Showing papers on "Slow-wave sleep published in 2000"

Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men.

Abstract: ContextIn young adults, sleep affects the regulation of growth hormone (GH) and cortisol The relationship between decreased sleep quality in older adults and age-related changes in the regulation of GH and cortisol is unknownObjectiveTo determine the chronology of age-related changes in sleep duration and quality (sleep stages) in healthy men and whether concomitant alterations occur in GH and cortisol levelsDesign and SettingData combined from a series of studies conducted between 1985 and 1999 at 4 laboratoriesSubjectsA total of 149 healthy men, aged 16 to 83 years, with a mean (SD) body mass index of 241 (23) kg/m2, without sleep complaints or histories of endocrine, psychiatric, or sleep disordersMain Outcome MeasuresTwenty-four–hour profiles of plasma GH and cortisol levels and polygraphic sleep recordingsResultsThe mean (SEM) percentage of deep slow wave sleep decreased from 189% (13%) during early adulthood (age 16-25 years) to 34% (10%) during midlife (age 36-50 years) and was replaced by lighter sleep (stages 1 and 2) without significant increases in sleep fragmentation or decreases in rapid eye movement (REM) sleep The transition from midlife to late life (age 71-83 years) involved no further significant decrease in slow wave sleep but an increase in time awake of 28 minutes per decade at the expense of decreases in both light non-REM sleep (−24 minutes per decade; P<001) and REM sleep (−10 minutes per decade; P<001) The decline in slow wave sleep from early adulthood to midlife was paralleled by a major decline in GH secretion (−372 µg per decade; P<001) From midlife to late life, GH secretion further declined at a slower rate (−43 µg per decade; P<02) Independently of age, the amount of GH secretion was significantly associated with slow wave sleep (P<001) Increasing age was associated with an elevation of evening cortisol levels (+193 nmol/L per decade; P<001) that became significant only after age 50 years, when sleep became more fragmented and REM sleep declined A trend for an association between lower amounts of REM sleep and higher evening cortisol concentrations independent of age was detected (P<10)ConclusionsIn men, age-related changes in slow wave sleep and REM sleep occur with markedly different chronologies and are each associated with specific hormonal alterations Future studies should evaluate whether strategies to enhance sleep quality may have beneficial hormonal effects

Analysis of a sleep-dependent neuronal feedback loop: the slow-wave microcontinuity of the EEG

Abstract: Increasing depth of sleep corresponds to an increasing gain in the neuronal feedback loops that generate the low-frequency (slow-wave) electroencephalogram (EEG). The authors derived the maximum-likelihood estimator of the feedback gain and applied it to quantify sleep depth. The estimator computes the fraction (0%-100%) of the current slow wave which continues in the near future (0.02 s later) EEG. Therefore, this percentage was dubbed slow-wave microconfinuity (SW%). It is not affected by anatomical parameters such as skull thickness, which can considerably bias the commonly used slow-wave power (SWP). In the authors' study, both of the estimators SW% and SWP were monitored throughout two nights in 22 subjects. Each subject took temazepam (a benzodiazepine) on one of the two nights, Both estimators detected the effects of age, temazepam, and time of night on sleep. Females were found to have twice the SWP of males, but no gender effect on SW% was found. This confirms earlier reports that gender affects SWP but not sleep depth. Subjectively assessed differences in sleep quality between the nights were correlated to differences in SW%, not in SWP. These results demonstrate that slow-wave microcontinuity, being based on a physiological model of sleep, reflects sleep depth more closely than SWP does.

Visual Discrimination Task Improvement: A Multi-Step Process Occurring During Sleep

Abstract: Performance on a visual discrimination task shows long-term improvement after a single training session. When tested within 24 hr of training, improvement was not observed unless subjects obtained at least 6 hr of post-training sleep prior to retesting, in which case improvement was proportional to the amount of sleep in excess of 6 hr. For subjects averaging 8 hr of sleep, overnight improvement was proportional to the amount of slow wave sleep (SWS) in the first quarter of the night, as well as the amount of rapid eye movement sleep (REM) in the last quarter. REM during the intervening 4 hr did not appear to contribute to improvement. A two-step process, modeling throughput as the product of the amount of early SWS and late REM, accounts for 80 percent of intersubject variance. These results suggest that, in the case of this visual discrimination task, both SWS and REM are required to consolidate experience-dependent neuronal changes into a form that supports improved task performance.

