Showing papers on "Slow-wave sleep published in 1991"
TL;DR: It appears that the pontomesencephalic cholinergic neurons play an important, active role in the generation of paradoxical sleep, this role may be conditional upon the simultaneous inactivity of noradrenaline and serotonin neurons, evidence for which derives from both pharmacological and recording studies.
396 citations
TL;DR: It is suggested that K complex related increases of MSA are signs of arousal which elicit both cortical EEG phenomena and activation of cerebral sympathetic centres in sleep-deprived healthy subjects.
Abstract: Muscle sympathetic activity (MSA) was recorded in the peroneal nerve during sleep in 14 sleep-deprived healthy subjects. Continuous noninvasive recordings of finger blood pressure were obtained in 7 subjects. In light sleep (stage 2 sleep) the number of sympathetic bursts/min decreased to 90 +/- 8% (mean +/- SEM) and total MSA (= burst/min x mean burst area) to 89 +/- 5% of the awake value (P less than 0.05, n = 14). In deep sleep (stage 3-4) total MSA decreased further, to 71 +/- 8% of the awake value (n = 5). There was no close correlation between variations of depth of sleep and variations of sympathetic activity but during continuously deepening sleep MSA decreased progressively with time. In stage 2 sleep, high amplitude K complexes were accompanied by short-lasting increases of sympathetic activity. Since these increases of MSA were not preceded by decreases of diastolic blood pressure, which is known to evoke increased sympathetic nerve traffic in muscle nerves, we suggest that K complex related increases of MSA are signs of arousal which elicit both cortical EEG phenomena and activation of cerebral sympathetic centres. During desynchronized (REM) sleep, total MSA increased to 124 +/- 12% of the value in awake state (n = 5). The increases occurred mainly in short irregular periods, often related to rapid eye movements and there was an inverse relationship between the duration of the desynchronized sleep and the increase of total MSA. Our findings are similar to the data obtained in animal experiments and may partly explain changes of blood pressure during synchronized and desynchronized sleep reported previously in man.
283 citations
TL;DR: Experimental evidence indicates that prostaglandins D2 and E2 are probably two of the major endogenous sleep‐regulating substances, one promoting sleep and the other wakefulness, in rats, dogs, rabbits, monkeys, and probably in humans as well.
Abstract: Although sleep-wake cycles are repeated every day and night and almost one-third of our lifetime is spent sleeping, the molecular mechanisms of sleep-wake regulation have remained little understood. Recent experimental evidence indicates that prostaglandins (PG) D2 and E2 are probably two of the major endogenous sleep-regulating substances, one promoting sleep and the other wakefulness, in rats, dogs, rabbits, monkeys, and probably in humans as well. Preliminary evidence indicates that the sites of action of PGD2 and E2 are located in the sleep and wake centers in or near the preoptic area and posterior hypothalamus, respectively.
238 citations
TL;DR: REM density appears to be a more likely candidate for a biologic marker for major depression than is REM latency, which was clearly affected by age, but there were no significant differences between patients and controls until the middle of the fourth decade of life.
233 citations
TL;DR: A deep-sleep-associated statistically highly significant 25% decrease in CMRO2 is found, a magnitude of depression according with studies of glucose uptake and reaching levels otherwise associated with light anesthesia.
Abstract: It could be expected that the various stages of sleep were reflected in variation of the overall level of cerebral activity and thereby in the magnitude of cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF). The elusive nature of sleep imposes major methodological restrictions on examination of this question. We have now measured CBF and CMRO2 in young healthy volunteers using the Kety-Schmidt technique with 133Xe as the inert gas. Measurements were performed during wakefulness, deep sleep (stage 3/4), and rapid-eye-movement (REM) sleep as verified by standard polysomnography. Contrary to the only previous study in humans, which reported an insignificant 3% reduction in CMRO2 during sleep, we found a deep-sleep-associated statistically highly significant 25% decrease in CMRO2, a magnitude of depression according with studies of glucose uptake and reaching levels otherwise associated with light anesthesia. During REM sleep (dream sleep) CMRO2 was practically the same as in the awake state. Changes in CBF paralleled changes in CMRO2 during both deep and REM sleep.
