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Query: UNIPROT:O75628 (REM)
 5,581 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phase of the REM sleep rhythm was studied in 10 normal subjects each of whom was sleep studied for 4 consecutive nights. For analysis, each night of sleep was aligned according to clock time and each minute was scored as REM or non-REM. With these data, REM probability was found as a function of clock time. Fractional harmonic analysis indicates a 90 min periodicity. The REM probability curve shows peaks occurring at 1:30 a.m., 3:15 a.m., 4:30 a.m., 5:45 a.m. and 7:00 a.m. Statistical measures comparing the time of REM sleep across subjects suggests that subjects tend to have REM sleep at the same time of the night as each other. The influence of elapsed time after sleep onset on REM sleep is also reestablished. Results indicate that the time of REM sleep is determined by both clock time and time of sleep onset, suggesting two clocks, one sleep dependent and the other related to the basic rest activity cycle (BRAC), which are responsible for driving REM sleep. Furthermore, the similarity of REM times across subjects indicates the possible existence of an extra-personae REM driving force linked to clock time and possibly the BRAC.
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PMID:Rapid eye movement sleep cycle, clock time and sleep onset. 7 28

Twelve patients aged 33--70 years (mean 49.5) underwent nightly recordings in the ICU and subsequently on the ward following acute myocardial infarction. Sleep patterns were analyzed according to night after infarct and ICU versus ward environment. Significant differences in nocturnal sleep patterns from matched controls initially after infarction included greater wakefulness, low REM sleep per cent, long REM latency, fewer REM periods, more awakenings, more stage shifts and decreased sleep efficiency. The usual circadian variation in HR was absent, and there was an estimated 8--10 h of unrecorded daytime sleep, which together suggested a quite generalized disruption of biological rhythms. With time, there was loss of daytime sleep, lowered nocturnal wakefulness and increased REM sleep. Slow-wave sleep (sometimes with very long duration delta waves) increased above normal over post-infarction nights 3--9, and sleep was otherwise renormalized by post-infarction night 9. No sudden sleep changes occurred with transfer from ICU to ward. The altered sleep patterns appeared mainly attributable to infarction itself. Twelve nocturnal anginal attacks occurred. Ten began in NREM sleep and two in REM periods without particularly intense phasic activity. Post-infarction nocturnal angina therefore appears to differ in pathogenesis from angina outside this period, which usually occurs in REM sleep. ECG changes could occur during sleep before awakening with pain, and overall decrease in ECG amplitude sometimes accompanied angina. Most attacks (10 of 12) occurred on post-infarction nights 4 and 5, indicating that undetermined that undetermined factors produce a secondary period of heightened risk at that time.
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PMID:Sleep patterns in the intensive care unit and on the ward after acute myocardial infarction. 7 74

EEG patterns recorded in the waking state and during sleep were studied in 6 rhesus monkeys inoculated with a strain of Kuru previously passaged in rhesus monkey (ENAGE strain, rhesus L6 56). The onset of the disease was confirmed by the appearance of various clinical signs in 4 monkeys 15 months after inoculation. At the 16th month, the first EEG modifications appeared during sleep, which became lighter. The waking EEG was abnormal during the mature phase of the disease; it was characterized by slow anomalies and scattered spikes. The sleep EEG still presented 3 stages of Slow Wave Sleep which, however, were totally unlike the physiological stages. REM sleep rapidly disappeared, as did the cyclic organization pattern. Irritative phenomena became very significant and, in particular, very frequent 'tonic seizures' were observed. Experimental Kuru thus appears, in the rhesus monkey, as an epileptogenic encephalopathy, which is differentiated from both the human disease and the experimental disease in the chimpanzee.
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PMID:Experimental kuru in the rhesus monkey: a study of EEG modifications in the waking state and during sleep. 8 63

Excessive daytime sleepiness is a complaint characterizing many disorders of the wakefulness--sleep cycle. This paper addresses the complaint of sleepiness objectively by an attempt to differentiate a group of control subjects from a group of patients with unambiguous narcolepsy. Fourteen control and 27 narcoleptic subjects were evaluated by one of three protocols involving nocturnal recordings, detailed interviews, and 5 or more 20-min opportunities to sleep offered at 2-h intervals beginning at 10.00 o'clock, +/- 30 min. Each 20-min opportunity to sleep was given to subjects lying in a darkened quiet room and asked to try to fall asleep. Polysomnographic variables were monitored and sleep was scored in 30-sec epochs by standard criteria. The interval from the start of each test to the first epoch of NREM (including stage 1 sleep) or REM sleep was called sleep latency. In two of the protocols, the subjects were awakened immediately after sleep onset. In the third protocol, the subjects were awakened after 10 min of sleep. Narcoleptics consistently fell asleep much more readily than did control subjects. We conclude that the Multiple Sleep latency test, in addition to providing opportunities to clinically document sleep onset REM sleep periods, can demonstrate pathological sleepiness. Based on these data, we suggest that an average sleep latency less than 5 min be set as the minimum cutoff point for pathological sleepiness.
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PMID:Excessive daytime sleepiness in man: multiple sleep latency measurement in narcoleptic and control subjects. 8 64

