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Biomedical subjects

T Roth

Publications and source records attributed to T Roth.

At least 55 records · Page 3Linked to original sources

Sleep extension in sleepy and alert normals.

Twenty-four healthy, young (21-35 years old) men with no complaints of daytime sleepiness, no habitual napping, and polysomnographically verified normal nocturnal sleep extended their time in bed (TIB) to 10 h for 6 consecutive nights to assess the effects of sleep extension on daytime sleepiness and performance. Twelve subjects had basal average daily sleep latencies of less than or equal to 6 min on the Multiple Sleep Latency Test and 12 had latencies of greater than or equal to 16 min before TIB was extended. The sleep extension improved daytime sleepiness differentially in the two groups. The degree of improvement was greater in the sleepy subjects than the alert subjects and the pattern of improvement differed between the groups. Sleepy subjects showed an immediate and uniform increase in alertness, while alert subjects did not show improvements until late in the extension. However, sleepy subjects never achieved the baseline level of sleepiness/alertness seen in the alert subjects.

Adult

Fragmented sleep, daytime somnolence and age in narcolepsy.

This study examined whether narcoleptics experience an age-related increase in nocturnal sleep disturbance and, if so, what impact that disturbance has on daytime sleepiness. To evaluate these questions, the records of 228 patients diagnosed as narcoleptic were assessed. Total sleep time (TST) and sleep efficiency (SE) significantly decreased, and wake during sleep (WDS), number of awakenings, and percentage of stage one significantly increased across the decades. This indicates an age-related elevation in sleep fragmentation. Daytime sleepiness, however, did not exhibit age effects. These data further support the theory that narcolepsy is a basic neural defect not confounded by excessive daytime sleepiness secondary to sleep fragmentation.

Adult

Predictors of objective level of daytime sleepiness in patients with sleep-related breathing disorders.

Excessive daytime sleepiness, the most prevalent symptom associated with the OSAS, is hypothesized to result from either fragmentation of sleep or hypoxemia during sleep. Measures of nocturnal sleep, respiration during sleep, and daytime sleepiness in 466 patients with apnea were collected to evaluate these two hypotheses. The various parameters were submitted to correlation and multiple regression analyses to predict daytime sleepiness as measured by the MSLT. The RAI, which measures the number of arousals from sleep associated with respiratory disturbances (best fragmentation correlation), produced a higher correlation with MSLT scores than did TMES (best hypoxemia correlation); however, the measures were highly intercorrelated, and multiple regression analyses to determine which parameters independently predicted MSLT showed the single best predictor to be the RAI. Additional independent variance in MSLT score was explained by TST and PSG1. Measures of hypoxemia provided little or no independent predictive information. These data support the hypothesis that sleep fragmentation is an important determinant of daytime sleepiness in patients with apnea.

Female

Recovery of alertness after CPAP in apnea.

Excessive daytime sleepiness is the most common symptom in OSAS. Administering CPAP improves breathing during sleep. We evaluated the time course of the recovery of alertness following CPAP therapy in OSAS patients. Thirty-nine patients with OSAS were treated with CPAP and evaluated after one, 14, or 42 nights of treatment, 13 patients being randomly assigned to each group. All received a diagnostic polysomnogram and MSLT before treatment. The three groups had similar baseline values for nocturnal respiratory disturbance, oxygenation during sleep, fragmentation of sleep, and level of EDS. CPAP treatment was associated with a significant improvement in sleep-related respiration, oxygenation, and sleep fragmentation. The EDS showed significant improvement after one night, and further significant improvement after 14 nights, but no further significant improvement after 42 nights. The differential rate of improvement in nocturnal parameters compared with that of primary complaint of EDS suggests that OSAS patients experience a chronic functional sleep loss. As with sleep deprivation, recovery of alertness in OSAS requires several nights of normal sleep.

Adult

The dose effects of zolpidem on the sleep of healthy normals.

This study determined the dose effects of zolpidem in 12 healthy males with normal sleep patterns. Subjects spent 7 weeks, 3 consecutive nights per week, in the laboratory and had a 4-night washout between treatments. The first week was a screening and adaptation week. Then subjects received zolpidem (2.5, 5.0, 7.5, 10.0, or 20.0 mg) or placebo on the first two nights for each of the next 6 consecutive weeks. Treatments were organized in a Latin square design and administered in a double-blind fashion. On the third night of each treatment, subjects always received placebo. The 5.0 mg and larger doses of zolpidem significantly decreased latency to persistent sleep and wake before sleep. Sleep maintenance measures were not affected by zolpidem. The 7.5 mg and higher doses of zolpidem significantly increased total sleep time. The only significant sleep stage effect was a decrease in percent of rapid eye movement sleep at only the 20 mg dose. No consistent discontinuation effects were found. Zolpidem was hypnotically active at doses as low as 5.0 and 7.5 mg, and sleep stage effects occurred only at the 20 mg dose, thus separating the dose range of hypnotic and sleep stage effects.

