Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SLEEP”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1992

Sleep onset rapid-eye-movement episodes in narcolepsy: REM sleep pressure or nonREM-REM sleep dysregulation?

Thirty-two narcoleptic subjects with excessive daytime sleepiness and cataplexy were recorded for 33 continuous hours. The continuous polysomnographic recording (CPSG) was followed by a standard MSLT at 2-h intervals. There were 64 sleep onset REM episodes (SOREMs) vs 64 sleep onset nonREM episodes (SONREMs) during the CPSG, and 102 SOREMs vs 50 SONREMS during the MSLT. Both sleep onset types peaked at 13-15 h during the CPSG while sleep onsets were evenly distributed during the MSLT. In the latter procedure, the mean sleep latency was significantly shorter with SOREMs occurrence than with SONREMs occurrence. Two factors were extracted in each procedure by means of a Varimax Rotated Factor Analysis. During the CPSG, SOREMs were related to the preceding nocturnal sleep parameters in the first factor, and to the daytime total sleep time and the total number of sleep onsets in the second factor. During the MSLT, SOREMs were related only to the mean sleep latency and the total number of sleep onsets. It was concluded that the occurrence of SOREMs is primarily due to the residual somnolence in narcoleptic subjects. However, their occurrence during the MSLT is largely independent of the prior history of sleep and waking. Thus, we propose a nonREM-REM sleep dysregulation hypothesis to account for the appearance of SOREMs in narcolepsy.

Journal Article↗
PubMed1987

Sleep onset REM periods observed after sleep interruption in normal short and normal long sleeping subjects.

Among about 1000 male college students, 6 short and 5 long sleepers were finally selected on the basis of their responses to a sleep habit questionnaire. The subjects slept in the laboratory for 6 consecutive nights. On nights 4, 5 and 6, deliberate sleep interruption was performed during the second sleep cycle. During interruption, subjects were asked to perform 3 different kinds of tasks on each of the 3 nights. Stage REM latencies after interruption were distributed bimodally with peaks at sleep onset after the interruption (sleep onset REM period: SOREMP) and 50-60 min later (non-SOREMP). SOREMPs were observed only in the sleep of short sleepers. Short sleepers showed a shorter sleep latency and a greater amount of stage REM in the 2nd and the 3rd sleep cycle of their baseline sleep record than did long sleepers. These characteristics of short sleepers' sleep and sleep interruptions probably affected the occurrence of SOREMPs. The mean duration of SOREMPs was significantly shorter than that of non-SOREMPs.

Adolescent↗
PubMed2000

Effects of sleep deprivation on sleep and sleep EEG in three mouse strains: empirical data and simulations.

Gene targeted mice can be used as models to investigate the mechanisms underlying sleep regulation. Three commonly used background strains for gene targeting (129/Ola, 129/SvJ and C57BL/6J) were subjected to 4-h and 6-h sleep deprivation (SD), and their sleep and sleep EEG were continuously recorded. The two-process model of sleep regulation has predicted the time course of slow-wave activity (SWA) in nonREM sleep after several sleep-wake manipulations in humans and the rat [3] [9]. We tested the capacity of the model to predict SWA in nonREM sleep on the basis of the temporal organization of sleep in mice. The strains differed in the amount and distribution of sleep and the time course of SWA. After spontaneous waking episodes of 10-30 min as well as after SD, SWA was invariably increased. Simulations of the time course of SWA were successful for 129/SvJ and C57BL/6J, but were not satisfactory for 129/Ola. Since the time constants are assumed to reflect the dynamics of the physiological processes involved in sleep regulation, the results provide a basis for the use of gene targeted mice to investigate the underlying mechanisms.

Animals↗
PubMed1979

Effects of sleep deprivation on sleepiness, sleep intensity, and subsequent sleep in the rat.

