Showing papers on "Non-rapid eye movement sleep published in 1999"

Comparison between subjective and actigraphic measurement of sleep and sleep rhythms

Abstract: Sleep is often assessed in circadian rhythm studies and long-term monitoring is required to detect any changes in sleep over time. The present study aims to investigate the ability of the two most commonly employed methods, actigraphy and sleep logs, to identify circadian sleep/wake disorders and measure changes in sleep patterns over time. In addition, the study assesses whether sleep measured by both methods shows the same relationship with an established circadian phase marker, urinary 6-sulphatoxymelatonin. A total of 49 registered blind subjects with different types of circadian rhythms were studied daily for at least four weeks. Grouped analysis of all study days for all subjects was performed for all sleep parameters (1062-1150 days data per sleep parameter). Good correlations were observed when comparing the measurement of sleep timing and duration (sleep onset, sleep offset, night sleep duration, day-time nap duration). However, the methods were poorly correlated in their assessment of transitions between sleep and wake states (sleep latency, number and duration of night awakenings, number of day-time naps). There were also large and inconsistent differences in the measurement of the absolute sleep parameters. Overall, actigraphs recorded a shorter sleep latency, advanced onset time, increased number and duration of night awakenings, delayed offset, increased night sleep duration and increased number and duration of naps compared with the subjective sleep logs. Despite this, there was good agreement between the methods for measuring changes in sleep patterns over time. In particular, the methods agreed when assessing changes in sleep in relation to a circadian phase marker (the 6-sulphatoxymelatonin (aMT6s) rhythm) in both entrained (n = 30) and free-running (n = 4) subjects.

Ageing and the circadian and homeostatic regulation of human sleep during forced desynchrony of rest, melatonin and temperature rhythms

Abstract: 1. The circadian timing system has been implicated in age-related changes in sleep structure, timing and consolidation in humans. 2. We investigated the circadian regulation of sleep in 13 older men and women and 11 young men by forced desynchrony of polysomnographically recorded sleep episodes (total, 482; 9 h 20 min each) and the circadian rhythms of plasma melatonin and core body temperature. 3. Stage 4 sleep was reduced in older people. Overall levels of rapid eye movement (REM) sleep were not significantly affected by age. The latencies to REM sleep were shorter in older people when sleep coincided with the melatonin rhythm. REM sleep was increased in the first quarter of the sleep episode and the increase of REM sleep in the course of sleep was diminished in older people. 4. Sleep propensity co-varied with the circadian rhythms of body temperature and plasma melatonin in both age groups. Sleep latencies were longest just before the onset of melatonin secretion and short sleep latencies were observed close to the temperature nadir. In older people sleep latencies were longer close to the crest of the melatonin rhythm. 5. In older people sleep duration was reduced at all circadian phases and sleep consolidation deteriorated more rapidly during the course of sleep, especially when the second half of the sleep episode occurred after the crest of the melatonin rhythm. 6. The data demonstrate age-related decrements in sleep consolidation and increased susceptibility to circadian phase misalignment in older people. These changes, and the associated internal phase advance of the propensity to awaken from sleep, appear to be related to the interaction between a reduction in the homeostatic drive for sleep and a reduced strength of the circadian signal promoting sleep in the early morning.

Leptin prevents respiratory depression in obesity.

