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Showing papers on "Slow-wave sleep published in 1990"


Journal ArticleDOI
TL;DR: Evidence supports a hypothesis that slow-wave sleep in mammals and birds is controlled by thermoregulatory mechanisms, and provides brain and body cooling as a primary homeostatic feedback process, and this concept provides a comprehensive model for analysis of sleep homeostasis.

369 citations


Journal ArticleDOI
TL;DR: It is concluded that anesthesia with upper abdominal surgery leads to a severe disruption of nocturnal sleep followed by the release of highly intense REM sleep about the middle of the first postoperative week.
Abstract: Characteristics of nocturnal sleep were investigated in six patients after anesthesia and cholecystectomy and in another six after anesthesia and gastroplasty. All night polysomnographic recordings were obtained while each patient slept in a private surgical ward room through two nights before and five or six nights after operation. Anesthesia included thiopental, N2O, isoflurane, and fentanyl. Postoperative analgesia was provided with parenteral morphine. Other aspects of care were routine. Nocturnal sleep was markedly disturbed after both surgical procedures. Throughout the operative night and subsequent one or two nights, sleep was highly fragmented with the usual recurring cycles of sleep stages completely disrupted. Slow wave sleep was suppressed and rapid eye movement (REM) sleep virtually eliminated. During the following 2-4 nights, as other aspects of sleep recovered, REM sleep reappeared and then increased to greater than the preoperative amount. This increased REM sleep was marked by a heavy density of eye movement activity along with frequent patient reports of unusually distressing dreams or vivid nightmares. It is concluded that anesthesia with upper abdominal surgery leads to a severe disruption of nocturnal sleep followed by the release of highly intense REM sleep about the middle of the first postoperative week.

301 citations


Journal ArticleDOI
TL;DR: It is hypothetized that energy requirements for maintaining membrane polarity are reduced during SWS because of a decreased rate of synaptic events and increased need for ion gradients maintenance while during REMS, cerebral glucose utilization is similar to that of wakefulness.

258 citations


Journal ArticleDOI
TL;DR: Analysis of data on 74 patients in a long-term maintenance treatment study for a minimum of 24 months demonstrates that the delta sleep ratio can predict survival time following discontinuation of drug treatment.
Abstract: • Slow wave sleep abnormalities have long been described in depression but were considered to be nonspecific indicators of psychopathology. Computerized techniques, including amplitude frequency measures and spectral analyses, are permitting new approaches to the examination of delta sleep. Early studies suggested that many depressed patients demonstrate lower delta wave intensity during the first non—rapid eye movement period than the second one. This finding, prominent in middle-aged depressed patients, has led to an examination of the ratio between the first and second non—rapid eye movement periods. This delta sleep measure seems to be a more robust predictor of recurrence than rapid eye movement latency. Analysis of data on 74 patients in a long-term maintenance treatment study for a minimum of 24 months demonstrates that the delta sleep ratio can predict survival time following discontinuation of drug treatment. Individuals with a high delta sleep ratio remain clinically remitted five times longer than those with a low delta sleep ratio.

231 citations


Journal ArticleDOI
TL;DR: It is concluded that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia, and other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.
Abstract: In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.

231 citations


Journal ArticleDOI
TL;DR: The present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep, and it is concluded that the time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote.
Abstract: In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

219 citations


Journal ArticleDOI
01 Oct 1990-Sleep
TL;DR: It is concluded that, in accordance with the two-process model of sleep regulation, slow wave activity in NREM sleep depends on prior waking and is not significantly influenced by circadian phase.
Abstract: Human sleep electroencephalograms, recorded in four experiments, were subjected to spectral analysis. Waking prior to sleep varied from 12 to 36 h and sleep was initiated at different circadian phases. Power density of delta and theta frequencies in rapid-eye-movement (REM) sleep and non-REM (NREM) sleep increased monotonically as a function of prior waking. The increase of power density in the theta frequencies contrasts with the reported decrease of theta activity as detected by period-amplitude analysis. Slow wave activity (power density, 0.25-4.0 Hz) in NREM sleep during the first 3 h of sleep did not deviate significantly from the homeostatic process S of the two-process model of sleep regulation. In contrast, visually scored slow wave sleep, stages 3 and 4, deviated from this prediction at some circadian phases. It is concluded that, in accordance with the two-process model of sleep regulation, slow wave activity in NREM sleep depends on prior waking and is not significantly influenced by circadian phase.

