Spectral analysis of the sleep onset period in primary insomnia.

Objective: To compare the EEG power spectra characteristics of the sleep onset period (SOP) in patients with sleep onset insomnia (SOI), sleep maintenance insomnia (SMI) and good sleepers (GS).

Methods: The time course of EEG power density (1-40Hz) during the SOP was examined in thirty subjects (SOI patients: N=10, SMI patients: N=10, GS: N=10).

Results: The EEG power of the beta2 frequency band (18-29.

The neuronal transition probability (NTP) model for the dynamic progression of non-REM sleep EEG: the role of the suprachiasmatic nucleus.

Little attention has gone into linking to its neuronal substrates the dynamic structure of non-rapid-eye-movement (NREM) sleep, defined as the pattern of time-course power in all frequency bands across an entire episode. Using the spectral power time-courses in the sleep electroencephalogram (EEG), we showed in the typical first episode, several moves towards-and-away from deep sleep, each having an identical pattern linking the major frequency bands beta, sigma and delta. The neuronal transition probability model (NTP)--in fitting the data well--successfully explained the pattern as resulting from stochastic transitions of the firing-rates of the thalamically-projecting brainstem-activating neurons, alternating between two steady dynamic-states (towards-and-away from deep sleep) each initiated by a so-far unidentified flip-flop.

State transitions between wake and sleep, and within the ultradian cycle, with focus on the link to neuronal activity.

The structure of sleep across the night as expressed by the hypnogram, is characterised by repeated transitions between the different states of vigilance: wake, light and deep non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. This review is concerned with current knowledge on these state transitions, focusing primarily on those findings that allow the integration of data at cellular level with spectral time-course data at the encephalographic (EEG) level. At the cellular level it has been proposed that, under the influence of circadian and homeostatic factors, transitions between wake and sleep may be determined by mutually inhibitory interaction between sleep-active neurons in the hypothalamic preoptic area and wake-active neurons in multiple arousal centres.

Spectral power time-courses of human sleep EEG reveal a striking discontinuity at approximately 18 Hz marking the division between NREM-specific and wake/REM-specific fast frequency activity.

Spectral power time-courses over the ultradian cycle of the sleep electroencephalogram (EEG) provide a useful window for exploring the temporal correlation between cortical EEG and sub-cortical neuronal activities. Precision in the measurement of these time-courses is thus important, but it is hampered by lacunae in the definition of the frequency band limits that are in the main based on wake EEG conventions. A frequently seen discordance between the shape of the beta power time-course across the ultradian cycle and that reported for the sequential mean firing rate of brainstem-thalamic activating neurons invites a closer examination of these band limits, especially since the sleep EEG literature indicates in several studies an intriguing non-uniformity of time-course comportment across the traditional beta band frequencies.

A unique pattern of sleep structure is found to be identical at all cortical sites: a neurobiological interpretation.

There is substantial evidence both at the cellular and at the electroencephalogram (EEG) level to support the view that the brainstem activating systems control the sleep-state (stage) progression over time that constitutes the overall sleep structure as seen at the EEG. We argue here that the brainstem therefore modulates the time-courses of spectral power in the different EEG frequency bands. These show during non-rapid eye movement (NREM) sleep a very particular interrelationship the origin of which has received little attention and for which the neuronal transition probability model for sleep structure has proposed a physiological explanation.

Beta EEG activity and insomnia.

To date there have been seven studies which find that beta EEG is elevated at around sleep onset and during polysomnographic sleep in patients with insomnia. These findings suggest that insomnia may be characterized by central nervous system (CNS) hyperarousal. In this article, the seven studies are critically reviewed, two theoretical perspectives on beta EEG are presented, and the concept of hyperarousal as a three component process is discussed.