Abstract: Human obesity leads to an increase in respiratory demands. As obesity becomes more pronounced some individuals are unable to compensate, leading to elevated arterial carbon dioxide levels (PaCO2), alveolar hypoventilation, and increased cardiorespiratory morbidity and mortality (Pickwickian syndrome). The mechanisms that link obesity and hypoventilation are unknown, but thought to involve depression of central respiratory control mechanisms. Here we report that obese C57BL/6J-Lepob mice, which lack circulating leptin, also exhibit respiratory depression and elevated PaCO2 (> 10 mm Hg; p < 0. 0001). A role for leptin in restoring ventilation in these obese, mutant mice was investigated. Three days of leptin infusion (30 microg/d) markedly increased minute ventilation (V E) across all sleep/wake states, but particularly during rapid eye movement (REM) sleep when respiration was otherwise profoundly depressed. The effect of leptin was independent of food intake, weight, and CO2 production, indicating a reversal of hypoventilation by stimulation of central respiratory control centers. Furthermore, leptin replacement in mutant mice increased CO2 chemosensitivity during non-rapid eye movement (NREM) (4.0 +/- 0.5 to 5.6 +/- 0.4 ml/min/%CO2; p < 0.01) and REM (-0.1 +/- 0.5 to 3.0 +/- 0.8 ml/min/%CO2; p < 0.01) sleep. We also demonstrate in wild-type mice that ventilation is appropriately compensated when obesity is diet-induced and endogenous leptin levels are raised more than tenfold. These results suggest that leptin can prevent respiratory depression in obesity, but a deficiency in central nervous system (CNS) leptin levels or activity may induce hypoventilation and the Pickwickian syndrome in some obese subjects. O'Donnell CP, Schaub CD, Haines AS, Berkowitz DE, Tankersley CG, Schwartz AR, Smith PL. Leptin prevents respiratory depression in obesity.

Effects of early and late nocturnal sleep on priming and spatial memory

Abstract: A wordstem priming task (nondeclarative memory), and a mental spatial rotation task (declarative memory) were presented to subjects of an experimental "sleep" group (n = 11) and of a "wake" control group (n = 10). Repetition priming effects and recall of spatial memory were tested after 3-hr retention intervals, which followed learning and were placed either in the early or in the late half of the night. Sleep group subjects slept during the retention intervals while subjects of the wake group stayed awake. As expected, early retention sleep was dominated by slow wave sleep (SWS), whereas rapid eye movement (REM) sleep prevailed during late retention sleep. After early retention sleep, recall of spatial memory was superior to that after late retention sleep (p < 0.01), and also to that after retention intervals of wakefulness (p < 0.05). In contrast, priming was more effective after late than early retention sleep (p < 0.05). It appears that early sleep dominated by SWS facilitates consolidation of declarative memory whereas late sleep dominated by REM sleep facilitates consolidation of nondeclarative memory.

Time course of sleep inertia dissipation in human performance and alertness.

Abstract: Alertness and performance on a wide variety of tasks are impaired immediately upon waking from sleep due to sleep inertia, which has been found to dissipate in an asymptotic manner following waketime. It has been suggested that behavioural or environmental factors, as well as sleep stage at awakening, may affect the severity of sleep inertia. In order to determine the time course of sleep inertia dissipation under normal entrained conditions, subjective alertness and cognitive throughput were measured during the first 4 h after habitual waketime from a full 8-h sleep episode on 3 consecutive days. We investigated whether this time course was affected by either sleep stage at awakening or behavioural/environmental factors. Sleep inertia dissipated in an asymptotic manner and took 2-4 h to near the asymptote. Saturating exponential functions fitted the sleep inertia data well, with time constants of 0.67 h for subjective alertness and 1.17 h for cognitive performance. Most awakenings occurred out of stage rapid eye movement (REM), 2 or 1 sleep, and no effect of sleep stage at awakening on either the severity of sleep inertia or the time course of its dissipation could be detected. Subjective alertness and cognitive throughput were significantly impaired upon awakening regardless of whether subjects got out of bed, ate breakfast, showered and were exposed to ordinary indoor room light (approximately 150 lux) or whether subjects participated in a constant routine (CR) protocol in which they remained in bed, ate small hourly snacks and were exposed to very dim light (10-15 lux). These findings allow for the refinement of models of alertness and performance, and have important implications for the scheduling of work immediately upon awakening in many occupational settings.

