Biomedical subjects

T Roehrs

Publications and source records attributed to T Roehrs.

At least 55 records · Page 3Linked to original sources

PubMed1994

Residual sedating effects of ethanol.

To test for dose and duration effects of residual sedation, ethanol (0.0, 0.5, and 0.9 g/kg) was administered (at 0830, 1030, and 0730 hr, respectively) to 10 healthy, normal-sleeping men, aged 21-35 years. The Multiple Sleep Latency Test was conducted at 0930, 1130, 1330, 1530, 1730, 1930, and 2130 hr, and a divided attention performance assessment was done at 1400, 1600, 1800, and 2000 hr. Breath ethanol concentration for both doses was 0.04% at 1130 hr, 0.01% at 1330 hr, and 0 at 1530 hr. A significant reduction in sleep latency was observed from 0930 to 1530 hr, but not thereafter. Divided attention performance overall was significantly impaired on the 1400-hr test only. These data again showed residual sedation and suggest residual sedation is time limited and not affected in duration or intensity by dose.

Adult↗

PubMed1994

Sleepiness and ethanol effects on simulated driving.

Twelve healthy young men were assessed in each of four experimental conditions presented in a Latin Square design: 8-hr time in bed (TIB) and placebo, 4-hr TIB and placebo, 8-hr TIB and ethanol, and 4-hr TIB and ethanol. After consuming ethanol (0.6 g/kg) or placebo (0900-0930 hr) with 20% supplements at 1030 and 1100 hr, subjects were tested for sleepiness (Multiple Sleep Latency Test at 1000, 1200, 1400, and 1600 hr) and divided attention (1030 hr) performance on day 1, and for simulated driving and divided attention (1000-1200 and 1400-1600 hr) performance on day 2. In the morning testing, with breath ethanol concentrations (BECs) averaging 0.049%, sleepiness was increased, divided attention reaction times increased (on both days), and simulated driving performance was disturbed in the ethanol and 4-hr TIB relative to placebo. Similarly in the afternoon, with BECs averaging 0.013%, the ethanol and 4-hr TIB condition increased sleepiness and disrupted divided attention and simulated driving performance. The results show that sleepiness and low-dose ethanol combine to impair simulated automobile driving, an impairment that extends beyond the point at which BEC reaches zero. They provide a possible explanation for the incidence of alcohol-related automobile accidents at low BECs.

Adult↗

PubMed1993

Effects of ethanol, diphenhydramine, and triazolam after a nap.

This study assessed the capacity of a 60-minute nap to reverse the sedating and performance-disruptive effects of ethanol, triazolam, and Diphenhydramine. Twelve healthy, young men received (at 0800 to 0830) .6 g/kg ethanol and a placebo pill, .25 mg triazolam and ethanol placebo, 50 mg Diphenhydramine and ethanol placebo, and a placebo pill and ethanol placebo on each of 2 days in a Latin Square design. On one treatment day (at 0900 hour) subjects were allowed a 60-minute nap and on the other a sleep latency test (no nap). Then, sleep latency was tested (by Multiple Sleep Latency Test [MSLT] at 1100, 1300, 1500, and 1700) and divided attention performance assessed (at 1130). The nap reversed the sedative effects of ethanol and Diphenhydramine and reduced those of triazolam (on MSLT). The nap reduced the performance-disruptive effects of ethanol and Diphenhydramine but not those of triazolam. Given the differing neurobiological mechanisms of these drugs, the data suggest that some of their effects are nonspecific and result from activation of sleep mechanisms that a nap can reverse.

Adult↗

PubMed1993

Sedative effects and plasma concentrations following single doses of triazolam, diphenhydramine, ethanol and placebo.

Twelve, healthy, young men received 0.25 mg triazolam and ethanol placebo, 50 mg diphenhydramine and ethanol placebo, 0.6 g/kg ethanol and placebo pill and ethanol placebo and placebo pill in a double-blind Latin Square design. Each of the four treatments were administered for 2 days at 0900 hours with blood samples drawn on day one at 0830, 1030, 1230, 1430 and 1630 hours, and sleep latency and performance assessed on day two at 1000, 1200, 1400 and 1600 hours. Significant sedative effects of ethanol, triazolam and diphenhydramine relative to placebo were observed on the sleep latency and performance measures with the effects being detected over the full 6.5 hours of assessment. Among the active drugs, triazolam and diphenhydramine had similar sedative effects which differed from that of ethanol. Plasma concentration of each drug declined significantly over the 6.5 hours. Ethanol reached zero, but triazolam and diphenhydramine did not. Continued sedation (sedative effects after plasma concentration reached zero) was observed with ethanol.

