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Helli Merica

Publications and source records attributed to Helli Merica.

4 recordsLinked to original sources

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. We ascribe this tentatively to the sharp reversal of slope we have seen at approximately 18 Hz in our data and that of others. Here, therefore, using data for the first four ultradian cycles from 18 healthy subjects, we apply several criteria based on changes in time-course comportment in order to examine this non-uniformity as we move in 1 Hz bins through the frequency range 14-30 Hz. The results confirm and describe in detail the striking discontinuity of shape at around 18 Hz, with only the upper range (18-30 Hz) displaying a time-course similar to that of the firing-rate changes measured in brainstem activating neurons and acknowledged to engender states of brain activation. Fast frequencies in the lower range (15-18 Hz), on the other hand, are shown to be specific to non-rapid-eye-movement sleep. Splitting the beta band at approximately 18 Hz therefore permits a significant improvement in EEG measurement and a more precise correlation with cellular activity.

Adult↗

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. These two fundamentally different behavioural states are separated by the sleep onset and the sleep inertia periods each characterised by gradual changes in which neither true wake nor true sleep patterns are present. The results of sequential spectral analysis of EEG data on moves towards and away from deep sleep are related to findings at the cellular level on the generating mechanisms giving rise to the various NREM oscillatory modes under the neuromodulatory control of brainstem-thalamic activating systems. And there is substantial evidence at cellular level that transition to and from REM sleep is governed by the reciprocal interaction between cholinergic REM-on neurons and aminergic REM-off neurons located in the brainstem. Similarity between the time-course of the REM-on neuronal activity and that of EEG power in the high beta range (approximately 18-30 Hz) allows a tentative parallelism to be drawn between the two. This review emphasises the importance of the thalamically projecting brainstem activating systems in the orchestration of the transitions that give rise to state progression across the sleep-wake cycle.

Activity Cycles↗

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. We advance the hypothesis that if the brainstem is modulating these time-courses then they should show a marked similarity in shape and timing at all sites. Using data from 10 healthy subjects, we measure the degree of similarity of the time-courses over each of the first four NREM episodes at the frontal, central and parietal sites, for each of the frequency bands beta, sigma and delta, and also the cortically generated slow oscillation. All the cross- correlation coefficients are high and statistically significant, indicating that the shape and timing of these time-courses are practically identical at different sites despite regional differences in their average power levels. These results tend to suggest that two processes may operate concurrently: the brainstem controls the shape and timing of the power time-courses while cortical-thalamic interaction controls their site-dependent average power.

Adult↗

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.

Journal Article↗