Sleep-Induced Changes in Associative Memory

Abstract: The notion that dreaming might alter the strength of associative links in memory was first proposed almost 200 years ago. But no strong evidence of such altered associative links has been obtained. Semantic priming can be used to quantify the strength of associative links between pairs of words; it is thought to measure the automatic spread of activation from a "node" representing one word to nodes representing semantically related words. Semantic priming could thus be used to test for global alterations in the strengths of associative links across the wake-sleep cycle. Awakenings from REM and nonREM (NREM) sleep produce a period of state carry-over during which performance is altered as a result of the brain's slow transition to full wakefulness, and cognitive testing in this period can provide information about the functioning of the brain during the prior sleep period. When subjects were tested across the night - before and after a night's sleep as well as immediately following forced awakenings from REM and NREM sleep-weak priming (e.g., thief-wrong) was found to be state dependent (p = 0.016), whereas strong priming (e.g., hot-cold) was not (p = 0.89). Weak primes were most effective in the presleep and REM sleep conditions and least effective in NREM and postsleep conditions. Most striking are analyses comparing weak and strong priming within each wake-sleep state. Contrary to the normal pattern of priming, subjects awakened from REM sleep showed greater priming by weak primes than by strong primes (p = 0.01). This result was seen in each of three protocols. In contrast, strong priming exceeded weak priming in NREM sleep. The shift in weak priming seen after REM sleep awakenings suggests that cognition during REM sleep is qualitatively different from that of waking and NREM sleep and may reflect a shift in associative memory systems, a shift that we hypothesize underlies the bizarre and hyperassociative character of REMsleep dreaming. Known changes in brainstem activity that control the transition into and maintenance of REM sleep provide a possible explanation of this shift.

Brain Gene Expression During REM Sleep Depends on Prior Waking Experience

Abstract: In most mammalian species studied, two distinct and successive phases of sleep, slow wave (SW), and rapid eye movement (REM), can be recognized on the basis of their EEG profiles and associated behaviors. Both phases have been implicated in the offline sensorimotor processing of daytime events, but the molecular mechanisms remain elusive. We studied brain expression of the plasticity-associated immediate-early gene (IEG) zif-268 during SW and REM sleep in rats exposed to rich sensorimotor experience in the preceding waking period. Whereas nonexposed controls show generalized zif-268 down-regulation during SW and REM sleep, zif-268 is upregulated during REM sleep in the cerebral cortex and the hippocampus of exposed animals. We suggest that this phenomenon represents a window of increased neuronal plasticity during REM sleep that follows enriched waking experience.

Heart rate variability during waking and sleep in healthy males and females.

Abstract: Study Objectives: The study goal was to investigate autonomic activity with heart rate variability analysis during different sleep stages in males and females. Design: The study utilized a 2 Groups (males, females) X 4 States (waking, stage 2 sleep, stage 4 sleep, rapid-eye movement sleep) mixed design with one repeated, within-subjects factor (i.e., state). Setting: The study was carried out in the sleep laboratory of the Thomas N. Lynn Institute for Healthcare Research. Participants: Twenty-four healthy adults (fourteen females and ten males). Interventions: NA Measurements and Results: All participants underwent polysomnographic monitoring and electrocardiogram recordings during pre-sleep waking and one night of sleep. Fifteen-minute segments of beat-to-beat heart rate intervals during waking, stage 2 sleep, stage 4 sleep, and REM sleep were subjected to spectral analysis. Compared to NREM sleep, REM sleep was associated with decreased high frequency (HF) band power, and significantly increased low frequency (LF) to (HF) ratio. Compared to females, males showed significantly elevated LF/HF ratio during REM sleep. Males also demonstrated significantly decreased HF band power during waking when compared to females. No significant sleep- or gender-related changes in LF band power were found. Conclusions: The results confirmed changes in autonomic activity from waking to sleep, with marked differences between NREM and REM sleep. These changes were primarily due to stage-related alterations in vagal tone. REM sleep was characterized by increased sympathetic dominance, secondary to vagal withdrawal. The data also suggested gender differences in autonomic functioning during waking and sleep, with decreased vagal tone during waking and increased sympathetic dominance during REM sleep in the males.

Breathing during sleep in patients with nocturnal desaturation.