The effects of 24 hr of sleep deprivation on cortical EEG and ventral hippocampus EEG recordings, ventral hippocampus spike rates, sleep stages percentages, and bout length measures were studied in rats. Two groups, differing only in the rate and distance they were forced to walk during deprivation by the water wheel method, were recorded continuously (23 hr per day) for one baseline, one deprivation, and two recovery days. During deprivation, microsleeps, increased hippocampal spike rates, and increased amplitude of the EEG recordings all suggested the intrusion of sleep processes. Nonetheless, there was no evidence to support the idea that these animals were not substantially deprived of sleep. No important differences were found in the recovery data of the two groups, even though one group walked three times as far as the other during deprivation. This supports the idea that, in conjunction with large amounts of sleep deprivation, changes in exercise and energy depletion may have little effect on sleep measures. During recovery, increased hippocampal spike rates and bout lengths, as well as increases in EEG amplitude, were interpreted in terms of increased sleep "intensity." High amplitude NREM sleep rebounded first, followed by rebounds in both paradoxical sleep and low amplitude NREM sleep. This pattern was compared to patterns previously reported for humans, cats, and rats. Finally, the tendency for some measures to fall below their baseline levels after an initial rebound was discussed in terms of "sleep inhibition" and servomechanism theory.

Animals↗
PubMed2005

Partial REM-sleep deprivation increases the dream-like quality of mentation from REM sleep and sleep onset.

STUDY OBJECTIVES: Sleep onset (SO) is cognitively and physiologically similar to rapid eye movement (REM) sleep, supporting the notion that REM sleep-related processes are 'covertly' active at this time. The objective was to determine if SO mentation is sensitive to REM sleep deprivation. DESIGN: Two-group cross-sectional design; sleep recordings for 3 nights. SETTING: Standard sleep laboratory with 24-channel polysomnography recording. PARTICIPANTS: Fourteen female, 13 male healthy volunteers (18-41 yrs, mean=24.8 +/- 6.07). INTERVENTIONS: On Night 2, half were and half were not partially REM sleep-deprived (REMD), recalled REM mentation, and rated it for dream-like quality (DLQ), sleepiness, and sensory attributes. On Night 3, all were awakened from SO substages 4 and 5 for mentation reports and further ratings. REMD measures were derived from scored sleep tracings. MEASUREMENTS AND RESULTS: REMD produced increases in DLQ for both REM and SO reports (P < .05); DLQ scores were higher for REM than for SO mentation (P < .001). Covarying sleepiness preserved the (REMD) effect but abolished the REM/SO difference. Whereas 2 sensory attributes (presence of self, visual intensity) tended to distinguish the REM-mentation reports of REMD and control subjects, only 1, self-movement, distinguished their SO mentation reports (P < .06). Multiple regression revealed that increased DLQ of both REM and SO mentation was associated with increased sleepiness and decreased REM sleep time on Night 2. CONCLUSIONS: SO mentation responds to REMD much like REM mentation does, a finding consistent with other work supporting the notion of covert REM-sleep processes at SO. DLQ may be mediated by both increases in REM-sleep propensity and a circadian process indexed by sleepiness ratings.

Adolescent↗
PubMedDate not supplied

[Electrophysiological recording of nocturnal sleep and the multiple sleep latency test in obstructive sleep apnea syndrome].

Polysomnographic studies were performed in 6 patients with obstructive sleep apnoea syndrome (OSA). The sleep study consisted of: electroencephalography, electromyography, electrooculography, electrocardiography, pulse oximetry and observation of respiration. During day multiple sleep latency tests were performed. In all patients fragmentation of sleep with prevalent stages 1. and 2. of NREM and occasionally deep sleep and REM phase were observed. Concomitantly with the appearance of electrophysiologic sleep stages the muscle tone decreased and episodes of obstructive apnoea occurred. The periods of sleep and apnoea alternated with wakefulness and breathing. In MSLF the mean latency was 3 +/- 2 min. In OSA syndrome episodes of obstructive sleep apnoea cause sleep fragmentation and prevalence of light sleep stages. Excessive daytime somnolence observed in this syndrome is caused by sleep disturbances. MSLT demonstrated pathologic hypersomnolence in OSA syndrome.

Adult↗
PubMed2003

Sleep and chronic pain: challenges to the alpha-EEG sleep pattern as a pain specific sleep anomaly.