Correlated and uncorrelated regions in heart-rate fluctuations during sleep.

Abstract: Healthy sleep consists of several stages: deep sleep, light sleep, and rapid eye movement (REM) sleep. Here we show that these sleep stages can be characterized and distinguished by correlations of heart rates separated by $n$ beats. Using the detrended fluctuation analysis (DFA) up to fourth order we find that long-range correlations reminiscent to the wake phase are present only in the REM phase. In the non-REM phases, the heart rates are uncorrelated above the typical breathing cycle time, pointing to a random regulation of the heartbeat during non-REM sleep.

Hallucinations, REM sleep, and Parkinson's disease: a medical hypothesis.

Abstract: Background: Patients with PD can have disabling visual hallucinations associated with dopaminergic therapy. Sleep disorders, including vivid dreams and REM sleep with motor behaviors (RBD), are frequent in these patients. Methods: The association of hallucinations and REM sleep both at night and during the day was examined in 10 consecutive nondemented patients with long-standing levodopa-responsive PD and hallucinations. Seven patients presented with paranoia and paranoid delusions. Overnight sleep recordings and standard multiple daytime sleep latency test were performed. The results were compared to those of 10 similar patients with PD not experiencing hallucinations. Results: RBD was detected in all 10 patients with hallucinations and in six without. Although nighttime sleep conditions were similar in both groups, hallucinators tended to be sleepier during the day. Delusions following nighttime REM period and daytime REM onsets were observed in three and eight of the hallucinators, and zero and two of the others. Daytime hallucinations, coincident with REM sleep intrusions during periods of wakefulness, were reported only by hallucinators. Postmortem examination of the brain of one patient showed numerous Lewy bodies in neurons of the subcoeruleus nucleus, a region that is involved in REM sleep control. Conclusion: The visual hallucinations that coincide with daytime episodes of REM sleep in patients who also experience post-REM delusions at night may be dream imagery. Psychosis in patients with PD may therefore reflect a narcolepsy-like REM sleep disorder.

Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans.

Abstract: The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1-2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep. Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.

The novel brain neuropeptide, orexin-A, modulates the sleep-wake cycle of rats.

Abstract: Orexin-A is a novel neuropeptide initially isolated from hypothalamic extracts but now known to be present in fibres distributed throughout the rat CNS including many regions associated with sleep–wake regulation. The recognition of a particularly dense innervation of orexinergic nerves in the locus coeruleus, together with the observed increase in firing rate of locus coeruleus neurons following application of orexin-A in vitro, further highlighted a potential involvement of the peptide in modulating the arousal state. The present study was undertaken to determine the effects of intracerebroventricularly (ICV) administered orexin-A on the sleep–wake cycle of conscious rats using electroencephalographic and electromyographic recordings. When administered at the onset of the normal sleep period, orexin-A (1, 10 or 30 μg/rat ICV) produced a dose-dependent increase in the time rats spent awake during the second and third hours after dosing. The enhancement of arousal was accompanied by a marked reduction in paradoxical sleep and deep slow wave sleep at the highest dose. The latency to the first occurrence of paradoxical sleep was also prolonged. This overall profile of increased arousal and decreased paradoxical sleep is consistent with a high rate of firing of locus coeruleus neurons as would be expected to occur following ICV administration of orexin-A. It is concluded that orexin-A may play an important physiological role in regulating the sleep–wake state, a hypothesis considerably strengthened by the recently reported narcoleptic phenotype of prepro-orexin (the precursor for orexin-A) knockout mice.

Sleep architecture and respiratory disturbances in children with obstructive sleep apnea.

Abstract: Little is known regarding sleep architecture in children with the obstructive sleep apnea syndrome (OSAS). We hypothesized that sleep architecture was normal, and that apnea increased over the course of the night, in children with OSAS. We analyzed polysomnographic studies from 20 children with OSAS and 10 control subjects. Sleep architecture was similar between the groups. Of obstructive apneas 55% occurred during rapid eye movement (REM) sleep. The apnea index, apnea duration, and degree of desaturation were greater during REM than non-REM sleep. OSAS data from the first and third periods of the night (periods A and C) were compared. Both the overall and the REM apnea index increased between periods A and C (11 to 25/h, p < 0.02; and 24 to 51/h, p < 0.01, respectively). There was no difference in SaO2 over time. Spontaneous arousals, but not respiratory-related arousals, were more frequent during non-REM than REM sleep; these did not change from periods A to C. We conclude that children with OSAS have n...