202 citations


Journal ArticleDOI
TL;DR: It is concluded that while sleep/wake patterns are significantly disturbed in AD, this phenomenon is not diagnostically useful for discrimination of mild stage AD.
Abstract: We examined the ability of sleep/wake measures to discriminate 45 control subjects from 44 mild Alzheimer's disease (AD) patients. Sleep fragmentation was observed as indicated by significant increases in time awake (37-52%) and number of awakenings (31-36%) during the night as compared to controls. Further, slow wave sleep (SWS) was significantly reduced (22%) in AD patients relative to controls. These findings are consistent with our earlier observations of increased wakefulness and decreased SWS in mild-moderate, moderate-severe, and severe stage AD patients. However, when we used these sleep/wake stage measures in discriminant analyses to classify the current AD subjects vs control subjects, the analyses failed to confirm our earlier high classification rate (90%). The present groups were discriminated at overall classification rates of only 63-67%. We conclude that while sleep/wake patterns are significantly disturbed in AD, this phenomenon is not diagnostically useful for discrimination of mild stage AD.

200 citations


Journal ArticleDOI
TL;DR: It is concluded that in the early part of the light period, 3 h waking prolongs non-REM sleep, whereas 6 h waking also enhances non- REM sleep intensity.

191 citations


Journal ArticleDOI
TL;DR: It is shown that the moderate reduction of slow wave energy in the deprivation nights induces only a minor enhancement ofSlow wave activity during recovery sleep; and that a REM sleep deficit gives rise to an immediate rebound when 'slow wave pressure' is low.

171 citations


Journal ArticleDOI
TL;DR: The data suggest that SWS sleep favors the restoration of cerebral proteins, and the occurrence of SWS is associated with higher rates of protein synthesis throughout the brain.

Journal ArticleDOI
TL;DR: In this paper, sleep, mood, and performance responses to acute sleep deprivation in healthy 80-year-olds and 20-yearolds were investigated, and the effects of total sleep loss in the 'old old' (i.e., 80-years old) were found to be more disruptive than for the young.
Abstract: Little is known about sleep and the effects of total sleep loss in the 'old old' (i.e., 80-year-olds). We investigated sleep, mood, and performance responses to acute sleep deprivation in healthy 80-year-olds (n = 10) and 20-year-olds (n = 14). The protocol consisted of three nights of baseline sleep, one night of total sleep deprivation, and two nights of recovery sleep. Mood and vigilance were tested using visual analog scales and a Mackworth clock procedure in the morning and evening of each study day. Daytime sleepiness was measured by five naps on the days following the third and sixth nights. Old subjects had lower sleep efficiency and less delta sleep than young subjects. However, sleep continuity and delta sleep were enhanced in both groups on the first recovery night, indicating that sleep changes in old subjects are at least partially reversible by this procedure. Surprisingly, young subjects had shorter daytime sleep latencies than the old, suggesting a greater unmet sleep need in the former group. Mood and performance were disturbed by sleep loss in both groups, but to a greater extent among the young. This suggests that acute total sleep loss is a more disruptive procedure for the young than for the old.

Journal ArticleDOI
TL;DR: The results revealed that the intracerebral dialysis technique provides a useful method to monitor changes in spontaneous neurotransmitter release during the sleep-waking cycle.

Journal ArticleDOI
TL;DR: Through this model of transient situational insomnia it was possible to outline different degrees of subjective complaint depending on 3 ranges of CAP/NREM, and a crucial role of CAP in the pathophysiological mechanisms of clinical insomnia is hypothesized.

