Morning and Evening-Type Differences in Slow Waves during NREM Sleep Reveal Both Trait and State-Dependent Phenotypes

Brain recovery after prolonged wakefulness is characterized by increased density, amplitude and slope of slow waves (SW, <4 Hz) during non-rapid eye movement (NREM) sleep. These SW comprise a negative phase, during which cortical neurons are mostly silent, and a positive phase, in which most neurons fire intensively. Previous work showed, using EEG spectral analysis as an index of cortical synchrony, that Morning-types (M-types) present faster dynamics of sleep pressure than Evening-types (E-types). We thus hypothesized that single SW properties will also show larger changes in M-types than in E-types in response to increased sleep pressure. SW density (number per minute) and characteristics (amplitude, slope between negative and positive peaks, frequency and duration of negative and positive phases) were compared between chronotypes for a baseline sleep episode (BL) and for recovery sleep (REC) after two nights of sleep fragmentation. While SW density did not differ between chronotypes, M-types showed higher SW amplitude and steeper slope than E-types, especially during REC. SW properties were also averaged for 3 NREM sleep periods selected for their decreasing level of sleep pressure (first cycle of REC [REC1], first cycle of BL [BL1] and fourth cycle of BL [BL4]). Slope was significantly steeper in M-types than in E-types in REC1 and BL1. SW frequency was consistently higher and duration of positive and negative phases constantly shorter in M-types than in E-types. Our data reveal that specific properties of cortical synchrony during sleep differ between M-types and E-types, although chronotypes show a similar capacity to generate SW. These differences may involve 1) stable trait characteristics independent of sleep pressure (i.e., frequency and durations) likely linked to the length of silent and burst-firing phases of individual neurons, and 2) specific responses to increased sleep pressure (i.e., slope and amplitude) expected to depend on the synchrony between neurons

Slow oscillations in human non-rapid eye movement sleep electroencephalogram: effects of increased sleep pressure

Slow oscillations (< 1 Hz) in the non-rapid eye movement (NREM) sleep electroencephalogram (EEG) result from slow membrane potential fluctuations of cortical neurones, alternating between a depolarized up-state and a hyperpolarized down-state. They are thought to underlie the restorative function of sleep. We investigated the behaviour of slow oscillations in humans under increased sleep pressure to assess their contribution to sleep homeostasis. EEG recordings (C3A2) of baseline and recovery sleep after sleep deprivation (eight healthy males, mean age 23 years; 40 h of prolonged wakefulness) were analysed. Half-waves were defined as positive or negative deflections between consecutive zero crossings in the 0.5-2 Hz range of the band-pass filtered EEG. Increased sleep pressure resulted in a redistribution of half-waves between 0.5 and 2 Hz: the number of half-waves per minute was reduced below 0.9 Hz while it was increased above 1.2 Hz. EEG power was increased above 1 Hz. The increase in frequency was accompanied by increased slope of the half-waves and decreased number of multi-peak waves. In both baseline and recovery sleep, amplitude and slope were correlated highly over a broad frequency range and positive half-waves were characterized by a lower frequency than the negative ones, pointing to a longer duration of up- than down-states. We hypothesize that the higher frequency of slow oscillatory activity after prolonged wakefulness may relate to faster alternations between up- and down-states at the cellular level under increased sleep pressure. This study does not question slow-wave activity as a marker of sleep homeostasis, as the observed changes occurred within the same frequency range

Ammonia-related changes in cerebral electrogenesis in healthy subjects and patients with cirrhosis

OBJECTIVE: To study the effect of hyperammonaemia on the wake electroencephalogram (EEG) of patients with cirrhosis and healthy volunteers. METHODS: Wake EEGs were recorded prior to and after the induction of controlled hyperammonaemia in 10 patients with cirrhosis and 10 matched healthy volunteers. RESULTS: At baseline, patients had higher ammonaemia than healthy volunteers and their dominant EEG rhythm was slower and of higher amplitude. Induced hyperammonaemia resulted in increased spectral power over most of the scalp in healthy volunteers and decreased frequency along the anterior-posterior midline in patients. CONCLUSIONS: These findings suggest different effects of hyperammonaemia on the wake EEG in relation to baseline/peak ammonia levels. SIGNIFICANCE: The wake EEG is sensitive to hyperammonaemia and power-based EEG parameters may help in its neurophysiological definition, which, to date, has generally been based on EEG frequency indices

Sleep EEG alterations: effects of different pulse-modulated radio frequency electromagnetic fields

Previous studies have observed increases in electroencephalographic power during sleep in the spindle frequency range (approximately 11-15 Hz) after exposure to mobile phone-like radio frequency electromagnetic fields (RF EMF). Results also suggest that pulse modulation of the signal is crucial to induce these effects. Nevertheless, it remains unclear which specific elements of the field are responsible for the observed changes. We investigated whether pulse-modulation frequency components in the range of sleep spindles may be involved in mediating these effects. Thirty young healthy men were exposed, at weekly intervals, to three different conditions for 30 min directly prior to an 8-h sleep period. Exposure consisted of a 900-MHz RF EMF, pulse modulated at 14 Hz or 217 Hz, and a sham control condition. Both active conditions had a peak spatial specific absorption rate of 2 W kg(-1) . During exposure subjects performed three different cognitive tasks (measuring attention, reaction speed and working memory), which were presented in a fixed order. Electroencephalographic power in the spindle frequency range was increased during non-rapid eye movement sleep (2nd episode) following the 14-Hz pulse-modulated condition. A similar but non-significant increase was also observed following the 217-Hz pulse-modulated condition. Importantly, this exposure-induced effect showed considerable individual variability. Regarding cognitive performance, no clear exposure-related effects were seen. Consistent with previous findings, our results provide further evidence that pulse-modulated RF EMF alter brain physiology, although the time-course of the effect remains variable across studies. Additionally, we demonstrated that modulation frequency components within a physiological range may be sufficient to induce these effects

Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness

The neurophysiological mechanisms by which anesthetic drugs cause loss of consciousness are poorly understood. Anesthetic actions at the molecular, cellular, and systems levels have been studied in detail at steady states of deep general anesthesia. However, little is known about how anesthetics alter neural activity during the transition into unconsciousness. We recorded simultaneous multiscale neural activity from human cortex, including ensembles of single neurons, local field potentials, and intracranial electrocorticograms, during induction of general anesthesia. We analyzed local and global neuronal network changes that occurred simultaneously with loss of consciousness. We show that propofol-induced unconsciousness occurs within seconds of the abrupt onset of a slow (<1 Hz) oscillation in the local field potential. This oscillation marks a state in which cortical neurons maintain local patterns of network activity, but this activity is fragmented across both time and space. Local (<4 mm) neuronal populations maintain the millisecond-scale connectivity patterns observed in the awake state, and spike rates fluctuate and can reach baseline levels. However, neuronal spiking occurs only within a limited slow oscillation-phase window and is silent otherwise, fragmenting the time course of neural activity. Unexpectedly, we found that these slow oscillations occur asynchronously across cortex, disrupting functional connectivity between cortical areas. We conclude that the onset of slow oscillations is a neural correlate of propofol-induced loss of consciousness, marking a shift to cortical dynamics in which local neuronal networks remain intact but become functionally isolated in time and space