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Biomedical subjects

T Roth

Publications and source records attributed to T Roth.

At least 109 records · Page 6Linked to original sources
PubMed1987

Fragmenting sleep diminishes its recuperative value.

The recuperative effects of naps fragmented by different rates of electroencephalographic (EEG) arousal were evaluated. Forty healthy subjects with normal hearing and daytime sleep tendency (measured by the Multiple Sleep Latency Test at 10:00 a.m., 12:00 p.m., 2:00 p.m., and 4:00 p.m.) were randomly assigned to one of five conditions. Each was deprived of sleep for one night and then at 8:30 a.m. was given 100 min of natural sleep, sleep with arousals 1/5 min, 1/3 min, 1/1 min, or no sleep. After the recovery nap at 12:00 p.m., 2:00 p.m., 4:00 p.m., and 6:00 p.m., sleep latencies were again evaluated. Mean sleep latencies increased linearly as the rate of arousal during the recuperative nap decreased. Latency in the high-arousal condition was similar to no sleep and lower than natural sleep. The sleep latency of the low-arousal condition was similar to natural sleep and higher than no sleep, whereas latency in the medium arousal condition was intermediate to and differed from both natural sleep and no sleep. Although the natural sleep provided recuperation relative to no sleep or fragmented sleep, it did not restore daytime sleepiness to the screening level.

Adult↗
PubMed1987

Ethanol and caffeine effects on daytime sleepiness/alertness.

Eighteen normal-sleeping young (mean age 25.6 years) volunteers received either ethanol (0.75 g/kg producing blood ethanol concentrations of 71.1 +/- 24.3 mg/100 ml on average) or caffeine (4.0 mg/kg dissolved in 300 ml of 97% caffeine-free instant coffee) at 0920-0950 h after spending 5, 8, or 11 h time in bed (TIB) the previous night. Latency to sleep onset was tested at 1000, 1200, 1400, and 1600 h. Mean sleep latency differed significantly between drugs on each day of testing, with subjects being sleepier after ethanol than caffeine. On day 2 the TIB manipulation produced significant differences in latency, with the 11-h condition differing from both the 8- and 5-h conditions. The significant interaction revealed that in fully rested subjects (11-h TIB), ethanol did not produce sleepiness to the degree it did after 5 or 8 h in bed. In this condition latencies were similar to those of the caffeine and 5- or 8-h TIBs.

Adult↗
PubMed1986

Sleep after transmeridian flights.

Nocturnal sleep and daytime sleep latencies, recorded electroencephalographically after westward and eastward flights across the North Atlantic involving time zone shifts of 5 h, were influenced by the time of the flight and by subsequent displacement of the rest period. After the westward flight there was sleep disturbance during the latter part of the first night. However, there was persistent disturbance of sleep after the eastward flight. A rapidly eliminated hypnotic may be useful for the first night or two after a westward flight and for a few nights after an overnight eastward flight.

Adult↗
PubMed1986

Dose-related effects of triazolam and flurazepam on a circadian rhythm insomnia.

Forty-eight normal subjects had sleep recordings and multiple sleep latency tests (an EEG measure of sleepiness) before and after a 12-hour shift of sleep-wake schedule. After 2 baseline days, subjects postponed sleep until 12:00 noon, then for three 24-hour periods were in bed from 12:00 noon until 8:00 PM. Treatment in parallel groups were administered before shifted sleeps. Sleep disturbance was greatest in the last quarter of shifted nights (6.5 to 8.5 hours after medication). Subjects taking placebo showed significant sleep loss on shifted nights and increased sleepiness the next day. Triazolam, 0.5 mg, reversed the sleep loss and consequent daytime sleepiness associated with the shifted sleep schedule. Triazolam, 0.25 mg, was not significantly better than placebo. In a dose-related manner, flurazepam mitigated the insomnia, but carryover effects left both dose groups more sleepy than were the placebo control subjects. Whether these laboratory results are applicable to clinically occurring forms of transient insomnia remains to be seen.

Adult↗
PubMed1986

Sleep-wake abnormalities in narcolepsy.

To evaluate the degree to which sleep (REM vs. NREM) intrudes into wake and wake intrudes into sleep in narcolepsy, 103 patients with narcolepsy were compared to 105 patients with other diagnoses of disorders of excessive sleep (DOES). Narcoleptic patients had more frequent REM onsets on the multiple sleep latency test (MSLT) and nocturnal polysomnograms. But the MSLT latencies to REM versus NREM in narcoleptic patients did not differ. Nocturnal measures of REM pressure, percentage of REM, and REM latency excluding the REM onsets, did not differ among patient groups. With respect to the intrusion of wake into sleep, narcoleptic patients had more and longer awakenings compared with other DOES patients, but the distribution of wake into REM and NREM sleep did not differ among groups. These data suggest that narcolepsy is not exclusively a REM-related disorder, but involves an inability to sustain a specific neural state for periods comparable to those in normal subjects or other DOES patients.

