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Biomedical subjects

T Roth

Publications and source records attributed to T Roth.

At least 199 records · Page 11Linked to original sources
PubMed1988

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.

Actuarial Analysis↗
PubMed1988

Daytime sleepiness in young adults.

The daytime sleepiness of a large sample (n = 129) of healthy, young (age 18-29) adults with no sleep-wake complaints was measured and compared with that of a sample (n = 47) of older (age 30-80) healthy, normal sleeping, subjects. Each spent 8 h in the laboratory on 1 night and received the Multiple Sleep Latency Test (MSLT) the following day. Sleep latency was measured at 1000, 1200, 1400, and 1600 h. Mean sleep latency ranged from 2 to 20 min within each group, but the shape of the distribution of latency between groups was different. The mean latency of young subjects (particularly college students) was shorter than that of the older subjects, with the differences occurring between the sleepiest 80% of each distribution. Among the college students, those with higher nocturnal sleep efficiencies (the previous night) were sleepier the following day than those with lower sleep efficiencies. The relation between nocturnal sleep efficiency and daytime sleepiness suggests that the increased sleepiness of average young adults is due to mild sleep restriction.

Adult↗
PubMed1987

Circadian fluctuation of plasma epinephrine in supine humans.

Previous studies have demonstrated circadian fluctuations of systemic catecholamines in man. However, methodological differences and conflicting results with epinephrine are apparent. In the present study, plasma and urinary epinephrine and norepinephrine and plasma cortisol were studied in healthy young adult males over 24 hr with 20 min plasma sampling and EEG monitoring of sleep. Plasma epinephrine did not have a circadian variation in supine subjects. Urinary epinephrine levels and small urinary circadian variations were increased by normal posture and activity. Sleep and sleep stage were not associated with different plasma epinephrine levels, and no ultradian fluctuation was observed. Levels of norepinephrine and cortisol were normal. Based on all studies to date, it appears that basal plasma epinephrine has either a very small amplitude or no circadian rhythm, but that changes in posture and activity or the rest/activity cycle may modify this pattern.

Activity Cycles↗
PubMed1987

Sedative effects of antihistamines.

The central effects of a newly developed, long-acting H1 antihistamine, loratadine (10 and 40 mg), were compared with those of a standard H1 antihistamine, diphenhydramine (50 mg three times a day) with measures of performance and daytime sleepiness (multiple sleep latency test). Sixteen healthy adults (six women and 10 men), 19 to 35 years of age, received each of the drugs and placebo for 2 days, separated by 5 days at home. Each day, the drug or placebo was administered at 8 A.M. and 12 and 4 P.M. Diphenhydramine was administered in three equal doses (50 mg), and loratadine was administered in a single dose followed by two placebo doses. Mean latency to sleep on tests done at 9 and 11 A.M. and 1, 3, and 5 P.M. was reduced significantly with diphenhydramine compared to placebo, whereas neither loratadine dose reduced sleep latency. Performance measured at 9:30 P.M. and 1:30 P.M. with a battery of tests, including reaction time, vigilance, digit symbol substitution, and symbol copying tasks demonstrated a significant reduction in symbols copied and digits substituted after diphenhydramine compared to both loratadine doses. These results demonstrate that loratadine (10 and 40 mg doses) did not have clinically significant central nervous system activity, whereas diphenhydramine increases sleepiness and disrupts performance efficiency.

Adult↗
PubMed1987

Hypercapnia and sleep O2 desaturation in chronic obstructive pulmonary disease.

There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the "pink puffer" (PP) and "blue bloater" (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BB. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 greater than 44 mm Hg) and without (PaCO2 less than or equal to 44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2, low sleep SaO2, and awake-low sleep SaO2, p less than 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PaO2 was similar in both groups, whereas PaCO2 was different (p less than 0.01). Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 desaturation in hypoxemic COPD.

Aged↗
PubMed1987

Experimental sleep fragmentation in normal subjects.

Recent research has suggested that sleep fragmentation in the absence of sleep loss is an important cause of excessive daytime sleepiness in certain clinical populations (e.g., sleep apnea syndrome or periodic leg movements). This study experimentally varied the number and rate of arousals in sleep to define more clearly the relation of sleep fragmentation and daytime sleepiness. Five male subjects participated in the study. Data from each were recorded for three consecutive nights (one baseline followed by two experimental nights) under three experimental conditions. All nocturnal polysomnograms were followed by a Multiple Sleep Latency Test (MSLT) the next day. The experimental conditions consisted of three different schedules of arousal produced by series of tones presented to subjects over headphones. The MSLT showed statistically significant changes after two nights of fragmented sleep, but the three fragmentation schedules did not differ from each other. Arousal threshold also changed significantly with sleep fragmentation from night one to night two.

Adolescent↗
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↗