OBJECTIVE: The alpha-EEG sleep anomaly has been associated with chronic benign pain syndromes. Although controversial, the anomaly is believed by some to be an important biologic correlate of certain otherwise poorly explained painful conditions (e.g., fibromyalgia and chronic fatigue syndrome). To shed further light on this phenomenon, this study compared the sleep and psychological characteristics of chronic pain patients who exhibited the alpha-EEG sleep anomaly with pain-free psychiatric and medical patients who also were found to exhibit the alpha-EEG anomaly. METHODS: The alpha-EEG sleep was identified in the polysomnographic records of 5% of over 1000 consecutive sleep patients. Objective sleep parameters, daytime sleepiness and psychological characteristics (Minnesota Multiphasic Personality Inventory [MMPI] scores) of patients exhibiting this anomaly were examined. RESULTS: The alpha-EEG anomaly was identified in only 5% of the total patient sample. Patients with the alpha-EEG anomaly could be further classified into three diagnostic subgroups: chronic pain, psychiatric and other medical/sleep disorders, The subgroups were compared on sleep parameters and psychological characteristics. Less than 40% of the patients exhibiting the alpha-EEG anomaly experienced chronic pain. Chronic pain patients evidenced disturbed sleep patterns and psychological characteristics that were for the most part similar to those observed in some pain-free medical and psychiatric patients. Only the medical subgroup exhibited objective daytime sleepiness. The alpha-EEG sleep disturbance was not accounted for by psychological characteristics. CONCLUSIONS: These findings challenge the notion that alpha-EEG sleep is of direct etiological significance in producing the pain complaint among patients with chronic pain since the alpha-EEG sleep was not a sufficient condition for pain.

Adolescent↗
PubMed1997

Sleep quality versus sleep quantity: relationships between sleep and measures of health, well-being and sleepiness in college students.

Two studies assessed whether measures of health, well-being, and sleepiness are better related to sleep quality or sleep quantity. In both studies, subjects completed a 7-day sleep log followed by a battery of surveys pertaining to health, well-being, and sleepiness. In subjects sleeping an average of 7 hours a night, average sleep quality was better related to health, affect balance, satisfaction with life, and feelings of tension, depression, anger, fatigue, and confusion than average sleep quantity. In addition, average sleep quality was better related to sleepiness than sleep quantity. These results indicate that health care professionals should focus on sleep quality in addition to sleep quantity in their efforts to understand the role of sleep in daily life.

Adaptation, Psychological↗
PubMed1985

Sleep apnea disorders. Introduction to sleep and sleep disorders.

This overview of normal and disordered sleep introduces techniques for recording and classifying sleep stages, physiological and temporal characteristics of sleep, age-related changes in sleep, consequences of sleep deprivation, theories on the function of sleep, and neurophysiological and biochemical mechanisms regulating sleep. Various categories of sleep disorders are briefly surveyed, with special emphasis on differential diagnosis of sleep apnea syndromes and other disorders characterized by symptoms of excessive daytime somnolence.

Adolescent↗
PubMed2002

Relationship of sleep hygiene awareness, sleep hygiene practices, and sleep quality in university students.

College students are known for their variable sleep schedules. Such schedules, along with other common student practices (e.g., alcohol and caffeine consumption), are associated with poor sleep hygiene. Researchers have demonstrated in clinical populations that improving sleep hygiene knowledge and practices is an effective treatment for insomnia. However, researchers who have examined relationships between sleep hygiene and practices in nonclinical samples and overall sleep quality have produced inconsistent findings, perhaps because of questionable measures. In this study, the authors used psychometrically sound instruments to examine these variables and to counter the shortcomings in previous investigations. Their findings suggest that knowledge of sleep hygiene is related to sleep practices, which, in turn, is related to overall sleep quality. The data from their regression modeling indicated that variable sleep schedules, going to bed thirsty, environmental noise, and worrying while falling asleep contribute to poor sleep quality.