222 citations
TL;DR: It is demonstrated that IL-1 promotes NREMS in the rat, however, unlike previously reported findings in rabbits, the circadian rhythm of sleep regulation strongly interferes with the sleep-promoting activity of IL- 1 in rats.
Abstract: Rats received various doses of interleukin 1 (IL-1) (range, 0.5-25.0 ng) or pyrogen-free saline intracerebroventricularly during the rest (light) and the active (dark) cycles of the day, and sleep-wake activity and brain temperature were determined for 6 h. Low doses of IL-1 (0.5 ng at night, 2.5 ng during the day) increased both the duration of non-rapid-eye-movement sleep (NREMS) and electroencephalogram (EEG) slow-wave activity during NREMS episodes. Increasing doses of IL-1 had divergent effects on NREMS duration and EEG slow-wave activity, and the direction of the changes depended on the diurnal cycle. Thus NREMS duration was promoted at night and EEG slow-wave amplitudes during the day, whereas NREMS duration during the day and EEG slow-wave amplitudes at night were suppressed after higher doses of IL-1. High doses of IL-1 also induced decreases in rapid-eye-movement sleep during both phases of the day. Each dose of IL-1 that promoted NREMS also tended to increase brain temperature. These results demonstrate that IL-1 promotes NREMS in the rat. However, unlike previously reported findings in rabbits, the circadian rhythm of sleep regulation strongly interferes with the sleep-promoting activity of IL-1 in rats.
205 citations
TL;DR: It is concluded that sleep homeostasis as conceptualized in the two-process model may be a general property of mammalian sleep.
177 citations
TL;DR: Nocturnal sleep was studied in inpatients with Huntington's disease and patients showed an increased density of sleep spindles, correlated in part with duration of illness, severity of clinical symptoms, and degree of atrophy of the caudate nucleus.
Abstract: Nocturnal sleep was studied in 16 inpatients with Huntington's disease. In comparison with healthy controls, patients exhibited a disturbed sleep pattern with increased sleep onset latency, reduced sleep efficiency, frequent nocturnal awakenings, more time spent awake and less slow wave sleep. These abnormalities correlated in part with duration of illness, severity of clinical symptoms, and degree of atrophy of the caudate nucleus. Patients showed an increased density of sleep spindles.
156 citations
TL;DR: The results suggest that corticosteroid-induced changes in SWS are mediated via MR-like central receptors in humans, whereas changes in REM sleep involve GR.
Abstract: Cortisol modulates brain functions in humans. This principal endogenous glucocorticoid in humans decreases rapid-eye-movement (REM) sleep and increases slow-wave sleep (SWS). Because cortisol exert...
153 citations
TL;DR: It was found that spike-wave discharges predominantly occur during light slow wave sleep and passive wakefulness, and a crucial role for the degree of stability of the level of vigilance in the genesis of absence seizures is suggested.
148 citations
TL;DR: The drug reduced REM sleep but did not significantly affect other sleep stages and subjective sleep parameters, and the pattern of the spectral changes was similar to those induced by other hypnotics that bind to the GABAA/benzodiazepine receptor complex.
Abstract: A single 10 mg dose of zolpidem, an imidazopyridine hypnotic, was administered to young, healthy male volunteers prior to bedtime. The drug reduced REM sleep but did not significantly affect other sleep stages and subjective sleep parameters. All-night spectral analysis of the EEG revealed that power density in nonREM sleep was reduced in the low-frequency range (1.25–2.5 Hz; 5.25–10.0 Hz) and increased in the spindle frequency range (12.25–13.0 Hz). Significant changes in the EEG spectrum were present in the first 4 h of sleep. The pattern of the spectral changes was similar to those induced by other hypnotics that bind to the GABAA/benzodiazepine receptor complex. There were no residual effects of zolpidem on psychomotor performance in the morning, on the self-rated state in the morning and at noon, and on sleep and EEG parameters in the subsequent drug-free night.