Journal ArticleDOI
TL;DR: It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.

Journal ArticleDOI
TL;DR: In this article, a substantial body of research in adults has established that certain sleep polysomnographic abnormalities are commonly found in depressed patients, including sleep continuity disturbances, reduced slow-wave sleep, shortened rapid eye movement (REM) latency, and increased REM density.
Abstract: • A substantial body of research in adults has established that certain sleep polysomnographic abnormalities are commonly found in depressed patients, including sleep continuity disturbances, reduced slow-wave sleep, shortened rapid eye movement (REM) latency, and increased REM density. To date, these abnormalities have not been documented in depressed children compared with age-matched controls. Three consecutive nights of polysomnographic recordings were obtained in 25 hospitalized depressed children and 20 age-matched healthy controls. The depressed patients had reduced REM latencies. The shortest single-night REM latency of each individual was the most sensitive discriminating value between depressed subjects and controls. The influence of different scoring criteria in distinguishing depressed children from healthy children is discussed. In addition, depressed children had an increased sleep latency and increased REM time but did not have stage 4 differences.

Journal ArticleDOI
TL;DR: Electroencephalogram (EEG) sleep recordings were compared in 34 normal controls and 31 inpatients with relatively pure primary alcoholism who had been abstinent for about 17 days, finding primary alcoholics took longer to fall asleep, slept less, and had poor sleep efficiency.

Journal ArticleDOI
TL;DR: It appears that reduced slow wave sleep may be related to a neurodevelopmental disorder related to the defect state in schizophrenia, and the pathophysiological significance of the defective REM rebound and the REM sleep abnormalities in schizophrenia remain uncertain.

Journal ArticleDOI
TL;DR: The observed effects of Org 3770 on normal human sleep suggest that it might ameliorate the sleep disturbances encountered in endogenous depression, which are characterized by a reduction in slow wave sleep, an increase in nighttime awakenings and shortening of REM sleep latency.
Abstract: The effect of a single dose (30 mg) of Org 3770 (metirzapine) on human sleep was assessed in a double blind, placebo controlled, cross over study in 6 young, healthy male volunteers. The sleep stage classification was based on visual scoring of 24 h electroencephalographic recordings according to the criteria of Rechtschaffen and Kales. Org 3770 30 mg p.o. given 2 h before bedtime had a sleep promoting action in all subjects, resulting in a shortened time to the onset of sleep. Bedtime waking and dozing (Stage 1) were reduced in favour of deep, slow wave sleep (Stages 3 and 4). Org 3770 increased the latency of REM sleep with respect to Stage 2 sleep in all subjects. It also caused a minor reduction in waking periods during REM sleep and a lower frequency of awakenings after periods of movement. No effect of Org 3770 was observed in reaction and vigilance tests on the post treatment day. The observed effects of Org 3770 on normal human sleep suggest that it might ameliorate the sleep disturbances encountered in endogenous depression, which are characterized by a reduction in slow wave sleep, an increase in nighttime awakenings and shortening of REM sleep latency.

Journal ArticleDOI
01 Aug 1990-AIDS
TL;DR: It is suggested that sleep disturbances occur early in the course of HIV infection and suggests that the observed alterations of sleep physiology may be a consequence of central nervous system involvement and/or immune defense mobilization in the early phases of HIV infections.
Abstract: To provide a better understanding of the etiology of subjective sleep complaints in HIV-infected individuals, a study to evaluate sleep/wake disturbances in 10 healthy HIV-infected male volunteers was performed. All subjects were HIV-infected but had no history of AIDS-related infections, and considered clinically asymptomatic. Interviews and sleep questionnaires revealed sleep complaints in nine subjects. Five healthy HIV-seronegative male subjects, with no history of sleep complaints, were also evaluated. Sleep architecture analyses detected that, in comparison to published normative data and to negative controls, there was a significant increase in the total percentage of slow wave sleep (SWS) and an increase in the percentage of SWS in the later sleep cycles. When compared with normative data, an increase in stage 1 shifts, rapid eye movement (REM) periods, and arousals were also observed in the HIV-infected group. Significant decreases in sleep latency, total percentage stage 2 sleep, and average REM durations were also observed in the HIV-infected group compared with normative data. These sleep architecture abnormalities could not be attributed to known sole primary sleep disorders, first night effect, medications, anxiety or depression. This study indicates that sleep disturbances occur early in the course of HIV infection and suggests that the observed alterations of sleep physiology may be a consequence of central nervous system involvement and/or immune defense mobilization in the early phases of HIV infection.

