Domien Beersma

EEG Power Density during Nap Sleep : Reflection of an Hourglass Measuring the Duration of Prior Wakefulness

The relation between the duration of prior wakefulness and EEG power density during sleep in humans was assessed by means of a study of naps. The duration of prior wakefulness was varied from 2 to 20 hr by scheduling naps at 1000 hr, 1200 hr, 1400 hr, 1600 hr, 1800 hr, 2000 hr, and 0400 hr. In contrast to sleep latencies, which exhibited a minimum in the afternoon, EEG power densities in the delta and theta frequencies were a monotonic function of the duration of prior wakefulness. The data support the hypothesis that EEG power density during non-rapid eye movement sleep is only determined by the prior history of sleep and wakefulness and is not determined by clock-like mechanisms.

Comparison of the Munich Chronotype Questionnaire with the Horne‐Östberg's Morningness‐Eveningness score

We report on results from an Internet survey of sleeping habits in a Dutch population using the Munich Chronotype Questionnaire (MCTQ), supplemented with the Horne‐Östberg Morningness‐Eveningness Questionnaire (MEQ). The MCTQ was completed by 5,055 responders, of which 2,481 also completed the MEQ. MEQ score correlated well with the MCTQ assessment of time of mid‐sleep on free days (MSF; r=− 0.73) and on workdays (MSW; r=− 0.61). MEQ was more strongly correlated with MSF (50% of sleep time) than with sleep onset (0%), rise time (100%), or with any other percentile (10 to 40, 60% to 90%) of sleep on free days. The study shows that chronotype (based on MSF as measured by the MCTQ) strongly correlates with morningness‐eveningness (as measured by the MEQ). However, the MCTQ collects additional detailed information on sleep‐wake behavior under natural conditions.

Seasonal affective disorder and latitude: a review of the literature.

BACKGROUND The aim of the study is to investigate the relationship between the prevalence of SAD and latitude. METHODS An overview of the epidemiological literature on the prevalence of SAD is given and studies relevant for the latitudinal dependency of prevalence will be analyzed and discussed. RESULTS The mean prevalence of SAD is two times higher in North America compared to Europe. Over all prevalence studies, the correlation between prevalence and latitude was not significant. A significant positive correlation was found between prevalence and latitude in North America. For Europe there was a trend in the same direction. CONCLUSIONS The influence of latitude on prevalence seems to be small and other factors like climate, genetic vulnerability and social-cultural context can be expected to play a more important role. Additional controlled studies taking these factors into account are necessary to identify their influence.

Subjective sleepiness correlates negatively with global alpha (8–12 Hz) and positively with central frontal theta (4–8 Hz) frequencies in the human resting awake electroencephalogram

Subjective sleepiness is part of the system controlling the decision to go to sleep in humans. Extended periods of waking lead to increased sleepiness, as well as to changes in cortical electroencephalogram (EEG) during waking. We investigated the association of sleepiness and awake EEG spectra during 40 h of wakefulness using multi-electrode EEG recordings for full coverage of the scalp. We found: (1). strong negative correlations of alpha (8-12 Hz) power with subjective sleepiness at all scalp locations, suggesting a negative association between sleepiness and general cortical activation; and (2). positive correlations of theta (4-8 Hz) power with subjective sleepiness with a focus on frontal locations, suggesting additional location specific associations between sleepiness and cortical activation. These findings support the notion that sleepiness is directly represented in the awake EEG.

All Night Spectral Analysis of EEG Sleep in Young Adult and Middle-Aged Male Subjects

The sleep EEGs of 9 young adult males (age 20-28 years) and 8 middle-aged males (42-56 years) were analyzed by visual scoring and spectral analysis. In the middle-aged subjects power density in the delta, theta and sigma frequencies were attenuated as compared to the young subjects. In both age groups power density in the delta and theta frequencies declined from NREM period 1 to 3. In the sigma frequencies, however, no systematic changes in power density were observed over the sleep episode. In both age groups the decay of EEG power (0.75-7.0 Hz) over successive NREM-REM cycles and the time course of EEG power during NREM sleep was analyzed. The decay rate of both EEG power density over successive NREM-REM cycles and EEG power density during NREM sleep was smaller in the middle-aged subjects than in the young subjects. It is concluded that the age-related differences in human sleep EEG power spectra are not identical to the changes in EEG power spectra observed in the course of the sleep episode. Therefore age-related differences in EEG power spectra cannot be completely explained by assuming a reduced need for sleep in older subjects. The smaller decay rate of EEG power during NREM sleep in the middle-aged subjects is interpreted as a reduced sleep efficiency. The results are discussed in the frame work of the two-process model of sleep regulation.