TL;DR: It is concluded that hypoventilation occurs in concert with reduced upper airway dilator muscle activation during PREM sleep by mechanisms that remain to be established.
Abstract: Several investigators have observed that irregular breathing occurs during rapid-eye-movement (REM) sleep in healthy subjects, with ventilatory suppression being prominent during active eye movemen...
TL;DR: The complaint of sleepiness in the hypersomnic bipolar depressed patient appears to be related to the lack of interest, withdrawal, decreased energy, or psychomotor retardation inherent in the anergic depressed condition, rather than an increase in true sleep propensity or REM sleep propensity.
Abstract: Objective: This study characterized objectively the hypersomnia frequently seen in the depressed phase ofbipolar affective disorder. On the basis ofprevious work in sleep and affective disorders, it has been hypothesized that the hypersomnia is related to greater REM sleep. This hypothesis was tested by using a multiple sleep latency test to compare bipolar affective disorder with narcolepsy, a well-defined primary sleep disorder associated with known REM sleep dysfunction. Method: Twenty-five bipolar depressed patients were selected on the basis ofcomplaints ofhypersomnia. They underwent 2 nights ofpolysomnography followed by a multiple sleep latency test. Data on their nocturnal sleep and daytime naps were compared with similar data on 23 nondepressed narcoleptic patients referred for sleep evaluation. & �yjj�� Despite their complaints of hypersomnia, no abnormalities were noted for the bipolar group in the results from the multiple sleep latency test. Contrary to the working hypothesis, REM sleep was notably absent during daytime naps in the depressed patients, in marked contrast to the findings for the narcoleptic group. Conclusions: The complaint of sleepiness in the hypersomnic bipolar depressed patient appears to be related to the lack of interest, withdrawal, decreased energy, or psychomotor retardation inherent in the anergic depressed condition, rather than an increase in true sleep propensity or REM sleep propensity. (AmJ Psychiatry1991; 148:1177-1181)
TL;DR: The WAG/Rij rat model for absence epilepsy was characterized with respect to the relationships between the level of vigilance, sleep-wake states and the occurrence of spike-wave discharges, and an increase of alertness decreased the amount of epilepsy.
TL;DR: The results further support an active role for histamine in the control of the Waking state and prevent the effects of (R)-α-methylhistamine on slow wave sleep and wakefulness.
TL;DR: It is concluded that bright light immediately affects core body temperature and that this effect is mediated via the eyes and the latency to sleep onset was increased after BL exposure.
Book•
01 Jan 1991
TL;DR: In this article, a conceptual review with new pharmacological data (P.Niedermeyer and C.E.Wieser) is presented, with an emphasis on automatic methods.
Abstract: 1. The neurophysiological basis of epileptic activity: a condensed overview (E.-J. Speckmann and C.E. Elger). 2. Epileptic manifestations and influence on sleep in the baboon Papio papio (R. Naquet, T. Tanaka and C. Cepeda). 3. Historical aspects of sleep and epilepsy (P. Passouant). 4. Sleep and epileptic activity (G.F. Rossi, G. Colicchio, P. Pola and R. Roselli). 5. The enforced nap: a simple effective method of inducing sleep activation in epileptics (H. Gastaut, M. Gomez-Almanzar and M. Taury). 6. Awakening epilepsy (`Aufwach-Epilepsie') revisited (E. Niedermeyer). 7. Sleep, arousal and electroclinical manifestations of generalized epilepsy with spike wave pattern (P. Halasz). 8. Runs of rapid spikes in sleep - A characteristic EEG expression of generalized malignant epileptic encephalopathies. A conceptual review with new pharmacological data (P. Halasz). 9. Sleep organization and epilepsy (J. Touchon, M. Baldy-Moulinier, M. Billard, A. Besset, J. Cadilhac). 