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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this clinical, psychometric and polysomnographic study, primary dysthymics (N = 20) were compared with anxious depressives (N = 22), and non-psychiatric controls (N = 11). Beck and MMPI depression scores were similar in the two affective groups. Prominent insomnia occurred in 82% of the anxious group; hypersomnia was more characteristic of the dysthymic group. On night 1, the anxious group had the poorest sleep efficiency (P less than 0.001), while dysthymics had the highest REM% (P less than 0.05) and shortest REM latency (P less than 0.01). On night 2, differences tended to be minimized, although the number of awakenings was still high (P less than 0.05) in the anxious group, and REM% was highest (P less than 0.01) and REM latency shortest (P less than 0.01) in the dysthymics. These findings suggest that patients with primary anxiety disorders experience greater sleep continuity difficulties on the adaptation night. Despite significant clinical overlap in depressive symptomatology between the two groups, REM% and REM latency appear as sturdy psychophysiological markers in differentiating primary dysthymics and anxious depressives on both nights. These data suggest that distinct anxious depressive and subaffective dysthymic subtypes can be distinguished within the universe of the atypical depressions.
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PMID:Chronic depressions. Part 2. Sleep EEG differentiation of primary dysthymic disorders from anxious depressions. 623 60

This study describes the effect of two weeks of delta-9-tetrahydrocannabinol (THC) administration upon normal sleep. The two subjects, two brothers in their 20s, slept in the laboratory for 27 consecutive nights and then, after four nights at home, for four additional nights. One subject, after an adaption night, received placebo for four baseline nights, 30 mg of THC for the next 14 nights, and placebo during four withdrawal nights. The other subject received placebo during this entire period. One year later the subjects alternated these conditions. The subjects had difficulty falling and staying asleep during the first two nights of placebo after 14 consecutive drug nights. This mild drug withdrawal insomnia was not accompanied by the increase of REM sleep which frequently accompanies withdrawal of other drugs. Starting after about a week of THC administration, and continuing for a week after drug discontinuance, there was a marked decrease in the type of sleep associated with slow waves in the electroencephalogram, nonREM sleep stages 3 and 4. The fact that prolonged, but not acute use, suppresses slow wave sleep indicates that this commonly used drug produces a poorly understood change in brain physiology.
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PMID:The effect of chronically administered delta-9-tetrahydrocannabinol upon the polygraphically monitored sleep of normal volunteers. 629 82

The purpose of this study was to evaluate the short- and intermediate-term (21 days) effectiveness, as well as the carryover and withdrawal effects of 7.5 mg of zopiclone, a new short-acting hypnotic agent. 6 patients with chronic insomnia, ranging in age from 33 to 57, participated in the study. Both EEG sleep recordings and subjective rating scales were used to evaluate the drug. Zopiclone increased the total sleep time throughout its 3-week administration period although only during the short-term period was this increase statistically above baseline. There was no carryover effect nor rebound insomnia upon drug withdrawal. The drug significantly increased the duration of stage 2 sleep, decreased stages 3 and 4 sleep, and had no effect on the duration of REM sleep. There were no reported side effects.
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PMID:Effects of zopiclone on the sleep of chronic insomniacs. 636 19