Adult↗
PubMed1987

Sleep EEG with or without sleep deprivation? Does sleep deprivation activate more epileptic activity in patients suffering from different types of epilepsy?

A sleep EEG of 190 patients without sleep deprivation was recorded, followed by a sleep EEG after 24 h of sleep deprivation on the next day. The patients suffered from various types of epilepsy, in their routine EEGs no epileptic discharges were seen. Both sleep EEGs were recorded under the same antiepileptic drugs. A waking EEG was recorded immediately before each sleep EEG. The activation rates of epileptic activity in 52.6% (without sleep deprivation) and 53.2% (with sleep deprivation) of the patients showed no significant differences. Also on classifying the epileptic discharges no real difference was found between the 2 methods (generalized: 29.5 vs. 29.5%, generalized with lateral emphasis: 11.1 vs. 9.5%, focal: 12.1 vs. 14.2%). Only in the waking EEG, recorded immediately before the sleep EEG after sleep deprivation, a few more patients showed epileptic discharges (33.6 vs. 27.4%). Without there being any significant differences between the 2 methods there were some different results in comparing the EEG with the clinical findings: significantly more epileptic activity was shown in patients who had their first seizure before the age of 20 (55.6 and 55.6% vs. 26.3 and 31.6%), amongst females (59.8 and 61.9% vs. 45.2 and 44.1%), in awakening grand mal (= primary generalized tonic-clonic seizures, 76.5 and 70%) and in absences (69 and 72.4%). The higher activation rates in young subjects, in patients with a family history of seizures, with pathological neurological findings, mental retardation and delayed psychomotoric development in early childhood, were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Time-course of sleep inertia upon awakening from nighttime sleep with different sleep homeostasis conditions.

BACKGROUND: We assessed the time-course of sleep inertia during the first 75 min after morning awakening from regular nocturnal sleep, as well as from nighttime sleep episodes with altered sleep homeostasis conditions. METHODS: Ten normal males slept for 6 nights in the laboratory: 1 adaptation (AD), 2 baseline (BSL, BSL-A), 2 selective Slow-Wave Sleep (SWS) deprivation (DEP-1, DEP-2), and 1 recovery night (REC). On morning awakening, performance was assessed by means of: a) Descending Subtraction Task (DST); b) Auditory Reaction Time task (ART); and c) Finger Tapping Task (FTT). The test battery, lasting about 13 min, was repeated for 5 times. RESULTS: In regard to DST, the Correct Response ratio (CR/NR) showed a great increase of sleep inertia on the first testing session of REC. Regarding sleep inertia time-course, a significant linear decrease across the testing sessions during the BSL-A and the DEP-2 was present, whereas a significant quadratic trend during the AD, the DEP-1 and the REC was found. On the other hand, ART performance showed a significant quadratic trend across testing sessions, while FTT performance did not show any significant variation. CONCLUSIONS: A uniform pattern of variation of time-course of sleep inertia as a function of the different sleep homeostasis conditions was not recognized. Performance accuracy (CR/NR) on the DST showed the hypothesized increasing linear trend across testing sessions only during 2 out of 6 nights, while the unexpected quadratic trend of ART performance is probably due to a fatigue effect. During sleep inertia, cognitive performance reached the baseline level about 30 min after awakening, while motor performance was still below the baseline levels 75 min after awakening. The finding that cognitive performance recovery is greater and more rapid than motor performance recovery could be very important for operational settings and in sustained operations.

Adult↗
PubMed1996

The diurnal distribution of sleep propensity: experimental data about the interaction of the propensities for slow-wave sleep and REM sleep.