10. Sleep and benign partial epilepsies of childhood (B. Dalla Bernardina, V. Sgro and R. Caraballo). 11. Temporal lobe epilepsy, sleep and arousal: stereo-EEG findings (H.G. Wieser). 12. Circadian distribution of generalized spike-wave-activity in relation to sleep (W. Burr, E. Korner and H. Stefan). 13. Nocturnal paroxysmal dystonia (E. Lugaresi, F. Cirignotta and P. Montagna). 14. Sleep polygraphic findings in epileptic encephalopathies from infancy to adolescence (C.A. Tassinari, R. Michelucci, O. Daniele, C. Dravet, M. Bureau, B. Dalla Bernardina, G. Rubboli, J. Picornell-Darder, F. Vigevano and J. Roger). 15. Influence of antiepileptic drugs on sleep pattern (A.C. Declerck and A. Wauquier). 16. Sleep and prolonged epileptic activity (status epilepticus) (W. Froscher). 17. Integrated sleep analysis with emphasis on automatic methods (Th. Penzel, K. Stephan, St. Kubicki and W.M. Herrmann). 18. General considerations of sleep and sleep deprivation (U. Jovanovi*g3). 19. Short term sleep EEG recordings after partial sleep deprivation as a routine procedure in order to uncover epileptic phenomena: an evaluation of 719 EEG recordings (St. Kubicki, W. Scheuler and H. Wittenbecher). 20. On the nature of the influence of sleep deprivation on the EEG (D. Klingler, H. Tragner and E. Deisenhammer). 21. Sleep and sleep deprivation in epileptology and comparing investigations with both methods (R. Degen and H.-E. Degen). 22. Sleep deprivation, epilepsy and the ability to operate a motor vehicle (J. Kugler, A. Heidl and R. Spatz). 23. Sleep deprivation and epileptological implications (E.A. Rodin). 24. Suppressive effects of enkephalins and REM sleep deprivation on seizures (M.R. Dzoljic, O.E. Ukponmwan, A.A.G. Baas, D.J. v.d. Berg, I. Rupreht and M.M. Dzoljic).
TL;DR: Overlap in the distribution of NREM alpha-like activity in sleep between the two groups indicated that it is not directly related to musculoskeletal symptoms.
TL;DR: It is hypothesized that low body temperatures during hibernation are incompatible with the restorative function of sleep as reflected in cortical slow-wave activity and animals must incur the energetic costs of periodic arousals from hibernation to receive the restrative benefits of euthermic slow- wave sleep.
Abstract: Hibernation is an adaptation for energy conservation, which probably evolved as an extension of non-rapid-eye-movement sleep mechanisms. Yet, during periodic arousals from bouts of deep hibernation, ground squirrels (Spermophilus lateralis) spend most of their time asleep. Spectral analysis of the electroencephalogram revealed that cortical slow-wave intensity during sleep is high at the beginning of a euthermic period and declines thereafter. Sleep slow-wave intensity is greater after longer bouts of hibernation than after shorter bouts. We hypothesize that low body temperatures during hibernation are incompatible with the restorative function of sleep as reflected in cortical slow-wave activity. Animals must incur the energetic costs of periodic arousals from hibernation to receive the restorative benefits of euthermic slow-wave sleep. The timing of arousals from hibernation may be a function of accumulated sleep debt.
TL;DR: It is demonstrated, that the EEG of slow wave sleep stages depicts a dimensionality, which is two units smaller than that of light or REM sleep.
Abstract: In order to perform an analysis of nonlinear EEG-dynamics we investigated the EEG of ten male probands during sleep. According to Rechtschaffen and Kales (1968) we scored the sleep-EEG and applied an algorithm, proposed by Grassberger and Proccaccia (1983) to compute the correlation dimension of different sleep stages. The correlation dimension characterizes the dynamics of the EEG signal and estimates the degrees of freedom of the signal under study. We could demonstrate, that the EEG of slow wave sleep stages depicts a dimensionality, which is two units smaller than that of light or REM sleep.
