Showing papers on "Slow-wave sleep published in 1986"
TL;DR: These REM sleep neurobehavioral disorders constitute another category of parasomnia, replicate findings from 21 years ago in cats receiving pontine tegmental lesions, and offer additional perspectives on human behavior, neurophysiology, pharmacology, and dream phenomenology.
Abstract: Four men, aged 67-72 years, had 4-month to 6-year histories of injuring themselves or their spouses with aggressive behaviors during sleep, often during attempted dream enactment. A 60-year-old woman had disruptive though nonviolent sleep and dream behaviors. Polysomnography did not detect seizures but did document REM sleep pathology with variable loss of chin atonia, extraordinarily increased limb-twitch activity, and increased REM ocular activity and density. A broad range of REM sleep behaviors was recorded on videotape, including stereotypical hand motions, reaching and searching gestures, punches, kicks, and verified dream movements. Stage 3-4 slow wave sleep was elevated for age in all patients. NREM sleep was devoid of harmful behaviors, although three men had periodic myoclonus. There was no associated psychiatric disorder, whereas serious neurologic disorder was closely associated in four cases: olivo-ponto-cerebellar degeneration, Guillain-Barre syndrome, subarachnoid hemorrhage, and an atypical dementia. Two patients had immediate and lasting sleep behavioral suppression induced by clonazepam, and another patient had the same response with desipramine. All instances of drug discontinuation prompted immediate relapse. In four cases there was associated dream hyperactivity, which resolved with behavioral control. These REM sleep neurobehavioral disorders constitute another category of parasomnia, replicate findings from 21 years ago in cats receiving pontine tegmental lesions, and offer additional perspectives on human behavior, neurophysiology, pharmacology, and dream phenomenology.
1,013 citations
TL;DR: In this article, three experiments were conducted to investigate the 24-hour structure of sleepiness after 1 night of sleep deprivation under two experimental conditions: instructing subjects to attempt to fall asleep or instructing subject to resist sleep.
420 citations
TL;DR: The single unit activity of presumed noradrenergic neurons in the area of the locus coeruleus (LC) was recorded in freely moving cats, consistent with a general role for NE-LC neurons inThe organism's adaptive response to environmental and physiological challenges.
318 citations
TL;DR: Delta activity showed a decreasing trend in all schedules and was enhanced as a function of prior waking, and theta activity and REM sleep were increased after 24 h SD.
305 citations
TL;DR: Electroencephalographic and behavioral findings seen following CRF and GRF are consistent with the behaviors frequently correlated with the known circadian timing of the release of corticosteroids and growth hormone during the sleep-waking cycle in rat and human.
Abstract: The effects of corticotropin-releasing factor (CRF) and growth hormone-releasing factor (GRF) on electroencephalographic (EEG) and behavioral signs of sleep and wakefulness following intracerebroventricular (ICV) administration was investigated in adult male rats. Visual scoring of EEG records as well as spectral analysis revealed that CRF (0.0015-0.015 nmol) produced decreases in slow wave sleep concomitant with significant decreases in spectral power in lower frequencies (1-6 Hz) and increases in high frequencies (32-64 Hz). In contrast, GRF (2.0 nmol) produced increased EEG and behavioral signs of slow wave sleep associated with significant increases in spectral power in the low frequencies (1-2 Hz) and decreases in high frequencies (32-64 Hz). ICV administration of GRF was also found to produce decreases in locomotion when administered during the active part of the rats' circadian cycle. These EEG and behavioral findings seen following CRF and GRF are consistent with the behaviors frequently correlated with the known circadian timing of the release of corticosteroids and growth hormone during the sleep-waking cycle in rat and human.
301 citations
TL;DR: Dramatic increase in IL‐1 activity along with changes in other immune functions occurred during sleep and were related to onset of slow wave sleep.
