Response of delta (0-3 Hz) EEG and eye movement density to a night with 100 minutes of sleep.

In one of a series of experiments aimed at gathering the empirical data required to formulate mathematically our recovery model of sleep, we recently (1) measured the increase in delta electroencephalogram (EEG) following one night of total sleep deprivation (TSD). We found that the delta rebound was confined to the first non-rapid eye movement period (NREM-P1) of recovery sleep; this unexpected result was documented with direct computer measurement of 0-3 Hz EEG, as well as with visual scoring of stages 3 and 4. We also found a robust decrease in eye movement density during the second and third REM periods, which we hypothesized to be due to the increased depth of recovery sleep. In the present experiment, we awakened young adult subjects after 100 min of sleep, a duration that includes the first cycle for this age group, and analyzed visual and computer measures of delta and eye movement density during recovery sleep. We again found eye movement density to be significantly reduced in REM-P2 and P3, but to a lesser degree than after total sleep deprivation, a condition that may be presumed to produce a greater increase in sleep depth. Delta increases were again limited to the first cycle, although all subjects completed this cycle on the 100-min night. The major difference between recovery sleep patterns following the total deprivation and the 100-min sleep conditions was that 0-3-Hz wave amplitude increased significantly after the former, but not after the latter. In both studies, recovery sleep showed increased 0-3-Hz wave density. The neurophysiological implications of a response of EEG amplitude as opposed to wave density are briefly considered; separate measurement of these variables is more readily accomplished with period-amplitude than with spectral analysis. Our results further illustrate the importance of measuring sleep by physiological units, such as the successive NREMPs and REMPs. They also support other data that indicate that NREM-P1 plays a special role in human sleep: it responds selectively to sleep deprivation, shows the greatest ontogenetic variation across the human lifespan, and is the component of sleep that is most frequently abnormal in psychiatric patients. As we have long argued, it is inappropriate to conceptualize this high priority component of NREM sleep as "REM latency" and as a measure of REM "pressure" exclusively.