Journal Article
TL;DR: It is proposed that the brain serotonergic system exerts a modulatory influence over its target structures so as to coordinate their activity with the organism's sleep-wake-arousal state (level of behavioral arousal).

Journal ArticleDOI
01 Jan 1990-Sleep
TL;DR: GHB administered before nocturnal or diurnal sleep increases stages 3 and 4 and decreases stage 1 non-rapid eye movement (NREM) sleep and slightly decreases REM latency when administered in the morning, and this effect is correlated with age.
Abstract: Gamma-hydroxybutyrate (GHB) is a drug currently used to treat narcolepsy. The present study documents its effect on sleep organization in healthy subjects. GHB and a placebo were given at bedtime and before a morning nap in a double-blind fashion. GHB administered before nocturnal or diurnal sleep increases stages 3 and 4 and decreases stage 1 non-rapid eye movement (NREM) sleep. In addition, GHB improves REM efficiency at night and reduces wake time after sleep onset when administered before a morning nap recording. GHB also slightly decreases REM latency when administered in the morning, and this effect is correlated with age. Hypotheses regarding mechanisms of action GHB and the involvement of hypothalamic structures in the regulation of REM sleep are discussed.

Journal ArticleDOI
TL;DR: Findings point to a direct inhibition of central cholinergic PGO-on neurons via a muscarinic autoreceptor and a difference in the mechanisms underlying the generation of tonic and phasic burst activity of PGO -on neurons occurring during waking and sleep.

Journal ArticleDOI
TL;DR: Slowing ofREM sleep-off cells in waking is hypothesized to counteract the functional effects of REM sleep loss on noradrenergic receptor sensitivity and may contribute to the loss of vigilance seen with sleep deprivation.

Journal ArticleDOI
TL;DR: It is demonstrated that even high-risk infants show behavioral states by 29 weeks CA and that considerable state development occurs over the preterm period, and additional research is needed to determine the effects of time of day, caregiving environments, and specific insults on state development.
Abstract: This study examined the development of sleeping and waking states in high-risk preterm infants. Thirty-seven preterm infants were observed from 7 p.m. to 11 p.m. weekly from the time their conditions were no longer critical until term age or hospital discharge. An average of 3.6 observations was conducted on each infant between 29 and 39 weeks conceptional age (CA). During the observations, the occurrence of eight sleep-wake states was recorded every 10 s. The intensity of rapid eye movements in active sleep and the regularity of respiration in quiet sleep were also rated. Similar state patterns were found at all ages, with active sleep the most frequent state, quiet sleep the second most frequent, and drowsiness and sleep-wake transition third and fourth. Waking states made up only small percentages of the observations at every age. Despite these similarities, four states exhibited significant changes over age: the amount of active sleep decreased, and fuss, cry, and quiet sleep increased. The organization of the sleep states also increased, as evidenced by an increase in the percent of active sleep with rapid eye movements and an increase in the regularity of respiration in quiet sleep. The severity of illness experienced by the infants had only minor effects on these patterns. These findings demonstrate that even high-risk infants show behavioral states by 29 weeks CA and that considerable state development occurs over the preterm period. Additional research is needed to determine the effects of time of day, caregiving environments, and specific insults on state development.