Abstract: Serial sampling of peripheral blood from six healthy adult male volunteers was performed during daytime waking and nighttime sleeping. In addition, sleep physiology was assessed in all subjects (Ss) and sleep stages scored blind by standard criteria. Samples of plasma were analyzed for cortisol (Co) levels, functional interleukin-1 (IL-1), and interleukin-2 (IL-2) activity. Peripheral blood monocytes (PBM) were assayed to evaluate natural killer (NK) activity and mitogen responsiveness. Dramatic increase in IL-1 activity along with changes in other immune functions occurred during sleep and were related to onset of slow wave sleep.
235 citations
TL;DR: The finding that a serotonin antagonist changed the architecture of sleep without producing insomnia is of fundamental importance and calls for a re-examination of traditional theories of sleep control which assign a facilitatory role to serotonin.
233 citations
TL;DR: It is noteworthy, therefore, that the central biochemical changes induced by GHB also appear comparable to those found naturally in narcolepsy.
Abstract: Previous studies on the effects of gamma-hydroxybutyrate (GHB) on the sleep and clinical response of patients with narcolepsy are reviewed. New information on 48 patients treated with GHB for as long as 9 years is presented. These studies indicate that 2.25 to 3.00 g of GHB, taken in conjunction with a low dose of a stimulant during the day, rapidly alleviate the symptoms of narcolepsy in most patients. Tolerance does not develop to this treatment regimen; neither have any patients discontinued the treatment because of side effects. In poor responders, daytime drowsiness and not cataplexy has been the most common residual symptom. Sleep studies reveal that GHB induces REM followed by slow wave sleep. Although total sleep time at night may be unchanged, sleep is less fragmented. GHB appears to be effective because it can induce the symptoms of narcolepsy and contain them at night. It is noteworthy, therefore, that the central biochemical changes induced by GHB also appear comparable to those found naturally in narcolepsy.
227 citations
TL;DR: These data lend particular support to a functional relation between wave A and the ascending reticular activating system and suggest that this potential may provide a unique and dynamic probe of tonic brain activity.
225 citations
TL;DR: Zolpidem is likely to prove useful in the management of transient and short-term insomnia in healthy middle aged individuals when impaired performance the next day is to be avoided.
Abstract: Effects of an imidazo-pyridine (zolpidem: 10, 20 and 30 mg) on overnight sleep and on performance the next day were studied in young adults and in middle aged individuals. The young adults were used particularly as an homogenous group to establish any possible adverse effects of the drug on sleep and on performance the next day, and the middle aged subjects with their less restful sleep were used to study efficacy. In the young adults zolpidem led to a marked increase in slow wave sleep with a reduction in stage 2 sleep. There were no significant changes in REM sleep, though there was a tendency for REM sleep to be delayed. In the middle aged there was a reduction in awake activity and drowsy sleep with an increase in stage 2 sleep. The latency to REM sleep was increased but the duration of REM sleep over the whole night was not reduced. Digit symbol substitution and a complex reaction time task were used to study performance, but there were no residual effects with zolpidem (9 h after ingestion). Zolpidem is likely to prove useful in the management of transient and short-term insomnia in healthy middle aged individuals when impaired performance the next day is to be avoided.
114 citations
TL;DR: It is concluded that LPS and lipid A are capable of modulating sleep and their effects were present primarily during the first 3 h postinjection.
Abstract: Some muramyl peptides derived from bacterial peptidoglycan enhance slow-wave sleep (SWS). The purpose of this study was to test whether another cell wall component, lipopolysaccharide (LPS), and its lipid A moiety also have an effect on sleep. When injected intravenously, both LPS and lipid A enhanced the duration of SWS, increased electroencephalogram delta-wave amplitudes, suppressed rapid eye movement (REM) sleep, and induced biphasic fevers. The effects of intravenously administered lipid A and LPS on SWS were present primarily during the first 3 h postinjection. Intraventricular lipid A administration enhanced SWS, did not suppress REM, and induced a monophasic fever; the SWS effect had a 3-h latency, whereas temperature started to rise during the second hour. Regardless of the route of administration, within the dose range used here, sleep was normal by the following criteria: sleep was episodic, animals could be easily aroused, and brain temperature, although elevated to "febrile" levels, continued to fluctuate during sleep-state transitions indistinguishably from control conditions. We conclude that LPS and lipid A are capable of modulating sleep.