Exposure to pulsed high-frequency electromagnetic field during waking affects human sleep EEG.

Abstract: The aim of the study was to investigate whether the electromagnetic field (EMF) emitted by digital radiotelephone handsets affects brain physiology. Healthy, young male subjects were exposed for 30 min to EMF (900 MHz; spatial peak specific absorption rate 1 W/kg) during the waking period preceding sleep. Compared with the control condition with sham exposure, spectral power of the EEG in non-rapid eye movement sleep was increased. The maximum rise occurred in the 9.75-11.25 Hz and 12.5-13.25 Hz band during the initial part of sleep. These changes correspond to those obtained in a previous study where EMF was intermittently applied during sleep. Unilateral exposure induced no hemispheric asymmetry of EEG power. The present results demonstrate that exposure during waking modifies the EEG during subsequent sleep. Thus the changes of brain function induced by pulsed high-frequency EMF outlast the exposure period.

Avoidance Task Training Potentiates Phasic Pontine-Wave Density in the Rat: A Mechanism for Sleep-Dependent Plasticity

Abstract: Behavioral studies of learning and memory in both humans and animals support a role for sleep in the consolidation and integration of memories. The present study explored possible physiological mechanisms of sleep-dependent behavioral plasticity by examining the relationship between learning and state-dependent phasic signs of rapid eye movement (REM) sleep. Cortical electroencephalogram, electromyogram, eye movement, hippocampal theta-wave, and pontine-wave (P-wave) measures were recorded simultaneously in freely moving rats after a session of conditioned avoidance learning or a control session. After learning trials, rats spent 25.5% more time in REM sleep and 180.6% more time in a transitional state between slow-wave sleep and REM sleep (tS-R) compared with that in control trials. Both REM sleep and tS-R behavioral states are characterized by the presence of P-waves. P-wave density was significantly greater in the first four episodes of REM sleep after the learning session compared with the control session. Furthermore, the P-wave density change between the first and third REM sleep episodes was proportional to the improvement of task performance between the initial training session and the post-sleep retest session. These findings show that the increase in P-wave density during the post-training REM sleep episodes is correlated with the effective consolidation and retention of avoidance task learning.

Daily social and physical activity increases slow-wave sleep and daytime neuropsychological performance in the elderly.

Abstract: Decreased levels of physical and social activity associated with aging can be particularly pronounced in residents of assisted living facilities. Reduced exposure to important behavioral and time-giving cues may contribute to the age-related changes in circadian rhythmicity and sleep. The present study was conducted to test the hypothesis that an enforced schedule of structured social and physical activity (0:900 to 10:30 and 19:00 to 20:30 daily for two weeks) can have beneficial effects on circadian rhythmicity, nocturnal sleep, daytime functioning, mood, and vigor. The subjects were 14 elderly residents of continued-care retirement facilities while a similar group of 9 elderly residents served as controls. The group exposed to structured activities had increased amounts of slow-wave sleep and demonstrated improvement in memory-oriented tasks following the intervention. Conversely, no significant changes were noted in the amplitude and phase of the body temperature rhythm or in subjective measures of vigor and mood. These results indicate that short-term exposure to structured social intervention and light physical activity can significantly improve memory performance and enhance slow-wave sleep in older adults without alterations to the circadian phase or amplitude of body temperature. This is the first report to demonstrate that low intensity activity in an elderly population can increase deep sleep and improve memory functioning. The high degree of interest in these activities paired with the simple nature of the tasks makes this a potentially practical intervention which can be adapted for both community dwelling and assisted-living elders.

The case against memory consolidation in REM sleep.

Abstract: We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40-85%) and sustained (30-50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.

Reduction of rapid eye movement sleep by diurnal and nocturnal seizures in temporal lobe epilepsy.