The effect of the nootropic drug, piridoxilate on normal and on exogenously (by traffic noise) disturbed sleep and awakening quality was investigated in a double-blind placebo-controlled study. 10 elderly subjects with a mean age of 62 years spent 13 nights in the sleep laboratory: 2 adaptation nights, 1 baseline night, 3 drug nights (placebo, 300 and 600 mg piridoxilate), as well as 2 drug nights with nocturnal traffic noise (placebo and 600 mg piridoxilate) and the subsequent wash-out nights. Polysomnographic recordings (including EEG, EMG and EOG) were carried out between 10:30 p.m. and 6.00 a.m. Traffic noise was pre-recorded at a busy Viennese street and presented continuously by a loudspeaker with a sound pressure level at the ear of between 68 and 83 dB (A) [mean 75.6 dB (A)]. In the morning the subjects completed a sleep questionnaire for the subjective evaluation of their quality of sleep and awakening. Thereafter objective awakening quality was measured by a psychometric test battery. Piridoxilate did not induce any significant changes in objective and subjective sleep variables. Nocturnal traffic noise produced a decrease in total sleep time and sleep efficiency, an increase in wakefulness and drowsiness (stage 1), as well as a decrease in REM and deep sleep stages, the last-mentioned being of statistical significance. Subjectively, the elderly subjects reported a deterioration in sleep quality due to traffic noise, an increase in middle and late insomnia, as well as a deterioration in awakening quality (dizziness, tiredness, headaches). Piridoxilate did not ameliorate these sleep disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of nootropic drugs on normal and disturbed sleep of the elderly: controlled studies with pyridoxilate and street noise]. 639 69

The effects of a single injection of parachlorophenylalanine (PCPA, 300 mg/kg i.p.) on sleep, motor activity and consummatory behavior were investigated in unrestrained rats which were continuously recorded with telemetric techniques on two control days and six drug days. Slow wave sleep (SWS) was defined as the non-REM sleep (NREMS) fraction with a low predominant EEG frequency. In the 24 h following PCPA administration, motor activity and food intake were reduced and sleep was increased. SWS was massively enhanced, while REM sleep (REMS) was depressed. The initial phase of sedation was followed by a phase of partial insomnia lasting 1-2 days. SWS and REMS were particularly depressed. A rebound phenomenon was observed at the end of recovery period when some of the SWS and REMS values exceeded the control level. The administration of tryptophan (Trp, 150 mg/kg i.p.) 28 h after PCPA pretreatment, causing a significant rise in the brain serotonin (5-HT) concentration, produced a temporary increase in SWS and REMS, and a reduction of motor activity. The experiments show that the depression of SWS and REMS, and the hyperactivity 1-2 days after PCPA administration, are a consequence of the reduced 5-HT level, whereas the involvement of serotonergic mechanisms in the initial sedative phase and in the recovery phase is less clear. The persistence of the daily distribution of sleep and activity, and of the specific pattern of SWS and REMS, indicates that the circadian sleep organization is little affected by 5-HT depletion.
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PMID:Effect of p-chlorophenylalanine and tryptophan on sleep, EEG and motor activity in the rat. 645 88

Adult cats were implanted with standard electrodes to record EEG, EOG, and EMG. After 15 days, morphine sulphate or saline placebo was given IP at 0.5, 1.0, 2.0, 3.0 mg/kg, at least 15 days apart. Cats were continuously recorded for 72 hr postinjection. Wakefulness, drowsiness, NREM and REM sleep percentages were scored from polygraphic features and statistically analysed. There was a dose-dependent suppression of NREM and REM sleep for at least 6 hours postmorphine, with a progressive sleep recovery thereafter. During the insomnia period there was an EEG/behavioral dissociation where bursts of high-voltage waves were seen over a background of desynchrony; meanwhile the animal was first aroused although quiet and later showed stereotypic behavior. There was a prolonged NREM sleep rebound which started later at the higher doses. A significant, relatively brief REM sleep rebound was seen only at the lowest dose. The latency for NREM and REM sleep onset was also dose-dependent. Possible brain sites of morphine actions and similarities with effects in other species are discussed.
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PMID:Reassessing morphine effects in cats: II. Protracted effects on sleep-wakefulness and the EEG. 654 2

