarify effects of hormonal and temperature rhythms on circadian fluctuations of sleep propensity. Ten healthy females underwent 24-h sleep deprivation and entered the circadian sleep propensity assessment setting under the ultra-short sleep-wake schedule. During the experiment, sleep propensity rhythm, rectal temperature, and 24-h serum hormone profiles (melatonin, cortisol and thyroid-stimulating hormone) were investigated. The circadian sleep propensity rhythms had two apparent peaks (afternoon and nocturnal peaks) and a trough (nocturnal sleep gate). The timings of the nocturnal sleep gate and the nocturnal peak were correlated exclusively with temperature and melatonin rhythms (P < 0.05), while that of the afternoon peak was significantly correlated with habitual wake time and melatonin rhythm. These results indicate that the circadian sleep propensity rhythm is influenced not only by the circadian pacemaker, but also by sleep habit.

Adult↗
PubMed2001

Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance.

Patients with obstructive sleep apnoea (OSA) are reported to have an increased risk of road traffic accidents. This study examines the nature of the impairment during simulated steering in patients with OSA, compared to normal subjects following either sleep deprivation or alcohol ingestion. Twenty-six patients with OSA and 12 normal subjects, either deprived of one night's sleep or following alcohol ingestion [mean (SD) alcohol blood level 71.6 mg dl(-1) (19.6)], performed a simulated steering task for a total of 90 min. Performance was measured using the tendency to wander (SD), deterioration across the task, number of 'off-road' events and the reaction time to peripheral events. Control data for OSA, sleep deprivation and alcohol were obtained following treatment with nasal continuous positive airway pressure (nCPAP), after a normal night of sleep, and following no alcohol, respectively. Patients with untreated OSA, and sleep-deprived or alcohol-intoxicated normal subjects performed significantly less well, compared to their respective controls (P<0.01 for all tests), with untreated OSA lying between that of alcohol intoxication and sleep deprivation. Alcohol impaired steering error equally throughout the whole drive, whilst sleep deprivation caused progressive deterioration through the drive, but not initially. Untreated OSA was more like sleep deprivation than alcohol, although there was a wide spread of data. This suggests that the driving impairment in patients with OSA is more compatible with sleep deprivation or fragmentation as the cause, rather than abnormal cognitive or motor skills.

Adult↗
PubMed2006

Correlates of sleep-onset REM periods during the Multiple Sleep Latency Test in community adults.

The diagnosis of narcolepsy without documented cataplexy is based on the observation of two or more sleep-onset REM periods (SOREMPs) during the Multiple Sleep Latency Test (MSLT). We report on the prevalence and correlates of SOREMPs in the community-based Wisconsin Sleep Cohort Study. MSLTs were conducted following nocturnal polysomnography (NPSG) and daily sleep diaries in 289 males and 267 females (age 35-70, 97% Caucasians). Multiple SOREMPs were observed in 13.1% of males and 5.6% of females. An MSLT mean sleep latency < or =8 min and > or =2 SOREMPs (diagnostic of narcolepsy) was observed in 5.9% (males) and 1.1% (females), all without cataplexy. Because of significant sex interactions, analyses were stratified by sex. Increased prevalence of HLA-DQB1*0602, a marker of narcolepsy, was observed in males but not in females with > or =2 SOREMPs. Males with multiple SOREMPs compared with those with no SOREMPs had shorter rapid eye movement (REM) latency during NPSG, were sleepier on the MSLT and reported increased sleepiness, hypnagogic hallucinations and cataplexy-like symptoms, suggesting a narcolepsy-like phenotype. In males only, the occurrence of SOREMPs increased with shift work and some indirect markers of sleep restriction, such as shorter sleep a day before NPSG. SOREMPs were unrelated to age, body mass index, depression (Zung Scale), anxiety (State-Trait Anxiety Scale) and the number of apnea and hypopnea events per hour of sleep (AHI), but were associated with decreased mean lowest oxygen saturation in males. Finally, we found that both males and females with SOREMPs reported taking more antidepressants, but those were of the types known not to suppress REM sleep. These results suggest a high prevalence of narcolepsy without cataplexy, as defined by the International Classification of Sleep Disorders, and/or a large number of false-positives for the MSLT.

Adult↗