Journal ArticleDOI
01 Jan 1990-Sleep
TL;DR: Improved sleep quality was reflected in improved daytime psychomotor performance and alertness and imply that benzodiazepine use may be beneficial in patients with central sleep apnea.
Abstract: It was hypothesized that triazolam might decrease central apneas associated with arousal periods in patients with central sleep apnea by hastening the onset of consolidated sleep Five male patients, diagnosed as having central sleep apnea on a screening night, participated in a double-blind randomized crossover study of the effect of placebo, 0125 mg triazolam, and 025 mg triazolam on sleep, respiration, and daytime function Results indicated that the medication increased total sleep and decreased central apnea index and number of brief arousals Improved sleep quality was reflected in improved daytime psychomotor performance and alertness These data, if replicated, imply that benzodiazepine use may be beneficial in patients with central sleep apnea

Journal ArticleDOI
TL;DR: Reduction in the activity of upper airway "dilator" muscles during sleep was shown to result from a sleep-related decline in the level of tonic muscle activity, and phasic inspiratory activity during wakefulness and sleep was exhibited in all subjects.
Abstract: Reduction in the activity of upper airway "dilator" muscles during sleep may allow the pharyngeal airway to collapse in some individuals. However, quantitative studies concerning the effect of sleep on specific upper airway muscles that may influence pharyngeal patency are sparse and inconclusive. We studied seven normal men (mean age 27, range 22-37 yr) during a single nocturnal sleep study and recorded sleep staging parameters, ventilation, and geniohyoid muscle electromyogram (EMGgh) during nasal breathing throughout the night. Anatomic landmarks for placement of intramuscular geniohyoid recording electrodes were determined from a cadaver study. These landmarks were used in percutaneous placement of wire electrodes, and raw and moving-time-averaged EMGgh activities were recorded. Sleep stage was determined using standard criteria. Stable periods of wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep were selected for analysis. The EMGgh exhibited phasic inspiratory activity during wakefulness and sleep in all subjects. In six of seven subjects, mean and peak inspiratory EMGgh activities were significant (P less than 0.05) reduced during stages 2 and 3/4 NREM sleep and REM sleep compared with wakefulness. This reduction of EMGgh activity was shown to result from a sleep-related decline in the level of tonic muscle activity. Phasic inspiratory EMGgh activity during all stages of sleep was not significantly different from that during wakefulness. Of interest, tonic, phasic, and peak EMGgh activities were not significantly reduced during REM sleep compared with any other sleep stage in any subject. In addition, the slope of onset of phasic EMGgh activity was not different during stage 2 NREM and REM sleep compared with wakefulness in these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Journal ArticleDOI
TL;DR: The prediction that in rats neonatal clomipramine (CLI) will produce adult animals that model endogenous depression was tested and it was found that neonatal treatment with CLI produced rats that at age 6 months had shorter REM latency, more sleep onset REM periods, and after RSD, had an abnormal temporal course of REM rebound in the presence of a normal total REM rebound.

Journal Article
TL;DR: The alpha-adrenergic receptor-blocking property of trazodone and a relative lack of noradrenaline reuptake blocking and the lack of anticholinergic effects are hypothesized to be responsible for the effects on sleep.
Abstract: The effects of trazodone on sleep were compared with those of placebo and the sedating tricyclic antidepressant trimipramine in a double-blind crossover study in six healthy young men. Only trazodone significantly increased deep sleep without otherwise altering the normal architecture of sleep. The alpha-adrenergic receptor-blocking property of trazodone and a relative lack of noradrenergic reuptake blocking and the lack of anticholinergic effects are hypothesized to be responsible for the effects on sleep.

Journal ArticleDOI
01 Jul 1990-Chest
TL;DR: Sleep studies should be performed on post-polio patients with excessive daytime sleepiness and respiratory complaints, including individuals already on respiratory assistance such as rocking beds who have features of respiratory failure who can be treated effectively with long-term nasal mechanical ventilation.