An electroencephalographic fingerprint of human sleep

Gennaro, Luigi De; Ferrara, Michele; Vecchio, Fabrizio; Curcio, Giuseppe; Bertini, Mario

doi:10.1016/j.neuroimage.2005.01.020

Cited by 230 publications

(216 citation statements)

References 53 publications

Supporting

Mentioning

191

Contrasting

Unclassified

Order By: Relevance

“…Whether a classification of cortical areas according to their respective deactivation times is physiologically sound and whether asynchrony in deactivation between the thalamic nuclei themselves also exists thus remain questions to be investigated. However, the possibility that these heterogeneities could be linked to the known intra- (14) and interindividual (7,8) local variations in cortical EEG power during sleep and in preceding local brain activities during waking periods (37-39) cannot be ignored. In addition to this challenge, our results reveal that extensive cortical territories remain activated for several minutes after the thalamic deactivation at sleep onset, a situation that may be propitious to the development of hypnagogic experiences so common during the wake-sleep transition (40,41).…”

Section: Discussionmentioning

confidence: 99%

“…intracranial recording | EEG | dimension of activation | thalamus | wake-tosleep transition A bundant electrophysiological and functional imaging data have revealed that sleep-related brain activity is not the result of a global deactivation of cerebral structures but rather is a multifocal process associated with local changes in brain activities (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Examples of such functional heterogeneities are, among others, the fronto-occipital gradient in cortical activity during sleep (1,2), the preponderant fronto-parietal localization of sleep spindles (3,4), and interhemispheric imbalanced activity (5,6).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Magnin

Rey

Bastuji

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

197

147

View full text Add to dashboard Cite

Thalamic and cortical activities are assumed to be time-locked throughout all vigilance states. Using simultaneous intracortical and intrathalamic recordings, we demonstrate here that the thalamic deactivation occurring at sleep onset most often precedes that of the cortex by several minutes, whereas reactivation of both structures during awakening is synchronized. Delays between thalamus and cortex deactivations can vary from one subject to another when a similar cortical region is considered. In addition, heterogeneity in activity levels throughout the cortical mantle is larger than previously thought during the descent into sleep. Thus, asynchronous thalamocortical deactivation while falling asleep probably explains the production of hypnagogic hallucinations by a still-activated cortex and the common self-overestimation of the time needed to fall asleep.A bundant electrophysiological and functional imaging data have revealed that sleep-related brain activity is not the result of a global deactivation of cerebral structures but rather is a multifocal process associated with local changes in brain activities (1-10). Examples of such functional heterogeneities are, among others, the fronto-occipital gradient in cortical activity during sleep (1, 2), the preponderant fronto-parietal localization of sleep spindles (3, 4), and interhemispheric imbalanced activity (5, 6). So far, very few studies have addressed the time course of these regional differences during transitions between vigilance states (11)(12)(13)(14), and most of these studies were based on scalp recordings performed during stable periods of wakefulness or sleep. Although reports that favor some asynchrony of sleep-onset activity between the different cortical areas are accumulating, there still is a firm belief that thalamic and cortical activities are tightly coupled, at both the cellular and integrative level, during wakefulness and sleep (15)(16)(17)(18). Recent intracranial data in humans, however, indicate that, during both paradoxical (rapid eye movement) sleep and sleep stage 2, thalamic and cortical activities may alternate periods of coupling and decoupling (19,20). In this context, the question is whether the dynamics of the neuronal deactivation that characterizes the transition from wakefulness to sleep is identical in thalamus and cortex, or, conversely, whether transient decoupling may occur at this transition time that would suggest different sleep-onset timing in these two structures. The opportunity to record thalamic and cortical activities simultaneously in epileptic patients chronically implanted with intracerebral electrodes allowed us to address this issue. In contrast to the generally accepted view that thalamic and cortical activities are tightly locked along the different vigilance states, we found that the thalamic activity most often decreased to sleep levels several minutes before the cortical activity started to abate. This finding suggests that the cortex remains neurophysiologically awake but decoupled from thalamic i...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Magnin