Abstract: The mechanisms leading to hypoxemia during sleep in patients with respiratory failure remain poorly understood, with few studies providing a measure of minute ventilation (V I) during sleep The aim of this study was to measure ventilation during sleep in patients with nocturnal desaturation secondary to different respiratory diseases The 26 patients studied had diagnoses of chronic obstructive pulmonary disease (COPD) (n = 9), cystic fibrosis (CF) (n = 2), neuromusculoskeletal disease (n = 4), and obesity hypoventilation syndrome (OHS) (n = 11) Also reported are the results for seven normal subjects and seven patients with effectively treated obstructive sleep apnea (OSA) without desaturation during sleep Ventilation was measured with a pneumotachograph attached to a nasal mask In the treated patients with OSA and in the normal subjects, only minor alterations in V I were observed during sleep In contrast, mean V I for the group with nocturnal desaturation decreased by 21% during non-rapid-eye-movement (NREM) sleep and by 39% during rapid-eye-movement (REM) sleep as compared with wakefulness This reduction was due mainly to a decrease in tidal volume (V T) Hypoventilation was most pronounced during REM sleep, irrespective of the underlying disease These data indicate that hypoventilation may be the major factor leading to hypoxia during sleep, and that reversal of hypoventilation during sleep should be a major therapeutic strategy for these patients

Melatonin as a therapy in REM sleep behavior disorder patients: an open-labeled pilot study on the possible influence of melatonin on REM-sleep regulation.

Abstract: REM sleep behavior disorder (RBD) is clinically impressive by virtue of its vigorous sleep behaviors usually accompanying vivid, striking dreams. The main feature of the disorder, REM sleep without muscle atonia, has been shown in a variety of diseases; therefore, the disorder might possibly be underestimated. In an open-labeled trial, we treated six consecutive RBD patients over a 6-week period with 3 mg melatonin given within 30 minutes before bedtime. There was a dramatic clinical improvement in five of the six patients within a week which extended beyond the end of treatment for weeks or months. A second polysomnogram performed 6 weeks after the beginning of treatment showed a significant tendency toward normalization of the percentage of REM sleep, a significant reduction of 30-second epochs, scored as REM sleep without muscle atonia, a significant reduction of stage-shifts in REM, and a significant reduction in epochs considered as movement time in REM. All other sleep parameters were not changed consistently. We hypothesize that internal desynchrony might be a part of the underlying pathophysiology in RBD. Our data might give first evidence to the hypothesis that exogenous melatonin, administered to patients with internal desynchrony at the time of the maximal rise of melatonin secretion, might increase the overall amplitude of the circadian pacemaker by reentraining the suprachiasmatic nucleus and thereby restore circadian driven rhythms, one of them being the circadian modulation of REM sleep.

Timing the end of nocturnal sleep.

Abstract: Some people can quite accurately time the end of their night's sleep at will, without using an alarm clock1, demonstrating that it is possible to voluntarily control a state of consciousness that is characterized by a loss of volition and attentional guidance2. Here we show that the expectation that sleep will come to an end at a certain time induces a marked increase in the concentration of the hormone adrenocorticotropin in the blood one hour before waking. The regulation of adrenocorticotropin release during nocturnal sleep is therefore not confined to daily rhythms; it also reflects a preparatory process in anticipation of the end of sleep.

Role of GABAA receptors in the regulation of sleep: initial sleep responses to peripherally administered modulators and agonists.