TL;DR: Results suggest that SRIF may be involved in the regulation of PS, and administration of cysteamine brought about a dose-dependent reduction of PS.
TL;DR: To determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep, normal young adults spent two 4-night periods in the laboratory.
TL;DR: Just prior to the onset of the first pronounced rise in plasma cortisol during sleep, episodes of slow wave sleep (SWS) became more frequent, which suggests that the offset of episodes of SWS may act as a trigger for thefirst pronounced nocturnal rise in Plasma cortisol.
TL;DR: Increased alertness was not strongly related to the sleep stage composition of the naps, the best predictor being minutes of slow wave sleep, and was not detected until the second latency test 4 hrs after napping.
Abstract: The effect of napping for varying durations after one night of sleep deprivation was examined. Sleep latency tests were used to determine levels of sleepiness/alertness at 2, 4, 6, and 8 hrs following a morning nap of 0, 15, 30, 60, or 120 min duration. Ten normal-sleeping, young adult volunteers spent two consecutive days and the intervening night in the sleep laboratory on each of five weeks. Baseline sleep latencies were recorded the first day, sleep was deprived that night, a nap was taken at 0900 hrs, and sleep latencies were again recorded on the second day. The naps had differential alerting effects related to their duration, but none of the naps returned mean sleep latency for the 8 hrs to its basal levels. Alertness increased with nap duration, reaching its highest level with a 60-min nap; the 120-min nap was no more alerting than the 60-min nap. During the second hour of the 120-min nap, sleep became more fragmented with more shifts to stage 1 sleep or wake. Increased alertness was not strongly related to the sleep stage composition of the naps, the best predictor being minutes of slow wave sleep. Increased alertness was not detected until the second latency test 4 hrs after napping.
TL;DR: Demonstration of selected EEG sleep variables discriminating between psychotic and nonpsychotic depression further supports psychotic depression as a distinct subtype of major affective disorder.
Abstract: • Electroencephalographic (EEG) sleep patterns were examined in 27 psychotic and 79 nonpsychotic subjects with major depression to evaluate the validity of the psychoticnonpsychotlc subtype dichotomy. Sleep in psychotic depression was characterized by increased wakefulness, decreased rapid eye movement (REM) sleep percentage, and decreased REM activity even after controlling for clinical differences in age, severity, and agitation. Psychotic depressive subjects also were more likely to have extremely short sleep-onset REM latencies. In psychotic depression EEG sleep varied as a function of total illness duration. Patients with recent-onset syndromes had profiles characterized by marked initial insomnia, Increased stage 1 sleep percentage, and long REM latency; patients with illnesses of longer duration had extremely short REM latencies. Demonstration of selected EEG sleep variables discriminating between psychotic and nonpsychotic depression further supports psychotic depression as a distinct subtype of major affective disorder.
TL;DR: It is suggested that the ability of older women to achieve slow wave sleep and to have long uninterrupted sleep in greater than that of men.
Abstract: Elderly women had better recovery sleep than elderly men following 36-h sleep deprivation, as evidenced by higher sleep maintenance/efficiency and more slow wave sleep (particularly in the amount of stage 4 sleep). During recovery sleep, both groups showed REM latency reduction (two men and three women had seven sleep-onset REM periods out of a total of 40 recovery nights), decrease in percentage of early REM sleep and increase in whole-night REM sleep time. Total Mood Disturbance scores on the Profile of Mood States increased in both men and women following sleep deprivation (reflecting a decrease in vigor and increase in fatigue and tension). While the increase tended to be greater in women, in both groups self-ratings of mood returned to baseline after 1 night of recovery sleep. These observations underscore the importance of gender in determining late-life sleep structure and suggest that the ability of older women to achieve slow wave sleep and to have long uninterrupted sleep in greater than that of men.
