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Biomedical subjects

D G Beersma

Publications and source records attributed to D G Beersma.

59 records · Page 4Linked to original sources

Timing of human sleep: recovery process gated by a circadian pacemaker.

A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.

Bed Rest↗

Refractive index of the fly rhabdomere.

The refractive index and the diameter of the fly rhabdomere were determined by comparing the experimental results derived from interference microscopy with the results of theoretical study on the scattering of plane waves by a homogeneous, isotropic cylindrical dielectric rod. It was found that the refractive index of the isolated rhabdomere of Calliphora erythrocephala is 1.363 +/- 0.003 in an area of the rhabdomere where its diameter is calculated to be 1.32 +/- 0.04 micrometers.

Animals↗

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.

Adult↗

The significance of sleep physiological disturbances in depression.

Since the discovery of the antidepressant effects of interventions in the sleep-wake cycle, a number of hypotheses have emerged according to which disturbances in sleep physiology are not merely expressions but essential components of the pathophysiology of depression. Three hypotheses are presented, the "Phase-advance", the "S-deficiency" and the "ACh-hypersensitivity" hypotheses. They explain the therapeutic effects of total, partial and selective sleep deprivation as consequences of the normalization of disturbed sleep regulation. The question is dealt with whether there are indications that the hypothesized sleep regulatory disturbances exist and whether there is a relationship between the effects of sleep deprivation on sleep regulation and clinical state. None of the hypotheses is totally supported, none can be fully rejected.

Circadian Rhythm↗