Abstract: This paper reviews the sleep effects of systemically administered agonistic modulators of GABAA receptors, including barbiturates, benzodiazepines, zolpidem, zopiclone and neuroactive steroids, and the selective GABAA agonists muscimol and THIP. To assess the involvement of GABAA receptors in the physiologic regulation of sleep, the article emphasizes the hypnotic properties shared by agonistic modulators and by the selective agonists of the GABAA receptor complex. In both rats and normal sleeping individuals, agonistic modulators are able to reduce sleep latency, increase sleep continuity, and promote non-rapid-eye-movement (NREM) sleep as well as the occurrence of spindles. Furthermore, nearly all of these compounds have been shown to attenuate slow-wave activity (SWA) and to suppress the occurrence of REM sleep. In the same species, GABAA agonist(s) do not seem to affect sleep latency or REM sleep time, but may increase sleep continuity and NREM sleep and augment SWA while depressing spindle activity in humans. The distinct sleep effects of GABAA agonists may be due to their unspecific stimulation of GABAA receptors throughout the brain, and to the fact that they are poor substrates for uptake and probably exert more tonic effects than liberated GABA. If so, the involvement of GABAA receptors in the various aspects of sleep can be inferred more accurately from the hypnotic effects of agonistic modulators. This implies that an activation of GABAA receptors plays a crucial role in the initiation and maintenance of NREM sleep and in the generation of sleep spindles, but disrupts the processes underlying slow EEG components and the triggering of REM sleep.

Effects of method, duration, and sleep stage on rebounds from sleep deprivation in the rat

Abstract: Total sleep deprivation (TSD) of rats for 24 hours or less by continually enforced locomotion has consistently produced subsequent rebounds of slow-wave or high-amplitude EEG activity in NREM sleep, which has contributed to the widely held view that this EEG activity reflects particularly "intense" or restorative sleep. These rebounds usually have been accompanied by substantial rebounds of REM sleep. In contrast, chronic TSD (2 weeks or longer) by the disk-over-water (DOW) method has produced only huge, long-lasting rebounds of REM sleep with no rebound of high-amplitude NREM sleep. To evaluate whether the different rebounds result from different methods or from different lengths of deprivation, rats were subjected to 24-hour TSD by the DOW method. Rebounds included increases in high-amplitude and slow-wave activity; i.e., the methods produced similar rebound patterns following short-term TSD. (Chronic TSD by continually enforced locomotion would be strategically difficult and severely confounded with motor fatigue.) Rats subjected to DOW-TSD for 4 days, well before the development of severe TSD symptoms, showed primarily REM sleep rebounds. Rats subjected to 1 day of selective REM sleep deprivation, but not their closely yoked control rats, showed large, significant REM sleep rebounds, which evidently were not induced by the stress of the deprivation method per se. The combined findings prompted reexamination of published evidence relevant to "sleep intensity," including "negative rebounds," rebounds in other species, the effects of stress and fatigue, depth of sleep indicators, and extended sleep. The review points out pitfalls in the designation of any specific pattern as intense sleep.

Half-awake to the risk of predation

Abstract: Birds have overcome the problem of sleeping in risky situations by developing the ability to sleep with one eye open and one hemisphere of the brain awake. Such unihemispheric slow-wave sleep is in direct contrast to the typical situation in which sleep and wakefulness are mutually exclusive states of the whole brain. We have found that birds can detect approaching predators during unihemispheric slow-wave sleep, and that they can increase their use of unihemispheric sleep as the risk of predation increases. We believe this is the first evidence for an animal behaviourally controlling sleep and wakefulness simultaneously in different regions of the brain.

Effect of Serotonin Uptake Inhibition on Breathing during Sleep and Daytime Symptoms in Obstructive Sleep Apnea

Abstract: Pharmacologic enhancement of serotonergic transmission by serotonin uptake inhibition has been suggested as one approach to improve upper-airway patency and thus nocturnal breathing in patients with obstructive sleep apnea (OSA). To test this hypothesis, we performed a double-blind, randomized, placebo-controlled crossover study testing the effect of paroxetine (20 mg od) on polysomnographic and psychopathologic outcomes in 20 male OSA patients (mean age 52.1 years, mean BMI 28.7 kg/m2, mean oxygen desaturation index on a previous screening 25.4/hour). The two treatment periods of 6 weeks and the separating washout period of 4 weeks were completed by 17 patients. Paroxetine reduced the apnea index during NREM sleep (-35%, p = 0.003), but not during REM sleep. No significant effect on hypopnea indices was found. With the exception of a previously described REM-postponing effect (p = 0.05), sleep architecture was not significantly influenced by paroxetine. Similarly, the effect of paroxetine on apnea was not associated with a significant overall alleviation of psychopathologic symptoms as rated on the Comprehensive Psychopathological Rating Scale or OSA-related daytime complaints assessed by visual analog scales. We conclude that enhanced serotonergic transmission improves breathing during NREM sleep in OSA. This effect is poorly related to effects on sleep architecture or daytime symptoms.

