Showing papers on "Delta wave published in 2008"

Spontaneous neural activity during human slow wave sleep

Abstract: Slow wave sleep (SWS) is associated with spontaneous brain oscillations that are thought to participate in sleep homeostasis and to support the processing of information related to the experiences of the previous awake period. At the cellular level, during SWS, a slow oscillation ( 140 μV) and delta waves (75–140 μV) during SWS in 14 non-sleep-deprived normal human volunteers. Significant increases in activity were associated with these waves in several cortical areas, including the inferior frontal, medial prefrontal, precuneus, and posterior cingulate areas. Compared with baseline activity, slow waves are associated with significant activity in the parahippocampal gyrus, cerebellum, and brainstem, whereas delta waves are related to frontal responses. No decrease in activity was observed. This study demonstrates that SWS is not a state of brain quiescence, but rather is an active state during which brain activity is consistently synchronized to the slow oscillation in specific cerebral regions. The partial overlap between the response pattern related to SWS waves and the waking default mode network is consistent with the fascinating hypothesis that brain responses synchronized by the slow oscillation restore microwake-like activity patterns that facilitate neuronal interactions.

Effects of Ibotenate and 192IgG-Saporin Lesions of the Nucleus Basalis Magnocellularis/Substantia Innominata on Spontaneous Sleep and Wake States and on Recovery Sleep after Sleep Deprivation in Rats

Abstract: The basal forebrain (BF) is known for its role in cortical and behavioral activation, and has been postulated to have a role in compensatory mechanisms after sleep loss. However, specific neuronal phenotypes responsible for these roles are unclear. We investigated the effects of ibotenate (IBO) and 192IgG-saporin (SAP) lesions of the caudal BF on spontaneous sleep-waking and electroencephalogram (EEG), and recovery sleep and EEG after 6 h of sleep deprivation (SD). Relative to artificial CSF (ACSF) controls, IBO injections decreased parvalbumin and cholinergic neurons in the caudal BF by 43 and 21%, respectively, and cortical acetylcholinesterase staining by 41%. SAP injections nonsignificantly decreased parvalbumin neurons by 11%, but significantly decreased cholinergic neurons by 69% and cortical acetylcholinesterase by 84%. IBO lesions had no effect on sleep-wake states but increased baseline delta power in all states [up to 62% increase during non-rapid eye movement (NREM) sleep]. SAP lesions transiently increased NREM sleep by 13%, predominantly during the dark phase, with no effect on EEG. During the first 12 h after SD, animals with IBO and SAP lesions showed lesser rebound NREM sleep (32 and 77% less, respectively) and delta power (78 and 53% less) relative to ACSF controls. These results suggest that noncholinergic BF neurons promote cortical activation by inhibiting delta waves, whereas cholinergic BF neurons play a nonexclusive role in promoting wake. Intriguingly, these results also suggest that both types of BF neurons play important roles, probably through different mechanisms, in increased NREM sleep and EEG delta power after sleep loss.

Slow-wave sleep, diabetes, and the sympathetic nervous system.

Abstract: Sleep oscillates between two different states: non-rapid eye movement (NREM) sleep and rapid-eye movement (REM) sleep. Slow-wave sleep (SWS) is a substate of NREM sleep, and its identification is based primarily on the presence of slow waves, i.e., low-frequency, high-amplitude oscillations in the EEG. Quantification of SWS is accomplished by visual inspection of EEG records or computerized methods such as spectral analysis based on the fast Fourier transform (FFT). Slow-wave activity (SWA; also referred to as delta power) is a quantitative measure of the contribution of both the amplitude and prevalence of slow waves in the EEG. The EEG oscillations reflect the field potentials associated with synchronized burst-pause firing patterns in cortical neurons (1). In view of these brain-based defining characteristics of SWS, it is not surprising that most theories on the functional significance of SWS have focused on the brain. In a recent issue of PNAS, Tasali et al. (2) draw attention to another aspect of SWS: the effects of SWS disruption on glucose tolerance and insulin resistance. What do these new data tells us about SWS and its functional significance? Is it for the body as well as the brain?

Neurobiology of sleep fragmentation: cortical and autonomic markers of sleep disorders.

Abstract: New insights into the physiopathological correlates of arousal and sleep fragmentation have recently been gained through experimental and clinical studies in healthy individuals and in patients with sleep disorders. The development of new analyses of autonomic system during sleep, has enriched the knowledge of sleep fragmentation derived from electroencephalographic analysis and has made possible the characterization of other phasic events arising from sleep, such as autonomic arousals. All of these studies provide evidence in support of the hypothesis that autonomic activations without cortical involvement are an epiphenomena of sleep fragmentation and altered sleep continuity, similar to that induced by cortical activation. This review begins by describing the latest findings on type of arousal response, with regards to the effect of arousing stimuli on the brain and the autonomic system. It then focuses on the hotly debated issue on experimental and clinical physiopathology of the arousals without cortical activation, highlighting the results of novel studies on the neural substrates mediating these response. Finally, we address the current question on clinical significance of sleep fragmentation to understand if arousal per se, cortical or autonomic, has an impact on daytime functioning, cardiovascular consequences and cognitive sequelae.