The aim of the present study was to assess the diurnal variation of sleep propensity by evaluating the temporal distribution of sleep onset latency (SOL) and REM- and slow-wave sleep (SWS) parameters in systematically scheduled daytime naps for 12 young males. To reduce the effect of prior SWS on subsequent REM sleep, a double-nap technique was used, i.e. two adjacent naps A and B, which were separated by a 10-min break. Nap duration was adjusted in such a way that nap A allowed 30 min of sleep and nap B one complete NREM-REM cycle. EEG slow wave activity (SWA, power density from 0.5-4 Hz) was estimated from nap A and REM sleep parameters from nap B. The time span between 08.00 hours and 24.00 hours was covered by nine double-naps at 2 h intervals. The order of the nap sessions was systematically varied within and across subjects. For each subject, the time between successive double-nap recordings was at least three days. SOL was shortest in the time interval 12.00 hours to 16.00 hours and significantly longer between 20.00 hours and 24.00 hours. REM sleep duration and the percentage of sleep onset REM episodes decreased continuously from 08.00 hours to the interval 18.00-20.00 hours and increased thereafter, with a time course inversely related to the one of body temperature, which was also measured continuously. SWA showed a steady, threefold increase from 08.00 hours to 24.00 hours. The study offers new data on the diurnal variation of sleep propensity which seems to be a composite function of the drives for SWS and REM sleep.

Adult↗
PubMed2003

Where should infants sleep? A comparison of risk for suffocation of infants sleeping in cribs, adult beds, and other sleeping locations.

OBJECTIVES: To ascertain whether the number of sudden infant deaths as a result of suffocation in cribs, in adult beds, on sofas or chairs, and on other sleep surfaces was increasing whether attributable to increased reporting, diagnostic shift, or an actual increase in suffocation deaths and to compare the risk of reported accidental suffocation for infants on sleep surfaces designed for infants with the risk on adult beds. METHODS: We reviewed all accidental suffocation deaths among infants < or =11 months of age reported to the United States Consumer Product Safety Commission from 1980 through 1983 and 1995 through 1998. We compared infants' ages and other demographic data, the sleep location and surface used, and the reported mechanism or pattern of death. For 1995-1998, we used data on sleep location from an annual survey of randomly selected households of living infants younger than 8 months, collected as part of the National Infant Sleep Position Study at the National Institute of Child Health and Human Development, to calculate risk for death as a result of suffocation in cribs, in adult beds, and on sofas or chairs. METHODS: The number of reported suffocation deaths by location were compared between the 1980s and 1990s using logistic regression modeling to calculate odds ratios (OR), 95% confidence intervals (CI), and P values. Comparative risks for suffocation deaths on a given sleep surface for infants in the 1990s were examined by calculating rates of death per 100 000 exposed infants and comparing the 95% CI for overlap. RESULTS: From the 1980s, 513 cases of infant suffocation were considered; from the 1990s, 883 cases. The number of reported suffocation deaths in cribs fell from 192 to 107, the number of reported deaths in adult beds increased from 152 to 391, and the number of reported deaths on sofas or chairs increased from 33 to 110. Using cribs as the reference group and adjusting for potential confounders, the multivariate ORs showed that infant deaths in adult beds were 8.1 times more likely to be reported in the 1990s than in the 1980s (95% CI: 3.2-20.3), and infant deaths on sofas and chairs were 17.2 times more likely to be reported in the 1990s than in the 1980s (95% CI: 5.0-59.3). The sleep location of a subset of cases from the 1990s, 348 infants younger than 8 months at death, was compared with the sleep location of 4220 living infants younger than 8 months. The risk of suffocation was approximately 40 times higher for infants in adult beds compared with those in cribs. The increase in risk remained high even when overlying deaths were discounted (32 times higher) or the estimate of rates of bedsharing among living infants doubled (20 times higher). CONCLUSIONS: Reported deaths of infants who suffocated on sleep surfaces other than those designed for infants are increasing. The most conservative estimate showed that the risk of suffocation increased by 20-fold when infants were placed to sleep in adult beds rather than in cribs. The public should be clearly informed of the attendant risks.

Accidents↗
PubMed2006

The contribution of intermittent hypoxia, sleep debt and sleep disruption to daytime performance deficits in children: consideration of respiratory and non-respiratory sleep disorders.

