Waking and sleeping最新文献

The various phases characterizing the sleep-wakefulness cycle were studied in rats. Electroencephalographic and electromyographic results were both analysed using classical visual methods and more sophisticated techniques such as spectral analysis and Hjorth parameters. The latter approach was very useful in obtaining a rapid characterization of regional and general brain activity and is applicable to the study of the EEG and EMG profiles of different pharmacological agents. Together with the conventional studies on the sleep-wakefulness cycle, the methodology reported here gives a powerful battery for the study of new centrally acting drugs.

Automated rat sleep analysis focuses on the statistically regular waveforms of the EEG, such as theta and delta rhythms. Such stochastic processes can be quantified in several manners. Time domain statistics such as auto- and cross-correlations produce outputs that are difficult to use and are best performed in software. Frequency domain statistics like spectral density accurately quantify the sleep state by power-frequency distributions but also require sophisticated computer processing. Continuous frequency analysis, using pass-band filtering, accurately measures signal power in an on-line fashion and employs relatively inexpensive hardware to estimate power by integrating the square of the signal. This method differs substantively from other previously reported systems which rely on signal amplitude analysis. Comparison of this system with a human scorer indicates high degrees of validity and reproducibility.

This study attempted to explain the variations of internal (brain and subcutaneous) temperature in the rat as a function of sleeping and waking. Temperature variations in cerebellum and hypothalamus were related to the changes in local cerebral blood flow (CBF) measured chronically with a thermal clearance method. CBF was stable and at a high level during slow wave sleep (SWS), decreased at the beginning of each wake (W) and paradoxical sleep (PS) phase, but tended to overshoot at the end of the PS phase. Subcutaneous temperature was related to the whole body thermogenesis (VO2) and to the sensible heat loss by radiation, convection and conduction. VO2 increased during W, decreased and plateaued during SWS, and was at a minimum level during PS. Sensible heat loss decreased during W, increased during SWS, and generally rose abruptly during PS. These variations in body and brain heat gain and heat loss are in agreement with the local temperature variations during sleeping and waking. The concomitant variations in vigilance states and internal temperature led to an apparent close relationship between the circadian rhythms of these variables, although their exact degree of liaison was not established.

A cable technique is described which allows continuous, unsupervised recording of cortical EEG and neck muscle EMG in rats over long periods. In addition, brain temperature is measured with an NTC-thermistor. After suitable adaptation the signals are computed for selected 8 s epochs into Hjorth parameters by means of a Normalised-Slope-Descriptor. These parameters are stored continuously on a digital magnetic tape. Off-line computer analysis of these parameters is used to examine changes in the EEG, EMG and brain temperature during waking and sleeping.

An evaluation of the spindle quality ranked by experienced human raters is described. The pattern discriminating criteria obtained from this evaluation are used for an automatic system based on the complex demodulation method. The performance of this automatic system is compared with both the human visual scoring and with a second automatic system employing phaselocked loop techniques. The performance of the complex demodulation is satisfactory. It also detects spindles buried in slow waves. It is not sensitive to the age of the subject. This method opens possibilities for research of either temporal or chemical (drugs etc.) effects on the characteristics of rhythmic activity, without being hampered by the arbitrary EEG jargon "alpha" or "sigma".

Report of a 56-year-old patient with a one-year-history of uncontrolable sleep attacks occurring at daytime and episodes of unsteadiness, dizziness, diplopia and dysarthria. The clinical evaluation revealed evidence of vertebrobasilar artery enlargement and insufficiency. He has become symptom-free under appropriate treatment. This raises the question of "symptomatic narcolepsy" caused by vascular brain stem disorder.

In an attempt to provide a more "physiological" measure of sleep onset, temperature of the great toe was monitored for 166 sleeper-nights in both insomniac and control groups. All subjects were women between 21 and 45 years of age. Earlier published reports had suggested that toe temperature elevation was the result of lowered sympathetic tone and marked a "vegetative preparedness for sleep." More recently, elevation of the toe temperature has been used to denote a level of chemical anesthesia sufficient for major surgery. In this study, however, the mean latency of the time course of the temperature elevation of the toe was uncorrelated with sleep onset determined by EEG criteria. Temperature elevations were frequently of large magnitude but were not uniformly observed across all subjects and all nights. It is suggested that the toe temperature elevation is reflective of metabolic adjustments which coincide with the onset of the night's first period of slow wave sleep.

The possibility of preventing endogenous depression may depend upon our understanding the brain mechanisms involved in the improvement of depression. Recent work in our laboratory has shed some light on these mechanisms. I will first describe this work and then suggest its possible preventive implications. Throughout this paper, the term depression means endogenous depression unless stated otherwise.

The lumbar cerebrospinal fluid (CSF) collected from 6 narcoleptic patients (three males and three females) aged between 31 and 47 years, as well as from 2 patients having Pickwickian syndromes with hypersomnia attacks (two males), aged 43-51 years, contained relatively high amounts of arginine vasotocin (AVT) only if the CSF was removed after a REM sleep period. The release was not induced by darkness since the same release of AVT occurred when the CSF was removed after a REM sleep period during daylight hours. No detectable AVT levels have been found in the CSF samples of four narcoleptics collected after a NREM period of sleep, either during night or daylight hours. The present results suggest a possible alteration of the rhythmical release of AVT both in narcolepsy and in narcoleptic syndromes.