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At least 19 recordsLinked to original sources
PubMed1975

Differential effects of chlorpromazine, imipramine, nitrazepam and amobarbital on REM sleep and REM density in man.

The effect of chlorpromazine (CPZ), imipramine (IMP), nitrazepam (NZP) and amobarbital sodium (AMOB) on the REM period of sleep (REMP) was investigated on four subjects by means of all-night sleep polygraphy with the schedule PPPDDDPP where P is placebo and D active drug. CPZ 25 mg resulted in a slight increase in %REMP, and no significant change in REM density (1 second fraction method) and total REM activity during the drug and withdrawal nights. IMP 25 mg produced moderate decrease in %REMP in the three drug nights, whereas REM density decreased only in the first drug night. NZP 5 mg resulted in a slight parallel suppression of %REMP, REM density and total REM activity during the drug nights. AMOB 200 mg produced a slight decrease in %REMP and marked decrease in REM density during the drug nights. Rebound increase of %REMP and a tendency of carry over decrease of REM density were observed in the withdrawal nights. Decrease in the REM density was more marked in AMOB than in NZP drug night. The importance of the simultaneous analysis of %REMP and REM density for the study of effects of psychotrophic drugs on sleep was emphasized.

Adult↗
PubMed1979

Sleep learning during stage 2 and REM sleep.

Pairs of subjects were presented with a 20-item picture series at bedtime. In the latter part of the night, a tape-recorded series of 10 words, the verbal equivalent of half the original series of pictures, was repeated 10 times during either Stage 2 or REM sleep. Morning recall and recognition for repeated words was found to be facilitated following repetition during Stage 2 sleep, but relatively unaffected following repetition during REM sleep. However, adjusting for recall, the number of additional words elicited through recognition was found to be significantly greater for REM repeated words than for Stage 2 repeated words. It was suggested that retrieval limitations, perhaps as a result of REM state dependency, rather than storage inhibition may be the main locus of the initial recall failure. By comparison, Stage 2 sleep would seem to present both a lower barrier to memory storage and retrieval compatibility with wakefulness.

Humans↗
PubMed1975

REM sleep predicts subsequent food intake.

REM sleep time in a 12 hr period was found to predict accurately food intake in the subsequent 12 hr period in undisturbed cats fed ad lib. In all but one of the cats, the correlation between REM sleep and subsequent food intake was negative. REM sleep was a better predictor of food intake than either waking, slow wave sleep or previous food intake. Cats were then fed only during the 12 hr day period. It was found that REM sleep at night, during which no food was available, no longer predicted food intake.

Animals↗
PubMed1979

An automated analysis of REM sleep in primary depression.

The REM sleep of 23 nonpsychotic patients with primary depression was studied by means of an automated REM analyzer during a drug-free period and again during amitriptyline administration. Initial drug administration (50 mg) was associated with an immediate reduction in the number, average frequency, and average size of the rapid eye movements. The average REM size remained suppressed with continued drug administration while the average REM frequency showed a rebound which was responsible for a partial recovery of the number of REMs and total REM intensity to predrug levels. With regard to individual REM periods, REM frequency and REM intensity were redistributed during tricyclic administration so that the second REM period became more "intense" than the first REM period. This automated REM analysis technique provides an objective set of measures for characterizing discrete aspects of REM sleep during a depressive episode and for evaluating the changes in REM sleep during psychotropic trials.

Adult↗
PubMed1979

Bimodal distribution of REM sleep latencies in depression.

The REM sleep latency of endogenously depressed patients was investigated by analyzing 90 polysomnograms of six patients during depression and 58 polysomnograms of four of these patients after remission. During depression the REM sleep latencies are distributed bimodally with peaks at sleep onset (sleep onset REM phases, SOREMPs) and 60 min later. During the follow-up examinations some time after remission, the occurrence of SOREMPs is very rare. A model is proposed according to which the occurrence of SOREMPs in the sleep of these patients is caused by a reduced amplitude of the circadian rhythm of the arousal system.

Adult↗
PubMed1979

Ventilatory responses to CO2 and lung inflation in tonic versus phasic REM sleep.

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.

Animals↗
PubMed1977

Individual variations in response of human REM sleep to amitriptyline and haloperidol.

The effect of amitriptyline and haloperidol on REM sleep was investigated in healthy human adults, with special attention to individual variations in these drugs' effects. In addition, an investigation was made of the rebound elevation of REM sleep occurring on the following night of partial differential REM deprivation (PDRD), again with emphasis being placed on individual variations in that effect. The administration of amitriptyline in a single oral dose of 25 mg was followed by an inhibition of REM sleep in all subjects. The per cent decrease in REM sleep was found to have a significant negative correlation with the per cent increase in REM sleep following PDRD in individual subjects. The amount of REM sleep during the recovery night following the night of amitriptyline medication tended to correlate with the per cent increase in REM sleep following PDRD in individual subjects. Haloperidol in a single oral dose of 1.5 mg caused REM sleep to augment in some subjects but inhibit in others. A significant correlation was noted to exist between drug-induced change in REM sleep and the per cent increase in REM sleep following PDRD.

