Showing papers on "Slow-wave sleep published in 1980"

Human sleep: its duration and organization depend on its circadian phase

Abstract: Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues. The duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime and not with the length of prior wakefulness. Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm.

Pubertal changes in daytime sleepiness.

Abstract: Nineteen children (8 girls, 11 boys) were evaluated in a total of 47 three-day sessions across three summers. Children were ranked according to Tanner's stages of secondary sexual characteristics. Nocturnal sleep was recorded from 2200 to 0800 hr each night. Multiple sleep latency tests were given at 2 hr intervals from 0930 each day. Nocturnal sleep time and REM sleep time remained constant across Tanner stages. Slow wave sleep time declined progressively across Tanner stages, with a 40% reduction from prepuberty to maturity. Daytime sleepiness was significantly greater in subjects at Tanner stages 3 and 4 than at Tanner stages 1 and 2. Subjects at Tanner stage 5 tended to be as sleepy as Tanner stage 3 and 4 subjects but did not differ significantly from the less mature subjects. No gender differences were found in daytime sleepiness for children at similar Tanner stages. More mature children were significantly sleepier at 1330 and 1530 than in the late afternoon and evening.

Improvement of Depression by REM Sleep Deprivation: New Findings and a Theory

Abstract: We compared sleep variables in 14 drug-free endogenous depressives and in 14 age- and insomnia-matched, nondepressed controls before and after brief rapid eye movement (REM) sleep deprivation by awakenings. Before REM sleep deprivation, compared with controls, depressives had lower REM latency, higher REM frequency, and--a new finding--an abnormal temporal distribution of REM sleep. Depression improvement by REM sleep deprivation correlated with the ameliorative effect of brief REM sleep deprivation on on indicator of the abnormal temporal distribution of REM sleep. Several findings suggest that the depressive abnormalities represent a "damaged," weakened sleep cycle "oscillator" and its correlate, a circadian rhythm disturbance, and that REM sleep deprivation improved depression to the extent that it stimulated the oscillator and corrected one manifestation of the circadian rhythm disturbance.

Distribution of REM sleep in entrained 24 hour and free-running sleep--wake cycles.

Abstract: One hundred thirty sleep episodes of 6 subjects, living on a natural 24 hr day, were compared with 116 sleep times of the same subjects living isolated from external time cues The polygraphic sleep recordings were analyzed for the distribution of REM sleep under both conditions Additionally, the relationship between body temperature and REM sleep was analyzed by comparing sleep episodes in which the temperature minimum occurred early in the sleep episode with those in which there was a late temperature minimum The results show that there is more REM sleep in the beginning of sleep in sleep episodes of free-running rhythms as compared to sleep episodes of entrained 24 hr rhythms This higher amount of REM sleep is due to a longer first REM episode and shorter first NREM episodes The comparison of the sleep episodes that differ in the position of the temperature minimum shows similar differences, ie, more REM sleep in the beginning of sleep episodes in which the temperature minimum occurs earlier as compared to episodes in which the temperature minimum occurs later It was hypothesized that the amount of REM sleep depends on the phase relationship between sleep and the circadian temperature cycle From this point of view, the difference in the distribution of REM sleep in the entrained 24 hr rhythm, on the one hand, and the free-running rhythm, on the other hand, can be explained by the different courses of body temperature during sleep That only the first REM episode is influenced by circadian parameters may indicate an exceptional role for this REM episode in contrast to the following episodes

Heterocyclic amphetamine derivatives and caffeine on sleep in man.