Evolution of time-keeping mechanisms: early emergence and adaptation to photoperiod

Virtually all species have developed cellular oscillations and mechanisms that synchronize these cellular oscillations to environmental cycles. Such environmental cycles in biotic (e.g. food availability and predation risk) or abiotic (e.g. temperature and light) factors may occur on a daily, annual or tidal time scale. Internal timing mechanisms may facilitate behavioural or physiological adaptation to such changes in environmental conditions. These timing mechanisms commonly involve an internal molecular oscillator (a ‘clock’) that is synchronized (‘entrained’) to the environmental cycle by receptor mechanisms responding to relevant environmental signals (‘Zeitgeber’, i.e. German for time-giver). To understand the evolution of such timing mechanisms, we have to understand the mechanisms leading to selective advantage. Although major advances have been made in our understanding of the physiological and molecular mechanisms driving internal cycles (proximate questions), studies identifying mechanisms of natural selection on clock systems (ultimate questions) are rather limited. Here, we discuss the selective advantage of a circadian system and how its adaptation to day length variation may have a functional role in optimizing seasonal timing. We discuss various cases where selective advantages of circadian timing mechanisms have been shown and cases where temporarily loss of circadian timing may cause selective advantage. We suggest an explanation for why a circadian timing system has emerged in primitive life forms like cyanobacteria and we evaluate a possible molecular mechanism that enabled these bacteria to adapt to seasonal variation in day length. We further discuss how the role of the circadian system in photoperiodic time measurement may explain differential selection pressures on circadian period when species are exposed to changing climatic conditions (e.g. global warming) or when they expand their geographical range to different latitudes or altitudes.

EFFECTS OF SEGANSERIN, A 5-HT2 ANTAGONIST, AND TEMAZEPAM ON HUMAN SLEEP STAGES AND EEG POWER SPECTRA

The effects of seganserin, a specific 5HT2 antagonist, on human sleep were assessed in two experiments and compared to the effects of temazepam and sleep deprivation. During daytime recovery sleep after sleep deprivation, seganserin did not significantly enhance visually scored slow wave sleep (SWS, stages 3 + 4) or the EEG power density in the delta frequencies. Under these conditions temazepam reduced the power density in the delta and theta frequencies. During nighttime sleep after a nap in the evening, seganserin caused an increase in SWS, a reduction in intermittent wakefulness, and an enhancement of the power density in the delta and theta frequencies during non-rapid eye movement (NREM) sleep. Temazepam induced a reduction in the power density in the delta and theta frequencies. It is concluded that the 5HT2 antagonist, seganserin, can induce SWS. However, since the spectral results showed that the changes in the sleep EEG were not identical to those induced by sleep deprivation it seems premature to conclude that 5HT2 receptors are primarily involved in NREM sleep regulation.

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density

SummaryThe relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Sepctral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25–15.0 Hz) over successive nonrapid eye movement — rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Accuracy of Circadian Entrainment under Fluctuating Light Conditions: Contributions of Phase and Period Responses

The accuracy with which a circadian pacemaker can entrain to an environmental 24-h zeitgeber signal depends on (a) characteristics of the entraining signal and (b) response characteristics and intrinsic stability of the pacemaker itself. Position of the sun, weather conditions, shades, and behavioral variations (eye closure, burrowing) all modulate the light signal reaching the pacemaker. A simple model of a circadian pacemaker allows researchers to explore the impact of these factors on pacemaker accuracy. Accuracy is operationally defined as the reciprocal value of the day-to-day standard deviation of the clock times at which a reference phase (0) is reached. For the purpose of this exploration, the authors used a model pacemaker characterized solely by its momentary phase and momentary velocity. The average velocity determines the time needed to complete one pacemaker cycle and, therefore, is inversely proportional to pacemaker period. The model pacemaker responds to light by shifting phase and/or changing its velocity. The authors assumed further that phase and velocity show small random fluctuations and that the velocity is subject to aftereffects. Aftereffects were incorporated mathematically in a term allowing period to contract exponentially to a stable steady-state value, with a time constant of 69 d in the absence of light. The simulations demonstrate that a pacemaker reaches highest accuracy when it responds to light by simultaneous phase shifts and changes of its velocity. Phase delays need to coincide with slowing down and advances with speeding up; otherwise, no synchronization to the zeitgeber occurs. At maximal accuracy, the changes in velocity are such that the average period of the pacemaker under entrained conditions equals 24 h. The results suggest that during entrainment, the pacemaker adjusts its period to 24 h, after which daily phase shifts to compensate for differences between the periods of the zeitgeber and the clock are no longer necessary. On average, phase shifts compensate for maladjustments of phase and velocity changes compensate for maladjustments of period.

REM-SLEEP DEPRIVATION DURING 5 HOURS LEADS TO AN IMMEDIATE REM-SLEEP REBOUND AND TO SUPPRESSION OF NON-REM SLEEP INTENSITY

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.