TL;DR: The results indicated that the descending noradrenaline locus coeruleus fibers and the "longitudinal catecholamine bundle," which course through the dorsal tegmentum, are not necessary for the generation of muscle atonia or the state of paradoxical sleep.
Abstract: A retractable wire knife was employed to transect the reticular formation at the pontomedullary junction in order to assess the respective importance of pontine and medullary reticular neurons and their pathways in paradoxical sleep. Thirteen cats were implanted with a standard array of electrodes for polygraphic recording of sleep-wakefulness states during 3 days in baseline condition and during 21 days after transections. Average electroencephalographic (EEG) amplitude, average electromyographic (EMG) amplitude, and ponto-geniculo-occipital (PGO) spike rate were measured per 1-min epoch for each day. A trivariate computer graphics display of 1 day's data revealed three major clusters of points that corresponded to wakefulness, slow wave sleep, and paradoxical sleep in baseline. (a) After transections through the entire reticular formation at the pontomedullary junction, paradoxical sleep was no longer evident in the trivariate computer graphics or polygraphic record, either by the presence of a high PGO spike rate or by that of muscle atonia in association with a low-amplitude EEG. These results indicated that the reticular fibers that pass through the pontomedullary junction and interconnect the pontine tegmentum and the medullary reticular formation are necessary for generating the cluster of electrographic variables that normally characterizes paradoxical sleep. (b) After transections through the dorsal half of the reticular formation, paradoxical sleep was still evident, though with a reduced PGO spike rate, and muscle atonia was normal. These results indicated that the descending noradrenaline locus coeruleus fibers and the "longitudinal catecholamine bundle," which course through the dorsal tegmentum, are not necessary for the generation of muscle atonia or the state of paradoxical sleep. (c) After transections through the ventral half of the reticular formation, paradoxical sleep was still apparent by the association of a moderate, though reduced, rate of PGO spiking in association with low-amplitude EEG activity and a high-amplitude EMG, indicating a loss of muscle atonia. The duration of the PS episodes, however, was greatly reduced. These results indicated that the descending "tegmentoreticular" and ascending reticulotegmental pathways, which course ventrally through the pontomedullary junction and interconnect the dorsolateral pontine tegmentum and the ventromedial medullary reticular formation, are essential for the muscle atonia of paradoxical sleep and important for the normal cyclic generation and maintenance of the state of paradoxical sleep.
TL;DR: Although the younger depressed patients showed increased numbers of delta waves, the middle-aged depressives showed greater average REM count and little statistical relationship between manual measures of slow-wave sleep and automated measures of delta sleep was found.
TL;DR: A statistical comparison of both experiments suggested that both steroids not only reduced REM sleep but also tended to enhance intermittent wakefulness, which represents a first demonstration of differential effects of synthetic and natural corticosteroids on sleep.
Abstract: The present two experiments were designed to investigate the effects of a synthetic and of a natural corticosteroid on nocturnal sleep in humans. Both experiments were held double-blind and designed according to a within-subject cross-over comparison. In the first experiment, 1 mg of dexamethasone applied orally prior to sleep (11.00 p.m.) led to a reduction of the percent of time spent in REM and in stage 4 sleep. The amount of stage 2 sleep tended to be increased after dexamethasone. In the second experiment, an infusion of 100 mg hydrocortisone throughout the night also reduced REM, but increased stage 4 sleep. A statistical comparison of both experiments suggested that both steroids not only reduced REM sleep but also tended to enhance intermittent wakefulness. This analysis also confirmed opposite effects on measures of slow-wave sleep of both substances. The results represent a first demonstration of differential effects of synthetic and natural corticosteroids on sleep, which has to be substantiated in further studies directly comparing effects of these steroids.
TL;DR: Challenges to the thermoregulatory system can be used as a vehicle to systematically alter sleep architecture in humans, and the ability to maintain a sleep state was significantly impaired during the cold stress.