Abstract: 1 Effects of the heterocyclic amphetamine derivatives, pemoline (20 and 40 mg), prolintane hydrochloride (5 and 10 mg), methylphenidate hydrochloride (10 and 20 mg) and fencamfamine hydrochloride (10 and 20 mg), and of caffeine anhydrous (100, 200 and 300 mg) on sleep, were compared with placebo in six young adults (20-31 years) using electroencephalography for sleep measures and analogue scales for subjective assessments of well-being and sleep quality. The study was double-blind. 2 No consistent effect was found with pemoline. 3 With prolintane there were no changes in sleep latencies, or in slow wave sleep (SWS). Rapid eye movement (REM) sleep was reduced during the first 2 h after sleep onset. 4 With methylphenidate and fencamfamine latencies to sleep onset and to stage 3 sleep were unchanged. The higher dose of each drug delayed the first and subsequent REM periods. Both drugs reduced the duration of REM sleep, and the higher dose of each drug reduced the percentage REM sleep. Methylphenidate also reduced total sleep time (TST). There was no evidence of reduced SWS with either drug. Impairment of sleep was reported with each drug. 5 With caffeine there were no changes in latencies to sleep onset or to the first REM period, though in one study with 300 mg subsequent REM periods were delayed. Awake activity and drowsy sleep were increased and TST and SWS were decreased. With 300 mg only, REM sleep was decreased though percentage REM sleep was not altered. Impaired sleep was reported with all doses of caffeine.

Effects of nocturnal gamma-hydroxybutyrate on sleep/waking patterns in narcolepsy-cataplexy.

Abstract: Continuous 48-hour polygraphic recordings of sleep/waking patterns were performed on 14 patients with narcolepsy-cataplexy before and after 7-10 days of treatment of their nocturnal sleep with gamma-hydroxybutyrate (GBH). GBH improved the quality of night sleep by increasing the amount of slow wave sleep, reducing stage I, increasing sleep efficiency (percentage of time in bed spent asleep), and reducing the number of periods of short sleep under 15 minutes. Also nighttime REM sleep was reduced in latency and became less fragmented. The daytime period contained less slow wave sleep and REM sleep, and fewer episodes of prolonged sleep. Patients experienced reduction or loss of daytime attacks of irresistible sleep, cataplectic attacks, and other auxiliary symptoms. Residual daytime drowsiness subsequently improved on low doses of methylphenidate. Tolerance did not develop and there were no serious toxic side-effects. Four of the patients had been refractory to previous combinations of antidepressants and high doses of stimulants.

Effect of alcohol on sleep and nighttime plasma growth hormone and cortisol concentrations.

Abstract: The acute and chronic effects of alcohol and alcohol withdrawal on sleep patterns and plasma GH and cortisol fluctuations occurring during sleep were studied. Five healthy men, aged 21-26 yr, consumed a placebo drink for 3 baseline nights, alcohol (0.8 g/kg) for 9 nights, and a placebo drink on final withdrawal night. All-night polygraphic sleep recordings and blood samples (every 20 min with a venous catheter) were collected for 1 placebo, 1 acute alcohol, 1 chronic alcohol (night 9), and 1 alcohol withdrawal night. Acute and chronic alcohol consumption reduced rapid eye movement sleep nonsignificantly during the first half of the night, whereas slow wave sleep (stages 3 and 4) was increased significantly after acute alcohol, returning to baseline values on the chronic alcohol night. On the withdrawal night, rapid eye movement sleep and slow wave sleep were not significantly different from placebo sleep. Alcohol significantly suppressed plasma GH values (70-75%) on acute and chronic nights. All measures of GH, including total integral for bedtime hours, mean hourly rate, and peak level, were similarly affected by alcohol. GH returned to placebo values on the withdrawal night. Measures of nighttime plasma cortisol were not significantly altered by alcohol or alcohol withdrawal at this dose level.

Distribution of REM sleep on a 90 minute sleep-wake schedule

Abstract: Ten young adult (ages 17-21) volunteers lived on a 90 min sleep-wake schedule for 86 (n = 5) or 96 (n = 5) consecutive 90 min periods. Subjects were permitted to sleep in 30 min episodes separated by 60 min of enforced wakefulness. These bedrest episodes were monitored by electroencephalogram, electro-oculogram, and electromyogram and were scored in 30 sec epochs using standard criteria. REM sleep episodes on this schedule occurred with a clear daily cycle; 74% of REM sleep time occurred during the rising phase of the body temperature cycle. REM showed a marked tendency to recur during alternate bedrest episodes. Finally, REM and slow wave sleep occurred together during only 27 of 910 bedrest episodes. The findings support a circadian influence on the temporal distribution of REM sleep. Neither the sleep-independent nor the sleep-dependent models of REM sleep were supported by findings on the 90 min schedule.