Adult↗
PubMed1986

Alerting effects of naps in patients with narcolepsy.

As part of their standard diagnostic evaluation, 45 patients with narcolepsy and 45 patients with other disorders of excessive sleepiness (DOES), primarily obstructive sleep apnea, each underwent one of three nap conditions that involved manipulating time in bed on the 1600 h latency test of the standard multiple sleep latency test (MSLT) and varying the time between the 1600-h latency test and a subsequent fifth latency test. Compared with the mean of tests 1-4, a 15-min nap at 1600 h (condition 1) increased latency to stage 1 sleep on a latency test 15 min later in both groups. However, the increase was greater for patients with narcolepsy than with other DOES. A 30-min nap at 1600 h (condition 2) produced increased latency 15 min later, but the increase was greater for patients with other DOES. While narcoleptic patients showed no change in latency as a function of increased nap duration, the other DOES patients had increased latencies. When tested 30 min after a 15-min nap (condition 3), narcoleptic patients had latencies that did not differ from those of tests 1-4, while the other DOES patients sustained their increased latencies.

Adult↗
PubMed1986

Hypnotic residual effects of benzodiazepines with repeated administration.

Performance measures were compared to the multiple sleep latency test (MSLT) as indices to assess tolerance to the residual effects of benzodiazepine hypnotics during repeated nightly administration. Twelve healthy, normal sleepers received flurazepam 30 mg, temazepam 30 mg, and placebo for nine nights in a repeated measures, Latin-square design with 19 nights of recovery separating the treatments. As compared to placebo, both drugs altered sleep stage parameters in the early (nights 1-2) and late (nights 8-9) phases of the study. Hypnotic effects were found for both drugs in the early phase, but diminished for both in the late phase. The subjects' performance the next day was disrupted following treatment with flurazepam, but not with temazepam, during the early phase. Mean sleep latency on the MSLT was reduced by both drugs during the early phase. During the late phase, flurazepam did not disrupt performance but still affected the MSLT. Temazepam affected neither index the next day during the late phase.

Adult↗
PubMed1986

Dose determinants of rebound insomnia.

A polysomnographic assessment in healthy normal sleepers of possible dose relations for rebound insomnia was conducted. As an additional measure of rebound the study included a direct test of sleep/wake tendency during the night of drug discontinuation. Twelve, healthy men (21-30 years) each received placebo, 0.25 mg and 0.50 mg triazolam for 6 consecutive nights followed by a discontinuation night and 14 nights of recovery at home. The three conditions were presented, double-blind, in a latin square design. On night 6 of drug administration both doses increased total sleep time compared to placebo, but 0.50 mg did not improve sleep beyond 0.25 mg. On drug discontinuation (night 7) wake time over the 8 h recording and sleep latency after an experimental awakening (02.30 h) were increased with 0.50 mg compared to placebo and 0.25 mg. On these measures of rebound 0.25 mg did not differ from placebo. Thus rebound insomnia occurred only at a dose (0.50 mg) which produced no additional hypnotic efficacy in these normal sleepers. Whether tests of sleep/wake tendency make a useful measure of rebound insomnia needs further clarification.

Adult↗
PubMed1986

Chronic hypnotic efficacy of estazolam.

The chronic hypnotic efficacy of estazolam 2.0 mg was studied in five female and seven male subjects. Subjects with a complaint of insomnia verified by polysomnography were included in the study. Following a screening and adaptation period, subjects spent two consecutive nights a week in the laboratory. The protocol for medication was placebo for weeks 1, 2, 9 and 10 and estazolam for weeks 3-8. Estazolam 2.0 mg significantly improved sleep onset and total sleep time for up to six weeks of nightly administration without consistent recovery effects upon discontinuation.

Adult↗
PubMed1986

Dose effects of temazepam tablets on sleep.

The dose effects of temazepam tablets (15 and 30 mg) were studied at two sleep centres in 48 volunteers who had objective polysomnographic evidence of sleep onset insomnia. Volunteers slept in the laboratory, retiring at their usual bedtime after taking placebo or temazepam 30 min earlier, and were monitored for 8 h using standard polysomnographic techniques. Acute (nights 5-7) and short term (nights 11-13) temazepam, both 15 and 30 mg, improved the sleep of these volunteers by reducing sleep latency and increasing sleep time compared to the placebo baseline (nights 2-4). Dose differences were found primarily on the measurement of sleep staging, with 30 mg having a greater or more consistent effect than 15 mg. No residual effects were observed on the basis of questionnaires and objective tests of performance and no consistent evidence of disturbed sleep after discontinuing treatment was seen.

