Effects of alcohol on the acoustic reflex threshold in the chinchilla.

The effect of ethanol on the acoustic reflex threshold was examined in a repeated measure design study in six chinchillas. Each subject was weighed and orally administered the control (water) at a dosage of 7.5 ml/kg. Commencing 1 h after alcohol ingestion, the acoustic middle ear reflex measures (AMRs) were taken every other hour, for a total of four recording sessions. Ascending and descending trials were alternated between each recording session. Two weeks later the same chinchillas were administered 35% alcohol by volume. AMRs were recorded under the same conditions and procedures as for the control. Alcohol produced AMRs that were significantly elevated over baseline values 1 h after alcohol ingestion and four of the five had AMRs that remained elevated 3 h after ingestion.

Effects of sleep on spontaneous activity in symptomatic diffuse esophageal spasm.

Diffuse esophageal spasm is a disease of unknown etiology in which neural or muscular control mechanisms malfunction, resulting in impaired and sometimes painful swallowing response, and inappropriate muscular contraction. An association between social stresses and disease activity suggesting elements of central control has been observed. In an effort to uncouple conscious central mechanisms from end organ response, we manometrically studied esophageal activity of four patients with symptomatic diffuse esophageal spasm while asleep (identified by electroencephalographic monitoring) as compared to wakeful states. We observed significant decreases from awake studies in number and duration of spontaneous contraction, during all sleep stages. We conclude that CNS mechanisms participate in the expression of the abnormal excitability of the esophagus in symptomatic diffuse esophageal spasm.

Dose-related sleep disturbances induced by coffee and caffeine.

In a 13-night sleep laboratory study, each of 18 normal young adult males twice received 1 cup of warm water, 1-, 2-, and 4-cup equivalents of regular coffee, a 4-cup equivalent of decaffeinated coffee, and a 4-cup equivalent of caffeine. All beverages were administered 30 min before bedtime according to a balanced Latin-square design. Regular coffee produced dose-related changes in most standard electroencephalogram-electrooculogram (EEG-EOG) sleep parameters, and the 4-cup equivalents of regular coffee and caffeine produced equivalent effects. Decaffeinated coffee had no effect. Regular coffee and caffeine caused rapid eye movement (REM) sleep to shift to the early part of the night and stages 3 and 4 sleep to shift to the later part. Coffee also produced dose-related changes in several subjects estimates of sleep characteristics. These results suggest that coffee and caffeine may be used in normal subjects to induce symptoms mimicking those of insomnia. Such a tool should promote further understanding of insomnia.

Stress, cardiac activity and sleep.

An overview is presented of the relationship between cardiovascular activity and sleep, emphasizing the interrelations between stage of sleep and cardiovascular dysfunction. Possible implications of the data are discussed, especially in relation to stress-related factors and possible treatment regimens.

Longitudinal sleep patterns during pubertal growth: four-year follow up.

There were little or no indications of differences in sleep outcomes between the sexes. Results indicate a disturbance of sleep on initial laboratory nights relative to later nights. The results reported here clearly document the persistence of these effects from year to year. For the most part, sleep characteristics during the 4 years immediately after onset of puberty appear to represent a typical phase in the gradual patterns of changes across all ages. Total sleep time decreased markedly from 560 min in age range 10-12 to 424 min in age range 20-29, with our puberty subjects as intermediate levels. Puberty subjects has an average of 2.5 awakenings/night in the first 2 years as compared with 1.2/night in the last 2 years. The number of sleep stage shifts during the night varied around a constant mean value of approximately 37/night throughout all ages. The number of rapid eye movement (REM) period during the night decreased sharply for individuals from childhood (6.9/night) through adolescence (4.0/night), remaining constant thereafter. Percentages of the various sleep stages were fairly constant for individuals from age range 10-12 through age 30-39. Our puberty subjects had percentage profiles in near perfect agreement with the normal ontogenetic process. Normative data suggest that slow wave sleep reaches a peak at some point during the teen years.