No abstract

Summary: This study explores the relationships between the standard sleep variables, particularly between those of NREM and REM sleep. A total of 399 nights of sleep was recorded in 147 adults who had no known pathology. This amount of data allowed for an accurate description of the generally nonnormal variable distributions and established the relative predominance of the intra-over the interindividual variability. Most correlations between variables were low, showing that there is little redundancy in the choice of variables. The relationships between stage 2 and 4 of NREM and REM sleep and between sleep stages and wakefulness were statistically significant. We found that a short latency of stage 2 predicted a sleep of poorer quality than did a longer latency and confirmed that stage 2 has a central role in transition between stages. Finally, there was an association between the variables describing sleep stability and those describing cyclic organization and sleep efficiency. However, it cannot be determined from these data whether the relationship is causal or permissive. In addition, these results suggest that further work on cycle structure is required and that future experiments should incorporate a larger number of observed nights per individual.

Ten healthy volunteers were injected i.v. with 5 mg Ro 15-1788, a specific benzodiazepine antagonist, or placebo in a double-blind randomised design. In the EEG, Ro 15-1788 led--with some topographical variations--to a diminution of theta and alpha power, an increase of alpha mean frequency and a decrease of delta mean frequency. In auditory evoked potentials, the N1P2 and P2N2 amplitudes decreased. The electrophysiological changes induced by Ro 15-1788 are consistent with a central stimulant action. Ro 15-1788 induced some slight behavioural and subjective changes.

A large body of data has been gathered on the sleep characteristics of normal subjects. The evolution of each sleep stage within each NREM/REM cycle is presented in detail, showing stage intensities minute by minute. There is a three-phase pattern in each stage intensity diagram: an initial phase of rapid change; a central phase of relative stability; and a terminating phase, again, of rapid change. The details of this pattern change progressively during the night. Throughout all cycles, there is a complementary relationship between the intensities of stage 2 sleep and the other stages that underlines the central role of stage 2 sleep in all stage transitions. Stage intensity diagrams for two groups, one group with and one group without stage 4 sleep, were compared. Subjects without stage 4 sleep tended to have a shorter duration and greater latency of stage 3 sleep. Surprisingly, cycles interrupted by abnormally long periods of continuous wake showed a negative correlation between the intensities of wake and slow wave sleep, and these interruptions did not appear to reset the cycle clock to zero. Sleep stage intensity diagrams may be useful to study the sleep patterns of populations of insomniac and depressive patients, as well as the effect of drugs on sleep.

The experiments reported here were designed to characterize in detail the spectrum of activity of flunitrazepam in human sleep. The direct and residual effects of flunitrazepam, as well as the antagonism by flumazenil, an antagonist of benzodiazepine receptors, were studied in 28 normal subjects recorded in the sleep laboratory. The five categories of variables--sleep-wake balance, sleep organization, orthodox sleep, phasic events in sleep, and sleep waveforms--were all modified by flunitrazepam. Some of these modifications were observed only on the drug night and were antagonized by flumazenil, whereas others persisted in the placebo postdrug night and were not antagonized by flumazenil. A few variables showed changes intermediate between these two types of reactivity. The results do not fit well with the multiple benzodiazepine receptors theory, but instead support the concept of spare receptors. Along these lines, the study of the reactivity of sleep components to ligands of benzodiazepine receptors can contribute to the better understanding of the neuronal systems involved in their control.