Linking stages of non-rapid eye movement sleep to the spectral EEG markers of the drives for sleep and wake.

The conventional staging classification reduces all patterns of sleep polysomnogram signals to a small number of yes-or-no variables labeled wake or a stage of sleep (e.g., W, N1, N2, N3, and R for wake, the first, second, and third stages of non-rapid eye movement sleep and rapid eye movement sleep, respectively). However, the neurobiological underpinnings of such stages remained to be elucidated. We tried to evaluate their link to scores on the first and second principal components of the EEG spectrum (1PCS and 2PCS), the markers of two major groups of promoters/inhibitors of sleep/wakefulness delineated as the drives for sleep and wake, respectively. On two occasions, polysomnographic records were obtained from 69 university students during 50-min afternoon naps and 30-s stage epochs were assigned to 1PCS and 2PCS. Results suggested two dimensionality of the structure of individual differences in amounts of stages. Amount of N1 loaded exclusively on one of two dimensions associated with 1PCS, amounts of W and N2 loaded exclusively on another dimension associated with 2PCS, and amount of N3 was equally loaded on both dimensions. Scores demonstrated stability within each stage, but a drastic change in just one of two scores occurred during transitions from one stage to another on the way from wakefulness to deeper sleep (e.g., 2PCS changed from >0 to <0 during transition W→N1, 1PCS changed from <0 to >0 during transition N1→N2). Therefore, the transitions between stages observed during short naps might be linked to rapid changes in the reciprocal interactions between the promoters/inhibitors of sleep/wakefulness.NEW & NOTEWORTHY In the present nap study, two dimensionality of the structure of individual differences in sleep stages was revealed. These results also suggested that individual variation in the sleep and wake drives associated with the first and second principal components of the EEG spectrum might underlie this structure. It seemed that each stage might be related to a certain, stage-specific combination of wake-sleep promoting/inhibiting influences associated with these drives for sleep and wake.

Differential relationship of two measures of sleepiness with the drives for sleep and wake.

PURPOSE: Since disagreement has been found between an objective sleep propensity measured by sleep onset latency (SOL) and subjective sleepiness assessment measured by the Epworth sleepiness scale (ESS) score, distinct underlying causes and consequences were suggested for these two sleepiness measures. We addressed the issue of validation of the ESS against objective sleepiness and sleep indexes by examining the hypothesis that these two sleepiness measures are disconnected due to their differential relationship with the antagonistic drives for sleep and wake. METHODS: The polysomnographic records of 50-min napping attempts were collected from 27 university students on three occasions. Scores on the first and second principal components of the electroencephalographic (EEG) spectrum were calculated to measure the sleep and wake drives, respectively. Self-assessments of subjective sleepiness and sleep were additionally collected in online survey of 633 students at the same university. RESULTS: An ESS score was disconnected with the polysomnographic and self-assessed SOL in the nap study and online survey, respectively. An ESS score but not SOL was significantly linked to the spectral EEG measure of the sleep drive, while SOL but not ESS showed a significant association with the spectral EEG measure of the opposing wake drive. CONCLUSIONS: Each of two sleepiness measures was validated against objective indicators of the opposing sleep-wake regulating processes, but different underlying causes were identified for two distinct aspects of sleepiness. A stronger sleep drive and a weaker opposing drive for wake seem to contribute to a higher ESS score and to a shorter SOL, respectively.