Sleep Problems in the Elderly

Abstract: Refreshing sleep requires both sufficient total sleep time as well as sleep that is in synchrony with the individual's circadian rhythm. Problems with sleep organization in elderly patients typically include difficulty falling asleep, less time spent in the deeper stages of sleep, early-morning awakening and less total sleep time. Poor sleep habits such as irregular sleep-wake times and daytime napping may contribute to insomnia. Caffeine, alcohol and some medications can also interfere with sleep. Primary sleep disorders are more common in the elderly than in younger persons. Restless legs syndrome and periodic limb movement disorder can disrupt sleep and may respond to low doses of antiparkinsonian agents as well as other drugs. Sleep apnea can lead to excessive daytime sleepiness. Evaluation of sleep problems in the elderly includes careful screening for poor sleep habits and other factors that may be contributing to the sleep problem. Formal sleep studies may be needed when a primary sleep disorder is suspected or marked daytime dysfunction is noted. Therapy with a benzodiazepine receptor agonist may be indicated after careful evaluation.

Activity of Midbrain Reticular Formation and Neocortex during the Progression of Human Non-Rapid Eye Movement Sleep

Abstract: To clarify the neural correlates and brain activity during the progression of human non-rapid eye movement (NREM) sleep, we examined the absolute regional cerebral blood flow (rCBF) during light and deep NREM sleep and during wakefulness in normal humans using positron emission tomography with H215O. Relative changes in rCBF during light and deep NREM sleep in comparison to the rCBF during wakefulness were also analyzed. During light NREM sleep, the rCBF in the midbrain, in contrast to that in the pons and thalamic nuclei, did not decrease when compared to that during wakefulness, whereas rCBF decreased in the left medial frontal gyrus, left inferior frontal gyrus, and left inferior parietal gyrus of the neocortex. During deep NREM sleep, the rCBF in the midbrain tegmentum decreased, and there was a marked and bilateral decrease in the rCBF in all neocortical regions except for the perirolandic areas and the occipital lobe. There have been three groups of brain structures, each representing one type of deactivation during the progression of NREM sleep. The activity of the midbrain reticular formation is maintained during light NREM sleep and therefore represents a key distinguishing characteristic between light and deep NREM sleep. Selective deactivation of heteromodal association cortices, including those related to language, occurs with increasingly deep NREM sleep, which supports the recent theory that sleep is not a global, but it is a local process of the brain.

Adenosinergic modulation of rat basal forebrain neurons during sleep and waking: neuronal recording with microdialysis

Abstract: 1. The cholinergic system of the basal forebrain (BF) is hypothesized to play an important role in behavioural and electrocortical arousal. Adenosine has been proposed as a sleep-promoting substance that induces sleep by inhibiting cholinergic neurons of the BF and brainstem. However, adenosinergic influences on the activity of BF neurons in naturally awake and sleeping animals have not been demonstrated. 2. We recorded the sleep-wake discharge profile of BF neurons and simultaneously assessed adenosinergic influences on wake- and sleep-related activity of these neurons by delivering adenosinergic agents adjacent to the recorded neurons with a microdialysis probe. Discharge rates of BF neurons were recorded through two to three sleep-wake episodes during baseline (artificial cerebrospinal fluid perfusion), and after delivering an adenosine transport inhibitor (s-(p-nitrobenzyl)-6-thioinosine; NBTI), or exogenous adenosine, or a selective adenosine A1 receptor antagonist (8-cyclopentyl-1, 3-dimethylxanthine; CPDX). 3. NBTI and adenosine decreased the discharge rate of BF neurons during both waking and non-rapid eye movement (NREM) sleep. In contrast, CPDX increased the discharge rate of BF neurons during both waking and NREM sleep. These results suggest that in naturally awake and sleeping animals, adenosine exerts tonic inhibitory influences on BF neurons, supporting the hypothesized role of adenosine in sleep regulation. 4. However, in the presence of exogenous adenosine, NBTI or CPDX, BF neurons retained their wake- and sleep-related discharge patterns, i.e. still exhibited changes in discharge rate during transitions between waking and NREM sleep. This suggests that other neurotransmitters/neuromodulators also contribute to the sleep-wake discharge modulation of BF neurons.