Nine volunteer poor sleepers, of mean age 61 years, took trazodone 150 mg nightly for 3 weeks, preceded by 2 weeks and followed by 1 week of matching blanks, in order to examine the effects of electrophysiologically-recorded and subjectively-rated sleep. The second of the initial weeks of matching blanks served as a baseline week. In the subjective ratings, sleep improved in quality on trazodone, significantly so in the first and second weeks of intake, though with significant rebound insomnia on the second withdrawal night. Trazodone halved the frequency of arousals interrupting sleep, and it reduced the time spent in stage 1 (drowsiness). It increased the duration of slow-wave sleep (stages 3 + 4), with a negative rebound following withdrawal. It reduced the time spent in REM sleep, with a rebound above baseline levels after withdrawal. Trazodone did not change total sleep duration, nor the time required to fall asleep. The effects of trazodone were sustained or became enhanced during the period of intake. They persisted for over 24 h after the last dose, and rebound effects were maximal on the second withdrawal night.
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PMID:Trazodone enhances sleep in subjective quality but not in objective duration. 661 88

This study investigated variation in respiratory disturbance during sleep. Sixty-six healthy elderly subjects (mean age = 67.2) underwent two consecutive nights of polysomnography. Respiratory disturbance was assessed by Respiratory Disturbance Index (RDI), the number of events per hour of sleep. Results indicated an increase in RDI from Night 1 to Night 2. Fourteen subjects increased their RDI by over 2.5, and eight by over 5.0, events per hour on Night 2. The increase was not a function of increased REM on Night 2. Age was positively related to RDI on individual lab nights but unrelated to nightly variation in RDI. Subjects without complaints of insomnia were more likely to show increases in RDI, perhaps reflecting the sounder sleep of this group on the second laboratory night. This study suggests that a single night of polysomnography is likely to underestimate the absolute level of respiratory disturbance seen in a subsequent recording night. Studies placing prevalence of such disturbance in the elderly at approximately 30% are thus likely to be underestimates. Whether this "error" is important will depend ultimately upon the meaning of various absolute levels of respiratory disturbance in healthy older persons.
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PMID:Nightly variation in sleep-related respiratory disturbance in older adults. 662 92

The effects of midazolam, a short-acting imidazobenzodiazepine, on the sleep cycle of insomniac patients were assessed by means of polygraphic recordings. Baseline placebo nights were compared with drug (30 mg p.o.) and placebo withdrawal nights. The compound was effective in inducing and maintaining sleep on short- and intermediate-term administration. Tolerance was not observed following two weeks of drug use. Subjective reports corroborated the effectiveness of midazolam as a hypnotic. In regard to its effects on sleep stages, midazolam markedly decreased Stage 3 and abolished Stage 4 sleep, while Stage 2 was augmented. REM sleep percentage was not significantly affected. Withdrawal of midazolam was followed by rebound insomnia, in which sleep latency, total wake time and wake time after sleep onset were increased above baseline. Side-effects related to midazolam administration included headache, muscular weakness and dizziness. They were mild and wore off 1-2 hours after awakening.
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PMID:Sleep laboratory study of the effects of midazolam in insomniac patients. 707 54

The short-term hypnotic efficacy of 15 mg flurazepam was evaluated in nine patients (mean age 37.2 +/- 15.9 years) who complained of insomnia and had polysomnographic evidence of disturbed sleep. Patients slept in the laboratory 14 consecutive nights, and their sleep was monitored using standard polysomnographic procedures. Prior to bedtime, they received a placebo the first four nights, 15 mg flurazepam on nights 5 through 11, and a placebo again on nights 12 through 14. Flurazepam significantly increased total sleep time while reducing the latency to stage 1 sleep, the number of awakenings in the night, and the amount of wakefulness after sleep onset. Sleep stage patterns also were altered significantly with flurazepam: percentage stage 2 sleep increased, and percentages of 3-4 sleep and REM sleep (on drug night 1 and nights 1-3) decreased. With the exception of REM sleep, most of these drug effects were first detected on the second night of administration, did not diminish over the next six nights, and persisted during the three-day withdrawal period. Subjective evaluations of sleep generally corresponded with the polysomnographic data. It was concluded that 15 mg flurazepam has significant hypnotic properties with minimal adverse side effects.
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PMID:Flurazepam for short-term treatment of complaints of insomnia. 710 76


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