In children, the most abundant available information regarding the effects of paediatric sleep disturbance on daytime function has been obtained by studying children with sleep disordered breathing (SDB). The purported underlying pathophysiological mechanisms responsible for these deficits include hypoxia secondary to obstructive apneas/hypopneas and/or disrupted sleep architecture from frequent arousals during sleep. This review will present evidence that, while hypoxia is likely to play a role for many children with SDB, sleep disruption is an important and often overlooked factor that can contribute to daytime deficits in children with SDB. Indeed, sleep deprivation and disruption appear to have a potent impact on the daytime functioning of the much larger number of children with non-respiratory sleep disorders. It is concluded that sleep deprivation, sleep disruption, and intermittent hypoxia independently may be sufficient to cause daytime effects in vulnerable children, and the combination of two or more of these factors can result in particularly impaired daytime functioning. These conclusions have significant implications for research and clinical practice.

Brain↗
PubMed1996

The transition from slow-wave sleep to paradoxical sleep: evolving facts and concepts of the neurophysiological processes underlying the intermediate stage of sleep.

Paradoxical sleep in rats, cats and mice is usually preceded and sometimes followed by a short-lasting (a few seconds) electroencephalogram (EEG) stage characterized by high-amplitude spindles in the anterior cortex and low-frequency theta rhythm in the dorsal hippocampus. The former is an index of advanced slow-wave sleep; the latter is an index of limbic activation since it occurs during active waking and paradoxical sleep. Barbiturates and benzodiazepines extend this intermediate stage at the expense of paradoxical sleep while concomitantly barbiturates suppress the pontine reticular activation characteristic of this sleep stage. During the intermediate stage, thalamocortical responsiveness and thalamic transmission level, which are controlled by brain stem activating influences, are the lowest of all sleep-waking stages. The unusual EEG pattern of this stage is otherwise only observed in the acute intercollicular-transected preparation. Therefore, forebrain structures may be functionally briefly disconnected from the brain-stem during this short-lasting stage, which could possibly account for the mental content of a similar sleep period in humans. In spite of strong evidence in favour of this forebrain deafferentiation hypothesis, other data indicate that the IS is in some way linked either to slow-wave sleep or to paradoxical sleep.

Animals↗
PubMed1997

The effects of REM sleep-inhibiting drugs in neonatal rats: evidence for a distinction between neonatal active sleep and REM sleep.

Neonatal active sleep (AS) has been considered to be homologous and continuous with rapid-eye-movement (REM) sleep in adult animals. We have recently proposed an alternative view that AS is an undifferentiated sleep state distinct from REM sleep. To test these opposing views on the relationship of AS and REM sleep, neonatal rats (P11, P14 and P20) were systemically injected with compounds that inhibit REM sleep in adults. Zimelidine (ZMI) and desipramine (DMI) are monoamine uptake inhibitors which increase synaptic concentrations of serotonin and norepinephrine, respectively. Serotonin and norepinephrine inhibit brainstem cholinergic neurons important in REM sleep generation. Atropine (ATR) is a muscarinic receptor antagonist that blocks the post-synaptic effects of cholinergic projections. Only DMI (5 mg/kg) suppressed AS at P11. ZMI (6 mg/kg) and ATR (6 mg/kg) did not suppress AS until P14. These data suggest that serotonergic and cholinergic regulation of AS are absent before P14. The fact that AS in P11 rats is not affected by cholinergic antagonists supports the hypothesis that AS and REM sleep represent different sleep states.

Adrenergic Uptake Inhibitors↗
PubMed1999

Prolonged effects of 24-h total sleep deprivation on sleep and sleep EEG in the rat.

Long-term effects of 24-h sleep deprivation (SD) on sleep and sleep EEG were analyzed in male rats during 4 recovery days (Rec). An increase of total sleep time and non-rapid eye-movement (NREM) sleep was present during Rec 1-4, and of REM sleep in Rec 1 and in the dark periods of Rec 2 and 3. After the initial increase of slow-wave activity (SWA, mean EEG power density in the 0.75-4.0 Hz range) in NREM sleep, SWA declined below baseline until Rec 3. Sleep continuity was increased in Rec 1. The persistent effects of SD which are probably due to homeostatic and circadian facets of sleep regulation, must be taken into account in the design of SD studies.

Animals↗