TL;DR: Findings suggest that subjectively poor sleep is not necessarily "light" sleep, and there was little relationship between reported habitual aspects of sleep and baseline polygraphically defined sleep variables.
Abstract: Ten insomniacs with age- and sex-matched controls had studies of baseline sleep, relation of polygraphically defined sleep to retrospective reports, and arousal thresholds to electronic tones or to a recording of a voice calling out the subject's name. The two groups differed in 10 out of 13 questions about habitual sleep and daytime feelings. In contrast, polygraphic measures of baseline sleep indicated only that insomniacs tended to have slightly less total sleep and had a small but significant increase in early morning awakening time. Unlike the descriptions of habitual sleep, the subjects' retrospective reports of the previous night's sleep differed significantly only for the variable of total sleep time, and there were virtually no differences in the description of their status at a given moment. Auditory arousal thresholds were similar in the two groups, and both went back to sleep and stayed asleep with equal facility. These findings suggest that subjectively poor sleep is not necessarily "light" sleep. For both groups, arousal thresholds differed across the sleep stages, and thresholds to hearing the subject's name were lower than those in response to electronic tones. Although insomniacs had as much polygraphically defined sleep as controls between the forced awakenings of the arousal threshold studies, they perceived their sleep to be only approximately half as long. Insomniacs described themselves as having been awake more frequently than controls in 8 out of 10 forced awakening situations. In one case, insomniacs also overestimated the time between awakenings. In both groups, there was little relationship between reported habitual aspects of sleep and baseline polygraphically defined sleep variables. On questionnaires the following mornings, however, in both groups there was a positive correlation of subjective quality of sleep on the baseline nights with percentage of rapid eye movement sleep, and a negative correlation to various aspects of slow-wave sleep.
TL;DR: The results show that homeostatic influences on sleep may be much larger than usually acknowledged and that SWS closely, although not perfectly, reflects the “active component’ of sleep homeostasis.
Abstract: Recent concepts of sleep/wake regulation have emphasized circadian influences and largely disregarded homeostatic ones. The present experiment was designed to study sleep loss homeostasis while minimizing confounding circadian influences. Eight male subjects participated in the study. Night sleep was curtailed across four conditions to yield 0, 2, 4, or 8 hrs of sleep. The effects were studied on subsequent day sleep begun at 1100h and spontaneously terminated. Total sleep time (TST), Stage 2 (S2), and Stages 3+4 (SWS) showed very strong dose-dependent increases with increasing loss. REM sleep did not respond. After maximum sleep loss TST and S2 doubled whereas SWS increased fivefold. Sleep did not terminate until the prior loss of SWS had been recovered. The total SWS recovery approximately matched the loss. TST, S2, and REM failed to recover more than limited amounts of the loss. The results show that homeostatic influences on sleep may be much larger than usually acknowledged and that SWS closely, although not perfectly, reflects the “active component’ of sleep homeostasis.
TL;DR: The Markov chain model simulates both probabilistic and the above-mentioned predictable dynamics of sleep, but only if these time-varying, individual rates are applied.
Abstract: Summary: A Markov chain model has been proposed as a mechanism that generates human sleep stages, A method for estimating the parameters of the model, i.e., the transition probabilities (rates) between sleep stages, has been introduced and applied to 95 hypnograms taken from 23 subjects. The rates characterize interindividual differences and nightly variations of the sleep mechanism, related to sleep-onset behavior, to the decreasing amount of slow wave sleep in the course of the night, and to the REM-NREM periodicity, The model simulates both probabilistic and the above-mentioned predictable dy namics of sleep, but only if these time-varying, individual rates are applied.
TL;DR: Intracellular electrical recordings in an in vitro slice preparation of the brainstem medial pontine reticular formation demonstrate a population of neurons that have a calcium-dependent, low threshold spike that may underlie changes in action potential firing patterns associated with behavioral state change.