Cross correlations between 4 homologous pairs of ear-reference derivations were calculated for 45-sec digitized samples of typical active and quiet sleep in 19 selected normal newborns at 21--70 h after term birth. Repeat recordings were obtained in 9 subjects 24 h after the original recordings and another set of cross correlations was calculated. For comparison, similar recordings were obtained from 4 asymptomatic young adults and cross correlations were calculated for 45-sec samples of typical stage 4 and stage REM sleep and for stage W both before and after sleep. Mean cross-correlation coefficients at zero time lag were generally higher for the adult sleep data than for the newborn data, but the differences were smaller than had been anticipated. The coefficients for active sleep data in the newborns were higher than for quiet sleep data, while in the adults the coefficients were higher for stage 4 than for stage REM. Coefficients were higher for convexity derivations than for temporal derivations in both newborns and adults. A review of the small available literature suggests that recording and analysis techniques may be significant variables determining the results obtained in such studies. The cross-correlation method of measuring interhemispheric synchrony may prove useful in identifying brain disorders in the postnatal period.
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PMID:Interhemispheric synchrony in the EEGs of full-term newborns. 8 66

Fine wire microelectrodes were used to record single unit activity from two of the intracerebellar nuclei, the interpositus and fastigius, during the sleep-waking cycle. The mean rates, interspike interval distributions and patterns of firing as revealed by autocorrelograms, were investigated. For each stage of the sleep-waking cycle and for as many units as possible the constancy of these measures was examined throughout several sleep cycles. Twenty-four interpositus units were recorded throughout at least one complete sleep-waking cycle. The firing rate of these units in paradoxical sleep without REM was equal to that in quiet wakefulness and greater than that occurring during slow wave sleep. The highest firing rates occurred during REM periods. Some interpositus units were found to have apparent eye movement related activity during REM periods but there was no correlation with waking eye movements. Eleven fastigial units were investigated throughout the sleep-waking cycle. At least half of these units were found to have rhythmic bursting activity during paradoxical sleep which did not appear to be tightly linked with REM periods. Fastigial and interpositus units were found to have slow shifts in their 'background' level of firing which occurred independently of the sleep-waking cycle. The results of these experiments are discussed in relation to the known inputs to the nuclei and in relation to previous studies on other groups of neurons during sleep and waking.
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PMID:Interpositus and fastigial unit activity during sleep and waking in the cat. 8 32

In 9 patients with implanted electrodes, the relationships between 13 deep subcortical structures and the premotor cortex were considered during different sleep stages, using both neuronal activities and slow electrical processes (including scalp EEG). Changes occurred asynchronously with a relative independence between the various brain structures during slow sleep. On the other hand, during REM sleep, all parameters reveal a high degree of synchronization of the activities. It is suggested that during slow wave sleep each of the separate rhythms display their own regulation, while in paradoxical sleep, it is their inter-relationships which are mainly controlled. The REM stage probably has some other function, associated with the fact that a neuronal population which has taken no part in any activity during wakefulness now reacts.
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PMID:The significance of different sleep stages for the regulation of electrical brain activity in man. 8 33

Full-term newborns with seizures exhibit EEG patterns that appear reliable in predicting neurological outcome in almost 75% of the cases in a prospective investigation. These patterns are unreliable for over 25% of infants with seizures and even more so for term and pre-term babies with other complications. Observations that such newborns often show maturational delay in various physiological and/or behavioral parameters, raises the issue of whether indices other than specific EEG patterns might prove reliable in predicting prognosis. As a prerequisite for testing such an hypothesis in prospective investigations of term and pre-term babies with 'risk' factors other than seizures, it appears necessary to obtain quantification of these parameters in normals. Hence a longitudinal study was designed to obtain simultaneously 3 parameters in a control group of newborns born after 30-32 weeks of gestational age, followed with serial polygraphic recordings at weekly intervals until a conceptional age of 43 weeks. The selected parameters were purposefully restricted to three that can be obtained and measured easily in routine recordings without need for more complex instrumentation and analysis. These were: the percentage of interhemispheric synchrony between bursts of 'trace alternant'; the number of spindle-delta complexes ('brushes') during 5 min of REM and NREM sleep; and the concordance between various parameters during the same 5 min epochs. The range of these indices was thus established in a group of normal prematures followed prospectively. Establishing such normative data will allow greater inter-study reliability, and form the basis for other prospective studies of infants 'at risk' to investigate whether those that lag behind the norm in these indices when followed serially during the newborn period differ prognostically from those who recover and reach expected norms for conceptional age.
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PMID:Quantified electrographic scales on 10 pre-term healthy newborns followed up to 40-43 weeks of conceptional age by serial polygraphic recordings. 8 42

Forty narcoleptic patients were given the Multiple Sleep Latency Test, consisting of 20 min opportunities to sleep offered at 10.00, 12.00, 14.00, 16.00 and 18.00 o'clock. Eleven patients had 2 episodes of REM sleep, 5 had 3, 11 had 4, and 13 had 5 before they were awakened. Fourteen control subjects given similar opportunities to sleep (reported in a companion article (Richardson et al. 1978)) had no REM sleep episodes. For the 10.00-18.00 o'clock opportunities respectively, there were 32, 29, 30, 28 and 27 REM sleep episodes. We conclude that this procedure can provide physicians with data useful in the diagnosis of narcolepsy.
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PMID:REM sleep episodes during the Multple Sleep Latency Test in narcoleptic patients. 8 44

The effect of apomorphine on the EEG of freely moving rats was studied. Apomorphine at the dose of 1 mg/kg caused stereotypy and a marked reduction of total sleep. On the contrary, acute subcutaneous administration of apomorphine at the dose of 100 microgram/kg, or less, markedly increased the amount of total sleep (corresponding mostly to synchronized sleep). Moreover, the infusion of apomorphine (80 microgram/kg/h) for 4 h doubled the duration of slow and REM sleep. The hypnotic effect of apomorphine was prevented by neuroleptics, such as pimozide, benzperidol and L-sulpiride, at doses which, per se, did not modify the EEG of the animals. These results suggest the existence in the CNS of DA receptors mediating sleep.
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PMID:Sleep induced by low doses of apomorphine in rats. 8 29


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