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.