Adult↗
PubMed1978

REM sleep in primary depression: a computerized analysis.

REM sleep in 35 inpatients with primary depression was automatically analyzed for 7 consecutive nights during placebo administration. For the total night of sleep, as well as each individual REM period, the number of REMs, their total voltage integral over time, the sum of their durations and the average REM size were automatically calculated. Validity of these automated REM measures was established by significant correlations with manually scored REM measures. Changes in REM sleep across the night were also investigated. Similar to findings in normal subjects, REM time did not change from REM period to REM period. Average REM size increased significantly from REM period 2-3 and 3-4. Contrary to what is seen in normal subjects, REM frequency was high during the first REM period, significantly decreased from the first to second REM period and then remained constant. Finally, a significant inverse correlation between REM frequency for the first REM period and REM latency was noted. This pattern of REM sleep is interpreted as indicating a high pressure for phasic REM at the beginning of the night which is dissipated by the first REM period.

Adult↗
PubMed1975

Apha-adrenergic receptor blockade increases human REM sleep.

1 An alpha-adrenergic receptor blocking agent, thymoxamine (150 mg i.v.) in the early night sleep of young adults increased REM sleep duration and also brief awakenings in the early night, while slow wave sleep, stage 3+4, was diminished. In the later night, however, stage 3+4 sleep was increased. Control experiments demonstrated that thymoxamine (i.v.) was without effect on blood pressure. 2 REM sleep duration may be inversely proportional to noradrenaline available at central alpha-adrenoceptors, but the control mechanisms for REM sleep appear interdependent with those for NREM sleep.

Adult↗
PubMed1975

A review of REM sleep deprivation.

Studies on the behavioral consequences of rapid eye movement (REM) sleep deprivation in animals and humans are critically reviewed. In animals, converging evidence--some reasonably well controlled--indicates that REM sleep deprivation probably heightens central neural excitability and increased motivational behavior, but has nuclear or inconclusive effects on learning. In humans, evidence indicates that REM sleep deprivation is not dream deprivation and is not harmful to schizophrenic, depressed, or healthy subjects. Controversy continues about whether or not (some) schizophrenic patients respond abnormally to REM sleep deprivation by having no REM rebound. Controlled but unconfirmed work indicates that that endogenous, but not reactive, depressive patients are improved by REM sleep deprivation, a finding consistent with the animal behavioral consequences of the procedure and with the unique REM-depriving properties of efficacious antidepressant drugs.

Adjustment Disorders↗
PubMedDate not supplied

[Excessive 7-14-sec positive spikes during REM sleep in monozygotic non-epileptic twins with speech retardation (author's transl)].

6-14/sec positive spikes (PS) (in our cases 7-14) were observed during 6 all-night sleep, recordings in one pair of monozygotic twins (aged 7 years), who had severe speech retardation, no epilepsy and were otherwise normal (CAT were normal). The EEG during wakefulness and sleep showed multifocal independent spikes over the left mid-temporal and right parieto-occipital area. The 7-14 PS, which were similar in both twins, occurred slightly during light sleep, were absent during slow sleep and were most prominent during REM sleep (mean=6.3 sec of PS bursts/min of REM). During REM sleep, the 7-14 PS bursts were negatively related to bursts of eye movements; PS were 7 times more frequent in the intervals between than during bursts of eye movements. In addition, long bursts of PS (up to 6 sec) might interupt the bursts of eye movements suggesting a functional antagonism between mechanisms (still unclear) responsible for PS and for REM. The predominance of PS during REM sleep and the inverse relationship with eye movements are not peculiar to our case, since similar findings have been reported in other cases (TSUZUKI 1967; OKUMA et al. 1968). During the sleep stages when Ps occurred spontaneously, PS could also be evoked by a click or a tone, with a latency of 1, 5-2 sec.

Auditory Perception↗
PubMed1975

REM sleep reduction effects on depression syndromes.

Thirty-four endogenous and 18 reactive, depressed patients (hospitalized and nonschizophrenic) were treated in a double-blind, crossover study of the hypothesis that rapid eye movement (REM) sleep reduction (by awakenings) relieves depression. In the endogenous group-but not in the reactive group-subjects deprived of REM sleep for three weeks improved significantly more than control subjects awakened from non-REM sleep. Therapeutic efficacy of REM sleep reduction appeared similar to reported efficacy of imipramine hydrochloride treatment of depression. Eight of nine endogenous patients, unimproved by REM sleep deprivation, did not improve with imipramine. Results suggested (1) that substantial REM sleep reduction has antidepressant activity, and (2) since imipramine and other drug antidepressants reduce REM sleep much more so than nonantidepressant drugs, that an antidepressant "mechanism" of drugs resides in their capacity to substantially reduce REM sleep.

Adjustment Disorders↗