Abstract: Intracellular electrical recordings in an in vitro slice preparation of the brainstem medial pontine reticular formation, a region thought to be important in mediation of desynchronized sleep phenomena, demonstrate a population of neurons that have a calcium-dependent, low threshold spike. This low threshold spike was inactivated at relatively depolarized membrane potential levels and, when this spike was deinactivated, it induced a burst of action potentials. The membrane potential dependence of the spike may underlie changes in action potential firing patterns associated with behavioral state change because the baseline membrane potential in neurons of the medial pontine reticular population depolarizes during passage from waking and slow wave sleep to desynchronized sleep, which is characterized by the absence of burst firing.
TL;DR: The hypothesis of a REM-inducing and regulating function of the right hemisphere is supported and will lead to a new understanding of sleep-controlling mechanisms.
Abstract: In 19 patients with cerebral infarctions in the middle cerebral artery territory, investigations of sleep using a mobile EEG recording system were performed. Sleep was found to be markedly altered compared to a normal group. Although an increase of time in bed and sleep period time was observed, total sleep time did not rise in a parallel manner, so that a distinct reduction of the sleep efficiency index was found. This increase of quantitative parameters was particularly caused by a higher amount of NREM time, whereas REM sleep was found to be deeply suppressed. Regarding the different NREM sleep stages, stage 0 (time spent awake during the night) and stage 1 had increased, whereas stage 4 was reduced. Inter-hemispheric differences were noticed referring to the sleep period time, which was found to be increased particularly in right-sided infarctions (because of an increase of NREM time) and a reduction of REM sleep in lesions of the right hemisphere (worsening of the REM to NREM ratio). Slow-wave sleep (stage 4), on the contrary, was found to be decreased in infarctions of the left hemisphere. These results support the hypothesis of a REM-inducing and regulating function of the right hemisphere and will lead to a new understanding of sleep-controlling mechanisms.
TL;DR: An increased frequency of sleep onset REM periods in psychotic depression and in elderly depressed patients (psychotic or nonpsychotic) and outpatients is suggested.
Abstract: Electroencephalographic (EEG) sleep changes in affective disorders have been characterized by sleep continuity, slow wave sleep, and rapid eye movement (REM) abnormalities. The most commonly cited feature, however, has been shortened REM latency. Because the diagnostic and prognostic significance of shortened REM latency has been debated, this issue was reexamined in a group of 186 psychotic and nonpsychotic depressed inpatients and outpatients. The analyses suggest an increased frequency of sleep onset REM periods in psychotic depression and in elderly depressed patients (psychotic or nonpsychotic).
TL;DR: The studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.
Abstract: Previous investigation in normal humans has demonstrated reduced ventilation and ventilatory responses to chemical stimuli during sleep. Most have interpreted this to be a product of decreasing central nervous system sensitivity to the normal stimuli that maintain ventilation, whereas other factors such as increasing airflow resistance could also contribute to this reduction in respiration. To improve our understanding of these events, we measured ventilation and occlusion pressures (P0.1) during unstimulated ventilation and rebreathing-induced hypercapnia during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Eighteen subjects (10 males and 8 females) of whom seven were snorers (5 males and 2 females) were studied. Ventilation was reduced during both NREM and REM sleep (P less than 0.05), but this decrement in minute ventilation tended to be greater in snorers than nonsnorers. Unstimulated P0.1, on the other hand, was maintained or increased during sleep in all groups studied, with males and snorers showing the largest increase. The hypercapnic ventilatory response fell during both NREM and REM sleep and tended to be lower during REM than NREM sleep. However, the P0.1 response to hypercapnia during NREM sleep was well maintained at the waking level although the REM response was statistically reduced. These studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.
TL;DR: It looks as though non-specific platform effects override the effects of PS deprivation, and it is improbable that the platform-pendulum controversy is due to differences in the amount ofPS deprivation or the other sleep parameters measured here.
TL;DR: REM sleep propensity, as measured by the number of naps with REM and the amount of REM sleep among those naps that contained REM, was affected only by the circadian phase of the nap, with trough naps containing significantly less REM, and SWS remained wake-responsive at both phases of the diurnal cycle.