Sleep apnea, narcolepsy, and dreaming: Regional cerebral hemodynamics

Abstract: Regional cerebral flow after inhalation of xenon 133 as well as polysomnography were recorded during daytime sleep and the awake state in patients with narcolepsy and sleep apnea. Brainstem-cerebellar (BSC) gray matter blood flow (Fg) values in the awake state were reduced below normal (p less than 0.05) in both narcolepsy and sleep apnea; in sleep apnea, bihemispheric Fg values were also reduced in the awake state. After sleep onset, Fg paradoxically increased in narcolepsy but decreased further in sleep apnea. Maximal regional Fg changes occurred in BSC regions in both groups of patients. Oral administration of methylphenidate hydrochloride (Ritalin) increased resting Fg values in awake narcoleptics, particularly in BSC regions, but attentuated Fg increases during sleep onset. Regional Fg values during visual dreaming or hypnagogic hallucinations in narcoleptics were maximally increased in right parietooccipital regions. In narcoleptics, impaired control of sleep-wake and REM mechanisms is attentuated by methylphenidate. In patients with sleep apnea, brainstem functional activity is low in the awake state but becomes critically reduced during sleep, culminating in apnea-stimulated arousal followed by repetitive cycles as sleep recurs.

Activity of the hypnotics, flunitrazepam and triazolam, in man.

Abstract: 1 Effects of flunitrazepam and triazolam (0.25 and 0.5 mg) on sleep and on performance were studied in six healthy adult males. Sleep was assessed by electroencephalography and analogue scales, and performance by a visuo-motor coordination task. 2 Over the same dose range triazolam had a more pronounced effect than flunitrazepam. Total sleep time was increased by 0.25 and 0.5 mg triazolam, and by 0.5 mg flunitrazepam. Both drugs decreased awake activity and drowsy sleep, though the effect of flunitrazepam was limited to the 0.5 mg dose and restricted to the first 6 h after sleep onset. There were no changes in slow wave sleep. 3 Latency to the first period of rapid eye movement (REM) sleep was increased with 0.5 mg triazolam, and when doses were combined (0.25-0.5 mg) the latencies with both drugs were increased. Both doses of triazolam reduced the duration and percentage of REM sleep during the early part of the night, though the whole night duration of REM sleep was not changed. 4 After the morning ingestion of 0.25 mg flunitrazepam performance was impaired for 2.0 h, but there were no residual effects when 0.25 or 0.5 mg were taken at night. With the morning ingestion of 0.25 mg triazolam performance was impaired from 0.5 to at least 5.0 h after ingestion. There were no residual effects with 0.25 mg overnight, but with 0.5 mg triazolam there was an effect on performance 10 h after ingestion with recovery within 1.5 h (11.5 h of ingestion). 5 Triazolam (0.25 mg) and 0.5 mg flunitrazepam provide useful hypnotic activity when impaired performance the next day is to be avoided. The activity of 0.5 mg triazolam is accompanied by only limited residual sequelae compared with some other benzodiazepines of comparable efficacy, and so may prove to be useful when a more powerful effect is required.

Sleep-wakefulness rhythms in mice after suprachiasmatic nucleus lesions.

Abstract: The experiment was performed in order to investigate whether the suprachiasmatic nucleus is a potent circadian pacemaker also in mice. Cortical EEG activity and neck muscle EMG were continuously recorded in 19 albino mice under 12 h light-12 h dark cycles. Computer analysis revealed that after bilateral suprachiasmatic nucleus (SCN) lesions, the diurnal rhythm in slow wave sleep (SWS) and paradoxical sleep (PS) stages was completely eliminated although ultradian rhythms with 2-4 h periodicity persisted. However, the daily amount of either slow wave sleep or paradoxical sleep did not show any significant change after small hypothalamic lesions with a complete destruction of SCN.