The Effect of Snoring and Obstructive Sleep Apnea on the Sleep Quality of Bed Partners

Abstract: Objectives To measure the effect of snoring and obstructive sleep apnea (OSA) on the sleep of snorers' bed partners and to determine whether a bed partner's sleep improves when snoring and OSA are treated. Materials and Methods We studied 10 married couples in which 1 member was undergoing polysomnography to evaluate suspected OSA. The patients and their spouses underwent simultaneous polysomnography. Midway through the 1-night study, the patients received nasal continuous positive airway pressure (CPAP) with the pressure adjusted to eliminate snoring and obstructive breathing events. Apnea-hypopnea index (episodes/hours of sleep time), arousal index (arousals/hours of sleep time), and sleep efficiency (percent time asleep) were calculated to measure sleep quality. Results The patients (all male) demonstrated a median (range) apnea-hypopnea index of 26 (3–75) that decreased to 7 (0–34) during the trial of nasal CPAP therapy (P Conclusion The elimination of snoring and OSA in these patients was associated with an improvement in the quality of their bed partners' sleep, as indicated by improved sleep efficiency and continuity, even when the spouses had been habitually exposed to snoring and OSA. Assuming that 480 minutes were spent in bed for sleep, a 13% improvement in sleep efficiency (ie, from 74% to 87%) translates to an additional 62 minutes of sleep per night for the spouses of snorers with OSA.

Circadian regulation of human sleep and age-related changes in its timing, consolidation and EEG characteristics.

Abstract: The light-entrainable circadian pacemaker located in the suprachiasmatic nucleus of the hypothalamus regulates the timing and consolidation of sleep by generating a paradoxical rhythm of sleep propensity; the circadian drive for wakefulness peaks at the end of the day spent awake, ie close to the onset of melatonin secretion at 21.00-22.00 h and the circadian drive for sleep crests shortly before habitual waking-up time. With advancing age, ie after early adulthood, sleep consolidation declines, and time of awakening and the rhythms of body temperature, plasma melatonin and cortisol shift to an earlier clock hour. The variability of the phase relationship between the sleep-wake cycle and circadian rhythms increases, and in old age sleep is more susceptible to internal arousing stimuli associated with circadian misalignment. The propensity to awaken from sleep advances relative to the body temperature nadir in older people, a change that is opposite to the phase delay of awakening relative to internal circadian rhythms associated with morningness in young people. Age-related changes do not appear to be associated with a shortening of the circadian period or a reduction of the circadian drive for wake maintenance. These changes may be related to changes in the sleep process itself, such as reductions in slow-wave sleep and sleep spindles as well as a reduced strength of the circadian signal promoting sleep in the early morning hours. Putative mediators and modulators of circadian sleep regulation are discussed.