Adult↗

PubMed1992

Comparative effects of pravastatin and lovastatin on nighttime sleep and daytime performance.

Pravastatin and lovastatin, two HMG-CoA reductase inhibitors with similar cholesterol-lowering effects, differ in their lipid solubility. The hydrophilic characteristics of pravastatin may explain why the drug has not been detected in cerebrospinal fluid. On the other hand, lovastatin, a lipophilic compound, has been detected in the cerebrospinal fluid. Previous reports have suggested that lovastatin administration may be associated with insomnia, which reflects an action in the central nervous system. The effects of the two drugs on nocturnal sleep and day-time performance in young, healthy men have been assessed in randomized, double-blind, placebo-controlled studies. Computer-based performance tests were administered on two consecutive days before drug administration and at the end of a 3-week active drug or placebo treatment period. Results from both sites were combined for analysis. Neither pravastatin nor lovastatin significantly affected nocturnal sleep or daytime sleepiness in this study population, but lovastatin significantly affected daytime performance. In subjects treated with lovastatin, the results showed that two measures of performance, divided attention (p less than 0.05) and vigilance (p less than 0.01), worsened significantly from baseline as did global performance (p less than 0.01). Performance was not affected in the pravastatin and placebo groups. These results provide preliminary evidence of an adverse effect of lovastatin on daytime performance.

Adolescent↗

PubMed1992

Rebound insomnia and hypnotic self administration.

Twenty-one (three groups of seven), men and women, 25-50 years of age were studied to determine whether or not rebound insomnia would increase the likelihood of self administering a benzodiazepine (triazolam 0.25 mg) hypnotic. The groups compared were patients with insomnia and disturbed sleep, insomnia and normal sleep, and healthy normals. Rebound insomnia, by both subjective and polysomnographic assessment, was induced. The experience of rebound insomnia did not increase the likelihood of self administering a benzodiazepine hypnotic in any of the groups. There were clear group differences in pill self administration with normals rarely and insomnia patients frequently, but not differentially (placebo versus active drug) self administering pills.

Adult↗

PubMed1992

Rebound insomnia in normals and patients with insomnia after abrupt and tapered discontinuation.

Rebound insomnia was studied in subjects, aged 25-50 years, with insomnia complaints and normal sleep, insomnia complaints and disturbed sleep, and normal sleep with no complaints (N = 21, n = 7 per group). Standard sleep recordings were collected on a baseline night and after abrupt discontinuation of 6 nights of 0.50 mg triazolam, tapered discontinuation (3 nights of 0.50 mg, 2 nights of 0.25 mg, and 1 night of 0.125 mg triazolam) and 6 nights of placebo. Significantly disturbed sleep on the discontinuation night compared to the baseline night was found. The relative degree of rebound insomnia was greater in the abrupt condition than in either the tapered or placebo conditions. The tapered condition reduced sleep time by half that of the abrupt condition which was twice the reduction found in the placebo condition. An overall (regardless of group or condition) difference in baseline versus discontinuation sleep was found, suggesting that pill discontinuation itself leads to sleep disturbance. Subjects did not differ in rebound insomnia as a function of pre-existing sleep disturbance.

Adult↗

PubMed1992

Sedating effects of ethanol and time of drinking.

Ethanol (0.5 g/kg) was administered to 12 healthy, normal-sleeping men, aged 21 to 45, at two different times of the day (0900 and 1700 hr). The Multiple Sleep Latency Test (MSLT) was conducted at 1000, 1200, 1400, and 1600 hr in the day drinking condition and at 1800, 2000, 2200, and 2400 hr in the evening drinking condition. On placebo, sleepiness was greater in the daytime testing hours than in the evening, replicating findings on the circadian rhythm of sleepiness/alertness. There was a time of drinking (day versus evening) by ethanol interaction. An ethanol effect on sleep latency was found in the daytime hours, when alertness was relatively low. Ethanol failed to have a significant effect on sleep latency during the evening hours when alertness levels were increasing. Performance on a divided attention task, administered 1 hr postconsumption, was impaired by ethanol consumption, but did not vary as a function of time of drinking (day versus evening). However, at 5 hr postconsumption, mean reaction time on the first 20 min of a 40-min auditory vigilance task was slowed by ethanol to a greater extent after day drinking then after evening drinking.