Abstract: Background: Patients with brief, complex partial seizures frequently suffer from tiredness and decreased productivity that continue well beyond the postictal period. A possible explanation is that seizures, even when occurring during the day, disrupt sleep the following night. Objective: To determine the effect of temporal lobe complex partial seizures on sleep structure and daytime drowsiness. Methods: Patients with temporal lobe epilepsy were admitted for video-electroencephalography monitoring. Allnight polysomnography was recorded under the following 3 conditions: seizure free, seizure during the day before the recording, and seizure during the recording. Percentage of time in each sleep stage, sleep efficiency, and time to first and second rapid eye movement (REM) period were compared for seizure vs control conditions. Daytime drowsiness was also measured, using a modified maintenance of wakefulness test and 2 subjective drowsiness tests. Results: Daytime seizures reduced REM from 18% ± 1% to 12% ± 2% (P = .003). Night seizures reduced REM from 16% ±1 % to 6.8% ±2 % ( P ,.001). Night seizures also significantly reduced stages 2 and 4 while increasing stage 1 sleep. Night seizures, but not day seizures, significantly reduced sleep efficiency, increased time to first REM period, and increased drowsiness as measured by the maintenance of wakefulness test. Conclusions: Temporal lobe complex partial seizures decrease REM sleep, particularly when occurring during sleep but also when occurring on the previous day. This may, in part, be responsible for the prolonged impairment of functioning that some patients report following seizures. Arch Neurol. 2000;57:363-368

Reported chronic insomnia is independent of poor sleep as measured by electroencephalography.

Abstract: OBJECTIVE Several behavioral, physiological, and subjective variables were examined in subjects reporting chronic insomnia (IN group) and subjects with no complaint of insomnia (NC group) to determine factors predictive of poor sleep as measured by electroencephalography (EEG sleep). METHODS A total of 177 subjects (121 in the IN group and 56 in the NC group) were evaluated on the basis of EEG sleep, subjective sleep, sleepiness, performance, mood, personality, and metabolic parameters during a 36-hour laboratory stay. RESULTS Equal percentages of subjects in each group had 0, 1, or 2 nights of poor EEG sleep, indicating that the IN group was not more likely to have impaired sleep in the laboratory. Results of the Minnesota Multiphasic Personality Inventory showed that subjects in the IN group had more pathological personality profiles, and results of laboratory studies showed that these subjects had worse mood ratings, less subjective sleepiness, poorer memory performance, and longer midafternoon sleep latencies. Subjects in the IN group also rated their laboratory sleep as poorer in quality with more time awake after sleep onset and longer sleep latencies, but no differences in EEG sleep were observed. Poor nights of EEG sleep were associated with being male, increasing age, and a history of more time awake after sleep onset; among the laboratory tests, poor EEG sleep was associated with worse mood ratings, poorer memory performance, longer sleep latencies (as indicated by higher scores on the Multiple Sleep Latency Test), higher sleep/wake ratios for metabolic parameters, lower ratings of sleep quality, and longer perceived sleep latencies. CONCLUSIONS A history of chronic insomnia does not predict poor EEG sleep. Both chronic insomnia and poor EEG sleep are associated independently with dysphoria, hyperarousal, diminished waking function, and negative subjective sleep quality. Separate arousal and sleep systems are posited to account for these results.

The spectrum of neuropsychiatric abnormalities associated with electrical status epilepticus in sleep.

Abstract: Electrical status epilepticus in sleep (ESES) is an electrographic pattern consisting of an almost continuous presence of spike-wave discharges in slow wave sleep. ESES is frequently encountered in pediatric syndromes associated with epilepsy or cognitive and language dysfunction. It can be present in various evolutionary stages of a spectrum of diseases, the prototypes of which are the 'continuous spikes and waves during slow wave sleep' syndrome (CSWS), the Landau-Kleffner syndrome (LKS), as well as in patients initially presenting as benign childhood epilepsy with centrotemporal spikes (BECTS). The purpose of this article is to review the literature data on the semiology, electrographic findings, prognosis, therapeutic options, as well as the current theories on the pathophysiology of these disorders. The frequent overlap of CSWS, LKS, and BECTS urges an increased level of awareness for the occasional transition from benign conditions such as BECTS to more devastating syndromes such as LKS and CSWS. Identification of atypical signs and symptoms, such as high discharge rates, prolonged duration of ESES, neuropsychiatric and cognitive dysfunction, lack of responsiveness to medications, and pre-existing neurologic conditions is of paramount importance in order to initiate the appropriate diagnostic measures. Prolonged and if needed repetitive sleep electroencephalographs (EEGs) are warranted for proper diagnosis.