TL;DR: Patients with suicide attempts had altered intranight temporal distribution of phasic REM activity, with increased REM activity in REM sleep period 2 (significant group x period interaction), which may be more traitlike or persistent than state-related.
Abstract: In a retrospective study of the electroencephalographic (EEG) sleep of major depressives with and without a history of suicide attempts, suicide attempters had longer sleep latency, lower sleep efficiency, and fewer late-night delta wave counts than normal controls. Nonattempters, compared to attempters, had less rapid eye movement (REM) time and activity in period 2, but more delta wave counts in non-REM period 4. Although both attempters and nonattempters were like controls in regard to REM period 2, patients with suicide attempts had altered intranight temporal distribution of phasic REM activity, with increased REM activity (by both visual and automated scoring) in REM sleep period 2 (significant group x period interaction). These findings, which may be more traitlike or persistent than state-related, are discussed in the context of current theories on the role of serotonin in the regulation of sleep and in suicidal behavior.
01 Jan 1991
TL;DR: New understanding of CBF and CMR during sleep provides significant and important information of the brain's mode of working during sleep, but it does not at its current state identify the physiological processes involved in sleep or the physiological role of sleep.
Abstract: A review of the current literature regarding sleep-induced changes in cerebral blood flow (CBF) and cerebral metabolic rate (CMR) is presented. Early investigations have led to the notion that dreamless sleep was characterized by global values of CBF and CMR practically at the level of wakefulness, while rapid eye movement (REM) sleep (dream sleep) was a state characterized by a dramatically increased level of CBF and possibly also of CMR. However, recent investigations firmly contradict this notion. Investigations on CBF and CMR performed during non-REM sleep, taking the effect of different levels of sleep into consideration, show that light sleep (stage II) is characterized by global levels of CBF and CMR only slightly reduced by 3-10% below the level associated with wakefulness, whereas CBF and CMR during deep sleep (stage III-IV) is dramatically reduced by 25-44%. Furthermore, recent data indicate that global levels of CBF and CMR are about the same during REM sleep as in wakefulness. On the regional level, deep sleep seems to be associated with a uniform decrease in regional CBF and CMR. Investigations concerning regional CBF and CMR during REM sleep are few but data from recent investigations seem to identify site-specific changes in regional CBF and CMR during REM sleep. CBF and CMR are reflections of cerebral synaptic activity and the magnitude of reduction in these variables associated with deep sleep indicates that overall cerebral synaptic activity is reduced to approximately one-half the level associated with wakefulness, while cerebral synaptic activity levels during REM sleep are similar to wakefulness. However, even though the new understanding of CBF and CMR during sleep provides significant and important information of the brain's mode of working during sleep, it does not at its current state identify the physiological processes involved in sleep or the physiological role of sleep.
TL;DR: A number of factors, broadly termed ascertainment biases, likely contribute to the paucity of reports from North America and the greater recognition of the syndrome in Europe and Japan.
Abstract: Electrical status epilepticus during sleep (ESES) is primarily an EEG-defined syndrome in children characterized by the occurrence of continuous spike and slow waves during non-rapid-eye-movement (non-REM) sleep, the paroxysmal abnormalities being substantially less frequent during the awake state and REM sleep. Etiologically, cases can be divided into symptomatic and cryptogenic varieties. Partial motor seizures, frequently nocturnal, precede the emergence of ESES, whereas absence seizures often occur during the phase of ESES. The emergence of ESES is associated with neuropsychological regression. The characteristic electrographic pattern and epilepsy generally disappear during adolescence and are associated with an improvement in neuropsychological function. However, if the cases reported in the literature are representative, then there is a high probability of considerable residual dysfunction. A number of factors, broadly termed ascertainment biases, likely contribute to the paucity of reports from North America and the greater recognition of the syndrome in Europe and Japan. The current information on ESES is critiqued in this review.
Book•
01 Jan 1991
TL;DR: In this paper, the role of EEG phasic events such as K-complexes, sequences of reactive slow waves and microarousals in the physiological organization of sleep and discusses their significance in insomnia, sleep apneas, epilepsy and other disorders.