Adult↗

PubMed1992

Multiple Sleep Latency Test: technical aspects and normal values.

Excessive daytime sleepiness is now recognized as an important medical problem. This paper describes the Multiple Sleep Latency Test (MSLT), a direct, objective method of measuring daytime sleepiness. The standard methodology of the MSLT is outlined, including a description of possible and sources of error in conducting an MSLT. Data regarding the reliability and validity of the MSLT are presented. Finally, normal values are offered, and clinical MSLT results in patients with disorders of excessive daytime sleepiness are interpreted.

Cerebral Cortex↗

PubMed1991

Rebound insomnia: duration of use and individual differences.

This study assessed consistency, duration of use, and individual difference in rebound insomnia. Eleven healthy men, 20-30 years old, with normal sleep by both subjective and polysomnographic criteria, received each of four treatments in a double-blind Latin Square design (triazolam 0.50 mg for 1, 6, and 12 nights and placebo for 12 nights), followed by two placebo discontinuation nights. Triazolam increased sleep compared with placebo without differences in effects between the first and last nights of treatment. On discontinuation following active drug, sleep efficiency was reduced compared with placebo, but duration of administration did not alter the likelihood or intensity of rebound insomnia. Those subjects (5) showing poorer sleep on discontinuation from the 12-night treatment also had poorer sleep in the 1- and 6-night treatment. Subjects with rebound insomnia had poorer baseline sleep and a greater drug effect than did subjects without.

Adult↗

PubMed1991

Alerting effects of caffeine after normal and restricted sleep.

To assess the alerting effects of caffeine after normal and restricted nocturnal sleep, 36 healthy, nonsmoking men, 19 to 35 years old, who reported normal sleep and daytime alertness received 0, 75, or 150 mg caffeine twice daily after 8 and 5 hours in bed the previous night. Sleep restriction reduced average daily sleep latency measured by the Multiple Sleep Latency Test (MSLT) and slowed auditory vigilance reaction time in the latter half of the 40-minute task. Caffeine (75 and 150 mg) increased average daily sleep latency and improved vigilance reaction time. However, sleep restriction did not alter the alerting effects of caffeine. The data show that, unlike ethanol, basal level of sleepiness/alertness does not interact with the effects of caffeine.

Adult↗

PubMed1990

Rebound insomnia: its determinants and significance.

Rebound insomnia is a sleep disturbance that occurs on discontinuation of benzodiazepine hypnotic drugs. It has been reported in both patients and healthy normal subjects and is characterized by increased wakefulness above the person's baseline levels. This article reviews that available information regarding determinants, possible mechanisms, and clinical significance of rebound insomnia. It is concluded that rebound insomnia is a disturbance of one or two nights' duration that primarily follows discontinuation of short- to intermediate-acting benzodiazepines. It occurs at high doses of a given drug, beyond which no additional hypnotic efficacy is evident. There seem to be clear individual differences in the experience of rebound insomnia, but no prospective studies have established which differences predict rebound. It is likely to be avoided by initiating treatment with the lowest effective dose and tapering the dose upon discontinuation.

Anti-Anxiety Agents↗

PubMed1990

Polysomnographic, performance, and personality differences of sleepy and alert normals.

The nocturnal sleep, performance, and personality of healthy, asymptomatic, normal young men, 18 who had unusually short sleep latencies on the Multiple Sleep Latency Test (average latency, less than or equal to 6 min) and 20 with unusually long latencies (average latency, greater than or equal to 16 min) were compared. On the nocturnal sleep recording, sleepy subjects had a shorter sleep latency, less waking time, and overall greater sleep efficiency than alert subjects. During the day, sleepy subjects performed more poorly than alert subjects on divided attention and vigilance performance tasks. The sleepy and alert subjects did not differ appreciably on the Minnesota Multiphasic Personality Inventory and Jenkins Activity measures of personality. On the Institute of Personality and Ability Testing Anxiety Scale, the sleepy subjects showed higher levels of anxiety than the alert subjects. The data were interpreted as indicating that the sleepy subjects had a sleep debt due to chronic sleep restriction.