Adaptation of the 24-h growth hormone profile to a state of sleep debt

Abstract: In normal men, the majority of GH secretion occurs in a single large postsleep onset pulse that is suppressed during total sleep deprivation. We examined the impact of semichronic partial sleep loss, a highly prevalent condition, on the 24-h growth hormone profile. Eleven young men were studied after six nights of restricted bedtimes (0100-0500) and after 7 nights of extended bedtimes (2100-0900). Slow-wave sleep (SWS) was estimated as the duration of stages III and IV. Slow-wave activity (SWA) was calculated as electroencephalogram power density in the 0.5- to 3-Hz frequency range. During the state of sleep debt, the GH secretory pattern was biphasic, with both a presleep onset "circadian" pulse and a postsleep onset pulse. Postsleep onset GH secretion was negatively related to presleep onset secretion and tended to be positively correlated with the amount of concomitant SWA. When sleep was restricted, both SWS and SWA were increased during early sleep. Unexpectedly, the increase in SWA affected the second, rather than the first, SWA cycle, suggesting that presleep onset GH secretion may have limited SWA in the first cycle, possibly via an inhibition of central GH-releasing hormone activity. Thus neither the GH profile nor the distribution of SWA conformed with predictions from acute sleep deprivation studies, indicating that adaptation mechanisms are operative during chronic partial sleep loss.

Sleep arousal response to experimental thermal stimulation during sleep in human subjects free of pain and sleep problems.

Abstract: Although the interaction between sleep and pain is generating considerable interest (NIH Technology Assessment Panel, 1996), it is still unknown if chronic pain is the cause or effect of poor sleep. To further this understanding, subjects free of pain and sleep problems need to be studied in order to assess their response to pain during sleep, defined as a behavioral and a physiological state in which sensory processing is altered. (For example, while auditory perception remains active, other sensory inputs are facilitated, attenuated, or suppressed (Velluti, 199746 degrees C) was statistically greater in the lighter sleep stage 2 (48.3%) than in the deeper stages 3&4 (27.9%). A nocifensive behavioral-motor response was associated with only 2.5% of the 351 heat pain stimuli. Two other markers of sleep quality-sleep stage shift and awakening-were not influenced by the thermal stimuli. None of the subjects demonstrated any burns in the morning following the thermal stimulations applied during sleep. We conclude that the processing of nociceptive inputs is attenuated across sleep stages.

Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.

Abstract: We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the ...

Circadian and homeostatic control of rapid eye movement (REM) sleep: promotion of REM tendency by the suprachiasmatic nucleus.

Abstract: The daily timing of rapid eye movement (REM) sleep reflects an interaction between the circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus (SCN) and a homeostatic process that induces compensatory REM sleep in response to REM sleep loss. Whether the circadian variation in REM sleep propensity is caused by active promotion, inhibition, or passive gating of REM sleep homeostasis by the SCN is unknown. To investigate these possibilities, compensatory responses to 24 hr REM sleep deprivation (RSD) were compared between SCN-lesioned (SCNx) and sham-lesioned rats at different times of day in constant dark. The attempts to enter REM sleep (REM tendency) increased during RSD in all rats and were modulated by circadian phase in sham-lesioned, but not SCNx rats. REM sleep homeostasis interacted with circadian time, such that REM tendency doubled during the rest phase in sham-lesioned rats relative to SCNx rats (F((6,93)) = 17.9; p = 0.0001). However, REM tendency was indistinguishable between SCNx and sham-lesioned rats during the activity phase, suggesting the SCN does not inhibit REM tendency at this time. By contrast, the amount of compensatory REM sleep examined 2, 6, 12, or 24 hr after RSD did not depend on circadian phase. Thus, transitions into REM sleep are facilitated by the SCN during the rest phase, but the amount of REM sleep, once initiated, is determined primarily by homeostatic mechanisms. This work supports a role for the SCN in the active promotion of REM sleep at specific times of day.