Rapid Eye Movement Sleep

Abstract: Eyelid Condition at Birth: Relationship to Adult Mammalian Sleep-waking Patterns, E Aserinsky Phylogeny and Evolution of Rapid Eye Movement (REM) Sleep, M G Frank Ontogenesis of REM Sleep, M Segawa Initiation of Rapid Eye Movement Sleep: Beyond the Brainstem, A R Morrison, L D Sanford, and R J Ross Muscle Atonia in REM Sleep, Y -Y Lai and J M Siegel PGO Wave Generation: Mechanism and Functional Significance, S Datta Norepinephrine and REM Sleep, P-H Luppi, D Gervasoni, C Peyron, C Rampon, B Barbagli, R Boissard, and P Fort New Directions for the Study of Cholinergic REM Sleep Generation: Specifying Pre- and Postsynaptic Mechanisms, M L Capece, H A Baghdoyan, and R Lydic Functional Role of Serotonin 5-HT1 and 5-HT2 Receptor in the Regulation of REM Sleep, J M Monti and D Monti Possible Role of GABA in the Regulation of REM Sleep with Special Reference to REM-OFF Neurons, B N Mallick, S Kaur, S K Jha, and J M Siegel Nitric Oxide: A Diffusible Modulator of Physiological Traits and Behavioral States, T O Leonard and R Lydic Neurotransmitters Changes and REM Sleep, T Kodama Spatio-Temporal Distribution of Neuronal Activities and REM Sleep, S Inoue, U K Saha, and T Musha Different Physiological Properties of Two Populations of PS-on Neurons in the Mesopontine Tegmentum, Y Koyama, Y Kayama, and K Sakai Hormones and REM Sleep, F Obal Jr and J M Krueger Endogenous Sleep Substances and REM Sleep, S Inoue, K Honda, M Kimura, and S-Q Zhang Brain Energy, Production, and Sleep Occurrence, R Cespuglio, H Faradji-Prevautel, and L Netchiporouk Rapid Eye Movement Sleep: From Cerebral Metabolism to Functional Brain Mapping, P Maquet and C Phillips REM Sleep and Apnea, D W Carley and M Radulovacki Thermoregulatory Control of the nonREM-REM Sleep Cycle, R Szymusiak, Md Noor Alam, and D McGinty REM Sleep Across Age and Sex, K Mishima, T Shimizu, and Y Hishikawa The Function of Fetal/Neonatal REM Sleep, M Mirmiran and Y G H Maas REM Sleep Deprivation Alters Factors Affecting Neuronal Excitability: Role of Norepinephrine and Its Possible Mechanism of Action, B N Mallick, H V A Adya, and s Thankachan REM Sleep Deprivation and Behavioral Changes, G W Vogel Cellular and Molecular Changes Occurring During REM Sleep, O Prospero-Garcia, L Navarro, E Murillo-Rodriguez, M Sanchez-Alavez, R Guzman-Marin, M Mendez-Diaz, M Gomez-Chavarin, A Jimenez-Anguiano, and R Drucker-Colin Intensity of REM Sleep, K Takahashi Why We Believe What We Believe About REM-Sleep Regulation, H Benington Hypothesis on REM Sleep from the Viewpoint of Neuronal Dynamics, M Nakao and M Yamamoto

Landau-Kleffner syndrome (LKS): long-term follow-up and links with electrical status epilepticus during sleep (ESES)

Abstract: We describe 11 patients affected by Landau–Kleffner syndrome (LKS) with a mean follow-up of 9 years and 8 months. EEG recordings during wakefulness, NREM and REM sleep showed a bitemporal electrical status epilepticus during sleep (BTESES) in all cases; four of them presented a shift from a BTESES towards an `intercalated electrical status epilepticus during sleep' (IESES) accompanied by a global regression of cognitive and behavioural functions in 3/4 of cases. At the last observation, only 18.2% of cases presented a complete language recovery and mental retardation was evident in 63.6%. The prognosis of LKS in our cases may depend on the interaction of different negative factors such as onset of aphasia before 4 years, its duration for longer than 1 year, long-lasting duration and continuity without fluctuations of BTESES/IESES, probably preexisting mild speech delay. It is important for the prognosis to utilize antiepileptic treatment and possibly neurosurgical techniques to eliminate EEG paroxysmal abnormalities. At present, no similar cases with clinical-EEG evolution from LKS to electrical status epilepticus during sleep (ESES) have ever been described. Our observation demonstrates that LKS and ESES classified as different clinical-EEG syndromes represent two aspects of the same brain dysfunction and they may exist separately or pass one into the other with a change in the clinical-EEG picture. The common origin of the two syndromes is confirmed by recent functional brain imaging, neurophysiological and neurosurgical techniques.