Long-term changes in sleep and electroencephalographic activity by chronic vagus nerve stimulation in cats.

Abstract: We previously reported the effect of vagus nerve electrical stimulation (VNS) on sleep and behavior in cats. The aim of the present study is to analyze the long-term effects of VNS on the electroencephalographic (EEG) power spectrum and on the different stages of the sleep-wakefulness cycle in the freely moving cat. To achieve this, six male cats were implanted with electrodes on the left vagal nerve and submitted to 15 rounds of 23 h continuous sleep recordings in three categories: baseline (BL), VNS and post-stimulus recording (PSR). The following parameters were analyzed: EEG power spectrum, total time and number of sleep phases, ponto-geniculo-occipital (PGO) wave density of the rapid eye movement (REM) sleep, and the number of times the narcoleptic reflex was present (sudden transition from wakefulness to REM sleep). Significant changes were detected, such as an enhancement of slow-wave sleep (SWS) stage II; a power increase in the bands corresponding to sleep spindles (8-14 Hz) and delta waves (1-4 Hz) with VNS and PSR; an increase in the total time, number of stages, and density of PGO wave in REM sleep with VNS; a decrease of wakefulness in PSR, and the eventual appearance of the narcoleptic reflex with VNS. The results show that the effect of the VNS changes during different stages of the sleep-wakefulness cycle. In REM sleep, the effect was present only during VNS, while the SWS II was affected beyond VNS periods. This suggests that ponto-medullar and thalamic mechanisms of slow EEG activity may be due to plastic changes elicited by vagal stimulation.

Enhancement of neocortical-medial temporal EEG correlations during non-REM sleep.

Abstract: Interregional interactions of oscillatory activity are crucial for the integrated processing of multiple brain regions However, while the EEG in virtually all brain structures passes through substantial modifications during sleep, it is still an open question whether interactions between neocortical and medial temporal EEG oscillations also depend on the state of alertness Several previous studies in animals and humans suggest that hippocampal-neocortical interactions crucially depend on the state of alertness (ie, waking state or sleep) Here, we analyzed scalp and intracranial EEG recordings during sleep and waking state in epilepsy patients undergoing presurgical evaluation We found that the amplitudes of oscillations within the medial temporal lobe and the neocortex were more closely correlated during sleep, in particular during non-REM sleep, than during waking state Possibly, the encoding of novel sensory inputs, which mainly occurs during waking state, requires that medial temporal dynamics are rather independent from neocortical dynamics, while the consolidation of memories during sleep may demand closer interactions between MTL and neocortex

Interaction between sleep EEG and ECG signals during and after obstructive sleep apnea events with or without arousals

Abstract: This is a preliminary attempt to directly investigate the interactions of sleep EEG and ECG signals during normal, OSA breathing event and events following its termination with or without arousal in non-REM(NREM) and REM sleep stages. ECG and EEG signals were collected from 10 patients with OSA and 5 healthy subjects. Coherence between two signals (CoherenceECG-EEG) over different frequency bands(range:0~40 Hz) were calculated for normal breathing events, OSA events and events following OSA terminations (with/without arousals) in NREM as well as REM sleep. In normal breathing events, overall CoherenceECG-EEG in REM sleep is higher than that in NREM sleep. Significant (p<0.01) differences of CoherenceECG-EEG between OSA events with and without arousals were found in NREM sleep over 0.5-25 Hz bands but in REM sleep over 3.0-12 Hz. This research could be useful in understanding cardiac dysfunction in sleep apnoea patient.

Modelling electrical activities of the brain and analysis of the EEG in general anesthesia

Abstract: An enhanced local mean-field (MF) model that is suitable for simulating the EEG in different depths of anesthesia (DOA) is presented. The main elements of the model are taken from the Steyn-Ross and Bojak & Liley models, and a new slow ionic mechanism is included in the basis model. The Wilson-Cowan sigmoidal function corresponding to excitatory population is redefined to be also a function of the slow ionic mechanism. This modification adapts the firing rate of neural populations to slow ionic activities of the brain. When an anesthetic is administered, the slow mechanism induces neural cells to alternate between two levels of activity (up and down states). The frequency of up-down switching is in the delta band and this is the main reason behind high amplitude, low frequency EEG in anesthesia. The model may settle in up state in waking, switch to up and down states in moderate anesthesia or remains in down state in deep anesthesia. The modulation of alpha waves by slower EEG activities is also investigated in various DOA on 10 children. The modulation is quantified by two parameters so-called phase and strength of modulation (POM, SOM). These parameters are calculated for various formations of delta sub-bands and are employed to isolate different mechanisms contributing to delta waves, and to determine DOA. According to SOM, delta band comprises three main sub-bands roughly in [0. 1?0. 5], [0. 5?1. 5] and [2?4] Hz (very slow, slow and fast delta). POM decreases with desflurane so it may help us for determining DOA as a neurophysiologic parameter. Analyses show that POM relating to [1. 7?4] Hz can distinguish deep and light anesthesia better than BIS index.