Adult↗

PubMed1990

The chronic efficacy of midazolam.

The chronic efficacy of midazolam 15.0 mg was studied in 2 male and 10 female subjects. Only subjects with a complaint of sleep latency insomnia which was verified by polysomnography were included in the study. Following a screening and adaptation period, subjects spent 3 consecutive nights in the laboratory during the weeks of the study. Placebo was administered 15 min before lights out on the initial 8 and final 2 nights, and midazolam for the intervening 35 nights. Midazolam significantly reduced sleep latency parameters and significantly increased total sleep time the entire 5 weeks of nightly administration. No within-night rebound insomnia, residual daytime effects, or rebound effects upon discontinuation appeared.

Adult↗

PubMed1990

Individual differences in the sedating effects of ethanol.

Twenty-four healthy, normal-sleeping, males aged 21-35 were screened for basal levels of sleepiness using the Multiple Sleep Latency Test (MSLT). Twelve subjects had basal average daily sleep latencies of less than or equal to 6 min (sleepy) and 12 had latencies of greater than or equal to 16 min (alert) on the MSLT. Subjects consumed either ethanol (0.75 mg/kg) or placebo at 0900-0930 after spending 8 hr time in bed (TIB) the previous night. Sleep latency was measured at 1000, 1200, 1400, and 1600 hr. Divided attention performance and the Stanford Sleepiness Scale (SSS) were assessed at 1100 hr. Breath ethanol concentration (BEC) was determined prior to each latency test. Ethanol decreased average daily sleep latency, divided attention scores and SSS ratings. There were individual differences in the sedating and impairing effects of ethanol, related to subjects' basal level of sleepiness/alertness. The alert subjects exhibited longer sleep latencies and higher performance scores after ethanol administration than the sleepy subjects after placebo. Subjectively the groups had a similar level of sleepiness on placebo and were similarly sedated with ethanol.

Adult↗

PubMed1990

Response to CPAP and UPPP in apnea.

Ninety-two consecutive patients with obstructive sleep apnea syndrome (OSAS) were studied before and six weeks after treatment with either nasal continuous positive airway pressure (CPAP) or uvulopalatopharyngoplasty (UPPP) (n = 46 per group). Assignment of patients to treatment was based on clinical considerations and patient preference. Patients were assessed by nocturnal polysomnography and performance on the Multiple Sleep Latency Test (MSLT) the following day. Before treatment, the CPAP and UPPP groups did not differ in sleep-related respiratory disturbance, oxygenation during sleep, fragmentation of sleep, or the level of excessive daytime sleepiness indicated by the MSLT. Both treatments produced significant improvement on all measures. However, improvement in UPPP patients was significantly less consistent than that of CPAP patients. To the extent that UPPP successfully reversed the respiratory disturbance (i.e., 50% reduction in respiratory events index), sleep continuity and daytime sleepiness were improved to a degree comparable to that of patients treated with CPAP.

Female↗

PubMed1990

Characteristics of chronic insomniacs examined in a multicenter 14-day study of flurazepam and midazolam.

One hundred seven chronic insomniacs (41 men, 66 women; mean age, 37.9 years) with a history of use of benzodiazepines were recruited for a multicenter study testing the relative efficacy of flurazepam 15 mg or 30 mg, midazolam 15 mg, or placebo during a 14-day treatment period. Average duration of the complaint of insomnia was 13.5 years. Most (74%) of the patients met criteria for a diagnosis of persistent psychophysiological sleep disorder for both initiating and maintaining sleep.

Adult↗

PubMed1990

Clinical safety of flurazepam and midazolam during 14-day use in chronic insomniacs.

Data from evening questionnaires, reports of side effects, laboratory findings, and all-night respiratory measurements were collected on the 99 chronic insomniacs examined in this multicenter study. These data were used to compare the clinical safety and desirability of a benzodiazepine hypnotic with a very short half-life, midazolam 15 mg, with a hypnotic with a longer half-life, flurazepam 15 and 30 mg; both compounds were compared with a placebo control. There were 2 prestudy placebo nights followed by 14 consecutive nights of treatment. Of the 107 patients accepted, 99 completed the study. No marked adverse reactions were found in any area for any group. There was no increase in sleep apneas during the treatment period for any group. Results of this study provide additional evidence of the safety of benzodiazepine hypnotics.

Adult↗