Rey

Bastuji

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

197

147

View full text Add to dashboard Cite

show abstract

“…This finding suggests that the sleep EEG qualifies as the most heritable trait known so far, matched only by heritabilities for brain architecture such as the distribution of grey matter in the cerebral cortex (Andretic et al, 2008). Considering the facts that functional brain connectivity and rhythmic brain oscillations are determined by common genetic factors (Posthuma et al, 2005) and that the frequencyspecific, regional distribution of EEG power in NREM sleep is highly stable (De Gennaro et al, 2005;Finelli et al, 2001), it is possible that these two traits are inter-related.…”

Section: Heritability Of Sleep Eegmentioning

confidence: 99%

Genetic determination of sleep EEG profiles in healthy humans

Landolt

2011

Progress in Brain Research

View full text Add to dashboard Cite

The contribution of slow brain oscillations including delta, theta, alpha, and sigma frequencies to the sleep electroencephalography (EEG) is finely regulated by circadian and homeostatic influences, and reflects functional aspects of wakefulness and sleep. Accumulating evidence demonstrates that individual sleep EEG patterns in non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep are heritable traits. More specifically, multiple recordings in the same individuals, as well as studies in monozygotic and dizygotic twins suggest that a very high percentage of the robust interindividual variation and the high intraindividual stability of sleep EEG profiles can be explained by genetic factors (> 90% in distinct frequency bands). Still little is known about which genes contribute to different sleep EEG phenotypes in healthy humans. The genetic variations that have been identified to date include functional polymorphisms of the clock gene PER3 and of genes contributing to signal transduction pathways involving adenosine (ADA, ADORA2A), brain-derived neurotrophic factor (BDNF), dopamine (COMT), and prion protein (PRNP). Some of these polymorphisms profoundly modulate sleep EEG profiles; their effects are reviewed here. It is concluded that the search for genetic contributions to slow sleep EEG oscillations constitutes a promising avenue to identify molecular mechanisms underlying sleep-wake regulation in humans.

show abstract

“…In fact, the spatial distribution of EEG oscillations in nonREM sleep is highly stable across multiple recordings within the same individual. Thus, sleep EEG topography was proposed to reflect an individual "fingerprint", which is genetically determined [32,47,48].…”

Section: Homeostatic Sleep-wake Regulationmentioning

confidence: 99%

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Landolt

2008

CPD

View full text Add to dashboard Cite

Abstract:To better understand the neurobiology of sleep disorders, detailed understanding of circadian and homeostatic sleep-wake regulation in healthy volunteers is mandatory. Sleep physiology and the repercussions of experimentallyinduced sleep deprivation on sleep and waking electroencephalogram (EEG), vigilance and subjective state are highly variable, even in healthy individuals. Accumulating evidence suggests that many aspects of normal sleep-wake regulation are at least in part genetically controlled. Current heritability estimates of sleep phenotypes vary between approximately 20-40 % for habitual sleep duration, to over 90 % for the spectral characteristics of the EEG in nonREM sleep. The molecular mechanisms underlying the trait-like, inter-individual variation are virtually unknown, and the human genetics of normal sleep is only at the beginning of being explored. The first studies identified distinct polymorphisms in genes contributing to the endogenous circadian clock and neurochemical systems previously implicated in sleep-wake regulation, to modulate sleep architecture and sleep EEG, vulnerability to sleep loss, and subjective and objective effects of caffeine on sleep. These insights are reviewed here. They disclose molecular mechanisms contributing to normal sleep-wake regulation in humans, and have potentially important implications for the neurobiology of sleep-wake disorders and their pharmacological treatment.

show abstract

An electroencephalographic fingerprint of human sleep

Cited by 230 publications

References 53 publications

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Thalamic deactivation at sleep onset precedes that of the cerebral cortex in humans

Genetic determination of sleep EEG profiles in healthy humans

Genotype-Dependent Differences in Sleep, Vigilance, and Response to Stimulants

Contact Info

Product

Resources

About