Adult

Narcolepsy in a pediatric population.

Narcolepsy, a sleep-wake disorder of unknown cause, has been reported as occurring in the pediatric population, but only two reports of cases in the literature have included polysomnographic data on children with narcolepsy. We compared the clinical and polysomnographic data on a series of eight patients 15 years of age or younger and an adult comparison group with narcolepsy. All patients presented with excessive daytime sleepiness, and no significant difference was found between groups for the incidence of cataplexy, hypnagogic hallucinations, and sleep paralysis. On polysomnographic evaluation the pediatric group had increased total sleep time, percent-stage 3/4 sleep, percent rapid eye movement sleep, and decreased stage 1 sleep, which all are expected age-related differences. The pediatric group also showed a greater degree of daytime sleepiness and an increased frequency of sleep-onset rapid eye movement periods. While pediatric patients with narcolepsy resemble adults in their mode of presentation and the incidence of accessory symptoms, the increase in severity of sleepiness highlights the importance of diagnosing narcolepsy in children as early as possible so that treatment can be initiated.

Adult

Sleep and memory.

Generally sleep is considered a time of amnesia. It is not uncommon for an individual to experience 8 h of sleep and have no memory for events during that time. Similarly, a substantial proportion of the population has no memory for dreams that occurred during the night, despite the fact that the literature on awakening during rapid eye movement (REM) sleep clearly shows that individuals normally have four to six "dream experiences" a night. Research on this issue seems to indicate that the lack of memory cannot be explained by the organisms' inability to perceive stimuli. The data indicate that although perceptual thresholds are elevated, organisms can clearly perceive stimuli, and, in fact, can discriminate between them during sleep. The amnesia also cannot be explained by a defect in long-term memory, as studies have indicated that stimuli put into the memory during wakefulness are more efficiently retrieved after a sleep period than after a comparable period of wakefulness. The most likely explanation for the amnestic property of sleep seems to be the inability of organisms to transfer information from short-term memory to long-term memory during sleep. There are several sources of evidence to support this hypothesis. First, the probability of remembering a stimulus given during wakefulness is related to the proximity of sleep onset to the stimulus. Generally, information put into the system within 5 min of sleep onset is lost from memory. Secondly, disorders of excessive daytime somnolence which cause individuals to have frequent microsleeps are often associated with complains of memory problems.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans

Reversal by caffeine of triazolam-induced impairment of waking function.

Twelve, healthy normal men aged 21-25 years received each of four treatments (triazolam placebo plus caffeine placebo, triazolam 0.50 mg plus caffeine placebo, triazolam 0.50 mg plus caffeine 4 mg/kg, triazolam 0.50 mg plus caffeine 8 mg/kg), double blind, in a Latin-Square design. Triazolam or placebo was administered at 0830 and caffeine or placebo at 1000 and 1245. On two memory tasks, administered at 1015 with an immediate recall and a delayed recall at 1230 following a 90 min nap (1030-1200), both immediate and delayed recall was impaired by triazolam. Neither caffeine dose reversed the impairments. Sleep latency and sleep efficiency were improved by triazolam and not reversed by caffeine. On a performance battery presented at 1300 most measures of performance were impaired by triazolam; in general the caffeine dose of 4 mg/kg partially reversed the effect while the dose of 8 mg/kg completely restored performance.

Adult

Daytime alertness in patients with chronic insomnia compared with asymptomatic control subjects.

Despite the subjective reports of patients with difficulty initiating and maintaining sleep (DIMS) that they are impaired during the day, consistent differences in daytime functions have not been found between normal sleepers and patients with insomnia. The present study compares polysomnography and Multiple Sleep Latency Test (MSLT) data from 70 clinic patients seeking evaluation for chronic insomnia with data from a group of 45 asymptomatic sleepers. The DIMS group was found to sleep significantly less than the control group; yet they were also significantly more alert than the control group the following day, as measured by MSLT. Within the insomnia diagnostic subgroups, a correlation of -0.67 (p less than 0.05) was found between nocturnal total sleep time and mean MSLT. The results are interpreted as supporting the existence of a tendency towards physiological hyperarousal in patients with chronic insomnia. This tendency may be exacerbated by other factors (e.g., personality disorder, periodic leg movements) also associated with insomnia.