Abstract: This volume examines the role of EEG phasic events such as K-complexes, sequences of reactive slow waves and microarousals in the physiological organization of sleep and discusses their significance in insomnia, sleep apneas, epilepsy and other disorders. The contributors show how an understanding of phasic events has shed new light on the mechanisms underlying sleep alteration and can aid in the clinical assessment of insomnia and other sleep-related disorders. Included are analyses of the spectral features of evoked microarousals, the functional relationship between microstructure and macrostructure of sleep, the characteristics of transient activation phases in sleep, and the influence of environmental factors on transient activation phases. Attention is given to the relation of K-complexes to spontaneous slow wave activity during sleep, the K-complex variability in normal subjects and the link between K-complexes and spike-and-wave mechanisms in epilepsy, as well as to the role of phasic events in nocturnal paroxysmal dystonia, narcolepsy and sleep apneas. Other studies examine levels of EEG background activity and sleep states during the first year of life and relate phasic events to apneas, oxygenation, sighs and body movements during sleep in newborns and children.
TL;DR: Data show that homeostatic processes are expressed in the EEG also when sleep is initiated at a circadian phase where REM sleep propensity is high, and comparison of the power spectrum in the first cycle of day-time recovery sleep with published data on recovery sleep at various circadian phases suggests that circadian factors influence the EEG spectra.
Journal Article•
TL;DR: The sleep of thirty elderly patients with recurrent unipolar depression was examined and the single best correlate of clinical change was prolongation of REM sleep latency, consistent with the concept that anti-depressant drug efficacy may depend upon strengthening of the homeostatic regulation of sleep and upon changes in the REM-sleep regulation.
TL;DR: A clear dose-response relationship was found for ritanserin with higher doses evoking increased duration of slow wave sleep.
Abstract: This study investigated the effects of placebo, 1 mg, 3 mg, 10 mg and 30 mg ritanserin and 10 mg diazepam on human sleep Twelve normal volunteers participated in this randomized, double-blind, placebo-controlled cross-over sleep study A clear dose-response relationship was found for ritanserin with higher doses evoking increased duration of slow wave sleep
TL;DR: Scopolamine inhibited rapid eye movement sleep and prolonged REM latency equally in depressed patients and the normal comparison group and partial tolerance to the REM inhibiting effect of scopolamine developed between the first and third night of treatment.
Journal Article•
TL;DR: The results demonstrate that the nocturnal growth hormone surge is largely sleep- dependent; temporal associations between GH and SWS are not reliable after sleep deprivation; although the cortisol rhythm is not sleep-dependent, the timing of the cortisol rise may be influenced by sudden changes in the sleep-wake schedule.
Abstract: The study investigated secretory patterns of growth hormone (GH) and cortisol in relation to sleep and wakefulness. Plasma hormone levels were monitored in 10 young men during baseline waking and sleeping, during 40 hours of wakefulness, and during sleep following deprivation. The normal nocturnal GH surge disappeared with sleep deprivation, and was intensified following sleep deprivation. Mean GH levels were higher during slow wave sleep (SWS) compared with other sleep stages. During sleep after deprivation, GH secretion was prolonged, and second GH peaks occurred in three subjects which were not associated with SWS. Average 24-hour cortisol levels were not altered by sleep deprivation or sleep following deprivation, but the nocturnal cortisol rise occurred approximately one hour earlier with sleep deprivation and one hour later with resumed sleep, compared to baseline. This effect on the timing of the rise is consistent with an initial inhibitory influence of sleep on cortisol secretion. The results demonstrate that: the nocturnal growth hormone surge is largely sleep-dependent; temporal associations between GH and SWS are not reliable after sleep deprivation; although the cortisol rhythm is not sleep-dependent, the timing of the cortisol rise may be influenced by sudden changes in the sleep-wake schedule.
TL;DR: The results suggest that during non-rapid eye movement sleep cerebral metabolism and thereby cerebral synaptic activity is correlated to cerebral readiness rather than to mental activity.