Mentation during sleep: REM and NREM recall reports.
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Biomedical subjects
Publications and source records attributed to A Kales.
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BACKGROUND: To our knowledge, the association between sleep-disordered breathing (SDB) and hypertension has not been evaluated in subjects from the general population with a wide age range while adjusting for the possible confounding factors of age, body mass index, sex, menopause and use of hormone replacement therapy, race, alcohol use, and smoking. METHODS: In the first phase of this study, we interviewed 4364 men and 12,219 women, aged 20 to 100 years. In the second phase of this study, 741 men and 1000 women, previously interviewed, were selected based on the presence of risk factors for SDB (snoring, daytime sleepiness, obesity, hypertension, and, for women, menopause). Each subject selected for the second phase of the study provided a comprehensive history, underwent a physical examination, and was evaluated for 1 night in the sleep laboratory. In terms of severity of SDB, 4 groups were identified: moderate or severe (obstructive apnea/hypopnea index > or =15.0), mild (snoring and an obstructive apnea/hypopnea index of 0.1-14.9), snoring, and no SDB, the control group. RESULTS: Sleep-disordered breathing was independently associated with hypertension when potential confounders were controlled for in the logistic regression analysis. The strength of this association decreased with age and was proportional to the severity of SDB. In the best-fitted model, neither sex nor menopause changed the relationship between hypertension and SDB. CONCLUSIONS: In the results of this study, SDB, even snoring, was independently associated with hypertension in both men and women. This relationship was strongest in young subjects, especially those of normal weight, a finding that is consistent with previous findings that SDB is more severe in young individuals.
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Triazolam (U-33030), an investigational hypnotic drug, was evaluated in seven insomniac subjects in the sleep laboratory. The protocol consisted of 22 consecutive nights: four placebo nights for adaptation and baseline, two weeks of drug administration (0.5 mg triazolam) for short- and intermediate-term drug effectiveness, and four placebo nights for withdrawal effects. With short-term drug use, both sleep induction and sleep maintenance improved, with total wake time decreasing markedly--a 45 per cent decrease from baseline. At the end of two weeks of drug use, none of the efficacy parameters was significantly decreased from baseline; there was only a 17 per cent decrease in total wake time. Following drug withdrawal, sleep difficulty significantly increased above baseline levels. Two of the subjects experienced episodes of amnesia during the drug administration period. The per cent of REM sleep decreased significantly during both short and intermediate drug conditions. Following drug withdrawal, the per cent of REM sleep was similar to baseline. Slow-wave (stages 3 and 4) sleep was significantly decreased for both drug conditions; and following drug withdrawal, it returned completely to the baseline leve. These data indicate that triazolam is effective for short-term use, loses most of its effectiveness with intermediate-term use, and its withdrawal is followed by a significant sorsening of sleep. These findings are discussed in relation to the potential labeling and promotion of triazolam. Finally, the findings of amnesia associated with triazolam administration need to be more thoroughly evaluated.
The effectiveness of 30 mg temazepam (SaH 47-603) for inducing and maintaining sleep was evaluated in the sleep laboratory in six insomniac subjects under conditions of short-, intermediate-, and long-term drug administration. Administration of temazepam had no effect on sleep induction. In addition, effectiveness was not demonstrated for sleep maintenance: wake time after sleep onset was not significantly decreased on any of the three drug conditions, while the number of nightly awakenings was significantly decreased on all three drug conditions. Total wake time was decreased only slightly with short-term drug administration and was similar to baseline with intermediate- and long-term use. The percent REM sleep was essentially unchanged throughout the drug administration period. On the initial set of withdrawal nights, the per cent REM sleep was slightly but no significantly increased over baseline. The per cent slow wave sleep decreased significantly with short-, intermediate-, and long-term drug administration. After withdrawal, the percent slow wave sleep returned to baseline values.
Lormetazepam, an investigational hypnotic, was evaluated for efficacy and withdrawal phenomena in doses of 0.5, 1.0, 1.5, and 2.0 mg in four separate sleep laboratory protocols, each including four placebo baseline nights, seven drug nights, and three placebo withdrawal nights. A moderate degree of efficacy was shown across the four doses, but this was quite variable. There was no dose-response effect for efficacy for either the first three or last three nights of this short-term administration period. In general, there was less efficacy on the later drug nights, indicating a potential for the development of tolerance over a relatively short period of time. Following drug withdrawal, there was a dose-related worsening of sleep above baseline levels (rebound insomnia). The peak degree of worsening of sleep following drug withdrawal was more than two times greater than the peak degree of improvement of sleep with drug administration.
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OBJECTIVE: The differential diagnosis of primary (idiopathic) vs. psychiatric hypersomnia is challenging because of the lack of specific clinical or laboratory criteria differentiating these two disorders and the frequent comorbidity of mental disorders in patients with primary hypersomnia. The aim of this study was to assess whether polysomnography aids in the differential diagnosis of these two disorders. METHODS: After excluding patients taking medication and those with an additional diagnosis of sleep-disordered breathing, we compared the nocturnal and daytime sleep of 82 consecutive patients with a diagnosis of either primary hypersomnia (N = 59) or psychiatric hypersomnia (N = 23) and normal control subjects (N = 50). RESULTS: During nocturnal sleep, patients with psychiatric hypersomnia showed significantly higher sleep latency, wake time after sleep onset, and total wake time and a significantly lower percentage of sleep time than patients with primary hypersomnia and control subjects (p < .05). In addition, the daytime sleep of patients with psychiatric hypersomnia was significantly higher in terms of sleep latency, total wake time, and percentage of light (stage 1) sleep and lower in terms of percentage of sleep time and stage 2 sleep than in patients with primary hypersomnia and control subjects (p < .05). The daytime sleep of patients with primary hypersomnia as compared with that of control subjects was characterized by lower sleep latency and total wake time and a higher percentage of sleep time (p < .05). Finally, a sleep latency of less than 10 minutes or a sleep time percentage greater than 70% in either of the two daytime naps was associated with a sensitivity of 78.0% and a specificity of 95.7%. CONCLUSIONS: Our findings indicate that psychiatric hypersomnia is a disorder of hyperarousal, whereas primary hypersomnia is a disorder of hypoarousal. Polysomnographic measures may provide useful information in the differential diagnosis and treatment of these two disorders.