Sleep Following Sustained Exercise

Abstract: This study was designed to assess the effect of individually calibrated sustained, static exercise on sleep. Normal subjects engaged in 80 min of static muscular activity at 40% of maximal levels. The exercise ended 2 hrs before bedtime. Standard polysomnographic measures were recorded during sleep. The time to sleep onset was significantly reduced relative to nonexercise nights. Other significant comparisons (increased slow-wave sleep and decreased movement time after exercise) were confined to the period preceding the first REM episode. The results indicated that the type of exercise may be related to the effect on sleep latency. The data supported a restorative theory of slow-wave sleep.

Absence of REM and altered NREM sleep in patients with spinocerebellar degeneration and slow saccades

Abstract: The pontine tegmentum contains the neurons responsible for generation of saccadic eye movements and certain phases of sleep. We studied two genetically unrelated patients with spinocerebellar degeneration and slow saccadic eye movements. Multiple all-night sleep studies in both patients disclosed absence of REM and stage 4 sleep with an extremely short stage 3 and long stage 2. Both patients had a sleep stage (X) not previously reported. These are the first awake and ambulatory humans in whom consistent absence of REM sleep has been demonstrated. Both behaved appropriately during wakefulness and showed no overt psychological abnormalities.

Studies on sleep and performance with a triazolo-1, 4-thienodiazepine (brotizolam)

Abstract: 1 Brotizolam, a triazolo-1,4-thienodiazepine, was studied in healthy young adults. Electroencephalographic sleep variables and subjective effects, and performance on a visuo-motor coordination task were measured. 2 In the sleep studies six males each ingested 0.2, 0.4 and 0.6 mg brotizolam overnight. All doses increased total sleep time, improved the sleep efficiency index, and reduced drowsy sleep and number of awakenings. Brotizolam 0.4 and 0.6 mg also reduced awake activity and increased stage 2 sleep. There was some evidence of a delay to the first REM period, but only 0.6 mg reduced the total duration of REM sleep. There were no changes in slow wave sleep. 3. In the performance studies six females each ingested 0.4 mg in the morning and 0.2, 0.4 and 0.6 mg brotizolam at night. After morning ingestion of 0.4 mg there was impaired performance from 0.5 to 5.5 h. There were no residual effects after 0.2 mg brotizolam, but with 0.4 mg there was a residual effect at 9.5 h, and 0.6 mg led to impairments up to 15.0 h after ingestion. 4 Brotizolam is a short-acting hypnotic. In doses around 0.2 mg it has useful hypnotic activity free of adverse effects on sleep and residual effects on performance. With 0.4 mg the hypnotic effect is enhanced with only minimal residual effects.

Conditioned modifications of arousal and unit activity in the rat hippocampus

Abstract: Two main types of neurons were recorded in the dorsal hippocampus of chronic rats. Type I neurons were characterized by a bursting mode of discharge. Their activity was higher during slow wave sleep (SWS) than during wakefulness (W) or paradoxical sleep (PS). They had an “inhibitory” response (decrease in spike frequency) to desynchronizing stimuli presented during a SWS episode. Type II neurons had a mean spike frequency greater than 10/s. Some of them, (group IIa), were more active during W and PS than during SWS and had an “excitatory” response (increase in spike frequency) to desynchronizing stimuli. Activity of other type II neurons, group IIb, had no relationship with the arousal level. An arousal response (neocortical EEG desynchrony) was classically conditioned to an acoustical CS. During that conditioning, most of the type I neurons rapidly displayed an inhibitory conditioned response (CR). This unit response was closely associated with the EEG CR. The majority of the type II neurons did not demonstrate signs of conditioning (group IIb). The others, group IIa, gradually developed an excitatory CR at moderate levels. This unit CR seemed to be independent of conditioned modifications of arousal.