Adult↗
PubMed1985

Determinants of residual effects of hypnotics.

Studies of hypnotics have generally focused on the effects the drugs have on sleep. It is now clear that they also have effects which can extend beyond the usual sleep period. These residual effects of hypnotics are assessed by studying the effects of these drugs on performance. This paper discusses the issues critical to evaluating studies of the effects of hypnotics on performance. Dose and half-life are important variables in determining the degree to which these daytime effects occur following nighttime use. However, a number of issues have yet to be clarified. Whether residual effects persist with chronic use is not clear. Whether any specific skill may be more or less sensitive to residual effects cannot be determined from the available information. Finally, the degree to which the decrements occur in different populations is not well understood.

Benzodiazepines↗
PubMed1985

Efficacy of a reduced triazolam dose in elderly insomniacs.

Elderly persons with insomnia are unique because the cause of their insomnia differs from that of younger people and their metabolism of benzodiazepine hypnotics differs as well. This study used nocturnal polysomnography and daytime sleep/wake tendency measures (Multiple Sleep Latency Test, MSLT) to assess the efficacy and safety of a reduced triazolam dosage (0.125 mg) in elderly subjects with insomnia. After 2 nights and an intervening day of screening each subject received triazolam and placebo for 2 consecutive nights presented in a counter-balanced design. Compared to placebo the reduced triazolam dose induced and maintained sleep thereby increasing total sleep time. Sleep stage distribution and the frequency of apneas and periodic leg movements was not altered. The improved sleep was associated with a restoration of the normal pattern of daytime alertness. The correspondence of this clinical data to known pharmacokinetic data is discussed.

Aged↗
PubMed1985

Pharmacological effects of sedative-hypnotics, narcotic analgesics, and alcohol during sleep.

This article briefly reviews the well known effects of sedative-hypnotics, alcohol and narcotics on sleep. These drugs also have respiratory depressant effects, and the limited information about their effects on sleep-related breathing disturbances is reviewed. They exacerbate obstructive sleep apnea syndrome and have moderate to minimal effects on occasional apnea or hypopnea, but do not induce breathing disturbances de novo.

Adult↗
PubMed1985

Eligibility requirements in hypnotic trials.

Forty-eight patients complaining of insomnia were studied at two sleep laboratories using an identical protocol to evaluate hypnotic efficacy. All met the screening requirement of a mean sleep latency of 30 min or greater on 3 laboratory nights following an adaptation night. Of these patients 34 still complaining of insomnia were screened a second time 2 to 6 months later. Sixteen of the 34 failed the second screen. Sleep parameters for the 34 on screen 1 compared with screen 2 were the same except for sleep latency (the eligibility criteria), which was significantly shorter. There was no evidence of a systematic difference between laboratories, a change in procedure from screen 1 to 2, or a systematic loss of patients from screen 1 to 2. The data show that the statistical phenomenon of regression toward the mean must be considered in designing hypnotic efficacy studies.

Adult↗
PubMed1985

The effects of midazolam and temazepam on sleep and performance when administered in the middle of the night.

A multicenter, double-blind, sleep laboratory and performance study was conducted to evaluate the hypnotic efficacy and residual effects of midazolam (15 mg) and temazepam (30 mg) compared to placebo when administered in the middle of the night. Eighteen volunteers with objectively verified sleep maintenance insomnia received placebo for 3 nights during week 1 (adaptation and screening). During weeks 2, 3, and 4 they received 2 consecutive nights of midazolam, temazepam, and placebo (one treatment per week) in a balanced crossover design. Treatment was administered in the middle of the night (3.5 hours after bedtime). Neither drug reduced the latency to return to sleep after the middle of the night awakening. Both drugs significantly increased total sleep time, reduced wake during sleep, and number of awakenings over 4.5 hours in bed after treatment. In the morning (5 to 6.5 hours postdrug) significant performance decrements and reduced daytime sleep latency (7 hours postdrug) were found with temazepam but not midazolam.

Adult↗
PubMed1985

Sleep-wake complaints in patients with sleep-related respiratory disturbances.

The relation of sleep complaint to sleep continuity and respiratory disturbance was studied by comparing 2 series of patients with sleep apnea, one group complaining of insomnia and the other of excessive daytime sleepiness. On polysomnographic evaluation, patients with insomnia complaints had fewer and shorter, primarily central, apneas that had little hypoxemic effects. Patients with excessive sleepiness complaints had more and longer, primarily obstructive, apneas that produced significant hypoxemia. Sleep of the excessively sleepy patients was lighter and longer, whereas that of the patients with insomnia was characterized by more wake time before and after sleep onset. The excessively sleepy patients were objectively sleepy on a test of daytime sleepiness, whereas patients with insomnia were alert.

Adult↗