Adult

Test-retest reliability of the MSLT.

The test-retest reliability of the Multiple Sleep Latency Test (MSLT) was evaluated in 14 healthy normal subjects. Each slept a single night in the laboratory (8 h time in bed) and received the MSLT the following day (1000, 1200, 1400, and 1600 h) on two occasions separated by 4-14 months. Mean sleep latency (four tests) was highly reliable from MSLT to MSLT (r = 0.97, p less than 0.001). The test-retest reliability did not change as a function of the interval of time between tests or as a function of the level of sleepiness (range = 4-20 min) within the population. However, as the number of tests comprising the MSLT was reduced below three, the reliability was reduced such that only 50% or less of the variance could be predicted.

Adult

The effects of acute sleep restriction and extension on sleep efficiency.

This study employed a repeated measures design to assess the relationship between sleep efficiency and time-in-bed (TIB). Fourteen subjects underwent three TIB conditions: (5 hour, 8 hour, and 11 hour), which were presented in a Latin Square design. Subjects slept a total of six nights (two nights per condition) while being monitored by a wrist actigraph to determine sleep time. Sleep efficiencies (sleep time/TIB) were analyzed with a two-way repeated-measures ANOVA. The main effect of night was not significant. The main effect of TIB and the interaction of nights and TIB were significant. In the 11-hour condition, sleep efficiency fell from night one to night two, and on night two both the 5-hour and the 11-hour conditions were significantly different from the 8-hour condition. Analysis of total sleep time (TST) yielded the same results with the addition of a significant night-to-night difference in the 5-hour condition. It was concluded that sleep efficiency systematically changes with an extension or restriction of TIB from 8 hour.

Adult

Increased daytime sleepiness enhances ethanol's sedative effects.

Thirty healthy men, 21 to 35 years old, received either 8.7, 13.0 or 17.4 mmol/kg (0.4, 0.6, or 0.8 g/kg) ethanol after 8 hours time in bed (TIB), one night of 5 hours TIB, and four nights of 5 hours TIB. Ethanol, administered as 80-proof vodka mixed 1:4 with tonic water, was consumed over 30 minutes (0900 to 0930 hours). Sleep latency was measured at 1000, 1200, 1400, and 1600 hours using standard sleep laboratory methodology. Breath ethanol concentration (BEC) was determined prior to each latency test. Mean latency to sleep on the four tests decreased from day 1 (8 hours TIB) to day 5 (fourth day of 5 hours TIB). On day 1 mean latency after 8.7 mmol/kg differed from that after 17.4 mmol/kg, with the 13.0 mmol/kg latency intermediate between the other two. On day 2 and day 5 during sleep restriction these dose differences were diminished. Latency on day 5 after 8.7 mmol/kg was similar to that of 13.0 mmol/kg on day 2, which was similar to that of 17.4 mmol/kg on day 1. The BEC did not change from day 1 to day 5 and significant dose differences between each dose remained consistent from day to day. These data show that increased basal levels of sleepiness enhance ethanol's sedative effects for even moderate ethanol doses.

Adult

Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients.

Although obstructive sleep apnea (OSA) has been studied in detail for over a decade, the mortality of this disorder is unclear. We calculated cumulative survival in 385 male OSA patients. We found that those with an apnea index (AI) greater than 20 had a much greater mortality than those with AI = less than 20. The probability of cumulative eight-year survival was .96 +/- 0.02 (SE) for AI = less than 20 vs. 63 +/- 0.17 for AI greater than 20 (p less than .05). This difference in mortality related to AI was particularly true in the patients less than 50 years of age in whom mortality from other causes is not common. None of the patients treated with tracheostomy or nasal CPAP died. Eight of the patients treated with uvulopalatopharyngoplasty (UPPP) died and the cumulative survival of the UPPP-alone treated group was not different from the survival curve of untreated OSA patients with an apnea index of greater than 20. We conclude that OSA patients with an apnea index of greater than 20 have a greater mortality than those below 20 and that UPPP patients be restudied after therapy. If the latter patients are found not to have marked amelioration of their AI, then they should be treated by nasal CPAP or tracheostomy.

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