Showing papers on "Rapid eye movement sleep published in 1975"

The effects of stress films on dream affect and on respiration and eye-movement activity during Rapid-Eye-Movement sleep.

Abstract: The effects of stress on the affective content of dreams and on rapid-eye-movement (REM) period eye-movement activity and respiration were studied. The experiment was also designed to examine the similarity between walking and sleeping states in the respiratory correlates of emotion. Sleep records and dream reports were collected following the viewing of stress and neutral films. The stress films significantly increased dream anxiety and also increased REM-period respiratory irregularity among those Ss who, in the walking state, showed irregular breath patterns in response to stressful film scenes. Some evidence was also found that dream affect is related to RFM-period respiratory irregularity among the Ss who are walking responders. These data are interpreted as supporting the hypothesized congruence between the waking und dream states in The relationship between affect and breathing irregularity.

Continuous intraventricular cerebrospinal fluid pressure recording in hydrocephalic children during wakefulness and sleep

Abstract: ✓ Continuous 24-hour recordings of intracranial pressure and electroencephalographic activity were made on five hydrocephalic children in whom, in the resting wakefulness state, the intracranial pressure (ICP) was considered normal. An increase in both the mean ICP and its oscillations related to cardiac systole was recorded during slow-wave sleep. Further episodic increases, up to a factor of 7 compared to wakefulness values, occurred during sleep. In three patients it was possible to correlate such episodic increases to the rapid eye movement phases of sleep. The authors discuss these phenomena and their possible implication in the progression of hydrocephalus.

Weight gain and the sleeping electroencephalogram: study of 10 patients with anorexia nervosa.

Abstract: The relation between reduced nutritional intake, with consequent weight loss, and sleep disturbance was studied by comparing certain sleep encephalogram patterns in a group of inpatients with anorexia nervosa before, during, and after a regimen of refeeding with a normal diet to a matched population mean weight. At low body weights patients had less sleep and more restlessness, especially in the last four hours of the night. During refeeding and weight gain slow-wave sleep initially increased and then tended to decrease during the final stage of restoration of weight back to matched population mean levels. With the overall weight gain, however, there was a significant increase in length of sleep and rapid eye movement sleep, the latter increasing especially during the later stages of weight gain. These results reaffirm that insomnia, and especially early morning waking, is associated with low body weight in anorexia nervosa, and their implications are discussed with particular reference to a hypothetical association between various anabolic profiles and the need for differing components of sleep.

Experimental Ethanol Ingestion: Sleep Variables and Metabolites of Dopamine and Serotonin in the Cerebrospinal Fluid

Abstract: Many previous investigators have reported the effects of ethanol on sleep. Yules, et al. (1966, 1967), Knowles and Laverty (1968), and Rundell, et al. (1972) have demonstrated that acute doses of ethanol given to normal subjects cause a decrease in rapid eye movement sleep followed by a compensatory increase, or rebound, during withdrawal. Ethanol also increases the amount of beta activity (16–18 Hz) in the sleep EEG, and causes an increase in both the heart and respiration rates. In clinical observations made on alcoholics following heavy drinking periods by Gross et al. (1966), and Greenberg and Pearlman (1967), and in experimental ethanol ingestion studies done by Johnson (1971) and Gross et al. (1971), profound effects on both rapid eye movement sleep and slow wave sleep were noted. In addition, Allen et al. (1971) have noted that REM sleep is fragmented and stage three and four sleep decreased for many weeks after abstinence began.

A Note on Rem Rebound during Experimental Alcohol Withdrawal in Alcoholics

Abstract: Until recently the effect of alcohol on rapid eye movement sleep (REM) appeared to be a relatively simple and clear aspect of the complicated relationship between alcohol and sleep. In normals, alcohol, even in moderate amounts, reduced REM (Gresham et al., 1963, Yules et al., 1966, Knowles et al., 1968). This was followed by a transient increase in REM, a “REM rebound,” and return to baseline. When increased REM was observed in patients in acute alcohol withdrawal, this was assumed to be a manifestation of the REM rebound following the reduction of REM by the alcohol (Gross et al., 1966, Greenberg and Pearlman, 1967, Gross and Goodenough, 1968, Johnson et al., 1970). Patients in delirium tremens were often observed to have very considerable increases of REM and a level of 100% REM was reported in several instances (Gross et al., 1966, Greenberg and Pearlman, 1967, Johnson et al., 1970). Under experimental conditions, alcoholics appeared to have the REM reduction during alcohol intake and transient REM rebound when alcohol intake was stopped (Greenberg and Pearlman, 1967, Gross et al., 1971, Gross et al., 1973a, Gross et al., 1973b). The high levels of REM observed clinically during alcohol withdrawal in alcoholics were assumed to be quantitative effects of more alcohol intake for longer periods of time than the alcohol administered to normals or experimentally given to alcoholics. There was no evidence that there might be anything more complex in the REM differences between normals and alcoholics than the alcoholics’ ability to tolerate greater alcohol intake, and thereby, produce greater REM reduction and subsequent rebound. The REM reduction and rebound effects appeared to be shared by the other sedative-hypnotics.

The neuroendocrinology of human sleep

Abstract: Sleep consists of several distinct patterns of CNS activation, including synchronized or slow wave sleep and desynchronized or rapid eye movement sleep. Specific areas of the brain as well as specific biogenic amine neurotransmitters appear to be responsible for the periodic shifts between sleep stages. Hypothalamic regulation of the anterior pituitary gland also is influenced by the same biogenic amine neurotransmitters, and the episodic release patterns of the anterior pituitary hormones suggest prominent CNS influences. This review considers the relationship of these hormone release patterns to the circadian sleep-wake cycle and to sleep staging within the sleep period itself.