28 research outputs found

    Reflex tachycardia with airway opening in obstructive sleep apnea

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    Arousal from sleep is traditionally defined as a visually discernible shift to higher frequency activity in the sleep EEG lasting > 3 sec, with > 15-sec shifts considered full awakening. Arousals can occur spontaneously without an obvious trigger or be elicited by virtually any sensory stimulus applied with sufficient intensity to reach the “arousal threshold,” which varies between individuals and according to the “depth” or stage of sleep. Rather than simply a return to wakefulness, arousal appears to reflect a transiently activated state with altered responses to sensory inputs compared to wakefulness. Rapid cortical re-activation along with augmented cardiorespiratory and metabolic activity accompanying arousal has clear survival advantages, since all may be required to support “fight or flight” responses to exogenous or endogenous threats arising during sleep.Australian National Health and Medical Research Counci

    The efficacy of transcranial current stimulation techniques to modulate resting-state EEG, to affect vigilance and to promote sleepiness

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    Transcranial Current Stimulations (tCSs) are non-invasive brain stimulation techniques which modulate cortical excitability and spontaneous brain activity by the application of weak electric currents through the scalp, in a safe, economic, and well-tolerated manner. The direction of the cortical effects mainly depend on the polarity and the waveform of the applied current. The aim of the present work is to provide a broad overview of recent studies in which tCS has been applied to modulate sleepiness, sleep, and vigilance, evaluating the efficacy of different stimulation techniques and protocols. In recent years, there has been renewed interest in these stimulations and their ability to affect arousal and sleep dynamics. Furthermore, we critically review works that, by means of stimulating sleep/vigilance patterns, in the sense of enhancing or disrupting them, intended to ameliorate several clinical conditions. The examined literature shows the efficacy of tCSs in modulating sleep and arousal pattern, likely acting on the top-down pathway of sleep regulation. Finally, we discuss the potential application in clinical settings of this neuromodulatory technique as a therapeutic tool for pathological conditions characterized by alterations in sleep and arousal domains and for sleep disorders per se

    NEUROLOGIE UND SCHLAFMEDIZIN

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    Neurology is frequently confrontated with sleep disturbances and/or their effects. Sleep disturbances may be early, main- or escort symptom, in addition as well a factor of risk for a neurological illness. Goal of this contribution is to mediate a small overview of usual organic sleep disturbances and to give an insight into sleep medicine ways of thinking.Die Neurologie ist mit Schlafstörungen bzw. deren Auswirkungen sehr häufig konfrontiert. Schlafstörungen können sowohl Früh-, Leit – oder Begleitsymptom, aber auch Risikofaktor für eine neurologische Erkrankung sein. Ziel dieses Beitrages ist es, einen kleinen Überblick über gängige organische Schlafstörungen, sowie einen Einblick in schlafmedizinische Denkweisen, zu vermitteln

    Linking the nature and functions of sleep: insights from multimodal imaging of the sleeping brain

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    Sleep and wakefulness are traditionally considered as two mutually exclusive states with contrasting behavioural manifestations and complementary neurobiological functions. However, the discoveries of local sleep in global wakefulness and local wakefulness in global sleep have challenged this classical view and raised questions about the nature and functions of sleep. Here, we review the contributions from recent multimodal imaging studies of human sleep towards understanding the relationship between the nature and functions of sleep. Through simultaneous tracking of brain state and mapping of brain activity, these studies revealed that the sleeping brain can carry out covert cognitive processing that was thought to be wake-specific (wake-like function in the sleeping brain). Conversely, the awake brain can perform housekeeping functions through local sleep of neural populations (sleep-like function in the awake brain). We discuss how the blurred boundary between sleep and wakefulness highlights the need to radically rethink the definition of brain states, and how the recently discovered fMRI signatures of global and local sleep can help to address these outstanding questions

    EEG functional connectivity prior to sleepwalking : evidence of interplay between sleep and wakefulness

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    Study Objectives: Although sleepwalking (somnambulism) affects up to 4% of adults, its pathophysiology remains poorly understood. Sleepwalking can be preceded by fluctuations in slow-wave sleep EEG signals, but the significance of these pre-episode changes remains unknown and methods based on EEG functional connectivity have yet to be used to better comprehend the disorder. Methods: We investigated the sleep EEG of 27 adult sleepwalkers (mean age: 29 ± 7.6 years) who experienced a somnambulistic episode during slow-wave sleep. The 20-second segment of sleep EEG immediately preceding each patient’s episode was compared with the 20-second segment occurring 2 minutes prior to episode onset. Results: Results from spectral analyses revealed increased delta and theta spectral power in the 20 seconds preceding the episodes’ onset as compared to the 20 seconds occurring 2 minutes before the episodes. The imaginary part of the coherence immediately prior to episode onset revealed (1) decreased delta EEG functional connectivity in parietal and occipital regions, (2) increased alpha connectivity over a fronto-parietal network, and (3) increased beta connectivity involving symmetric inter-hemispheric networks implicating frontotemporal, parietal and occipital areas. Conclusions: Taken together, these modifications in EEG functional connectivity suggest that somnambulistic episodes are preceded by brain processes characterized by the co-existence of arousal and deep slee

    The brain network organization during sleep onset after deprivation

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    Objective: Aim of the present study is to investigate the alterations of brain networks derived from EEG analysis in pre- and post-sleep onset conditions after 40 h of sleep deprivation (SD) compared to sleep onset after normal sleep in 39 healthy subjects. Methods: Functional connectivity analysis was made on electroencelographic (EEG) cortical sources of current density and small world (SW) index was evaluated in the EEG frequency bands (delta, theta, alpha, sigma and beta). Results: Comparing pre- vs. post-sleep onset conditions after a night of SD a significant decrease of SW in delta and theta bands in post-sleep onset condition was found together with an increase of SW in sigma band. Comparing pre-sleep onset after sleep SD versus pre-sleep onset after a night of normal sleep a decreased of SW index in beta band in pre-sleep onset in SD compared to pre-sleep onset in normal sleep was evidenced. Conclusions: Brain functional network architecture is influenced by the SD in different ways. Brain networks topology during wake resting state needs to be further explored to reveal SD-related changes in order to prevent possible negative effects of SD on behaviour and brain function during wakefulness. Significance: The SW modulations as revealed by the current study could be used as an index of an altered balance between brain integration and segregation processes after SD

    Circadian dynamics in measures of cortical excitation and inhibition balance

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    Several neuropsychiatric and neurological disorders have recently been characterized as dysfunctions arising from a ‘final common pathway’ of imbalanced excitation to inhibition within cortical networks. How the regulation of a cortical E/I ratio is affected by sleep and the circadian rhythm however, remains to be established. Here we addressed this issue through the analyses of TMS-evoked responses recorded over a 29h sleep deprivation protocol conducted in young and healthy volunteers. Spectral analyses of TMS-evoked responses in frontal cortex revealed non-linear changes in gamma band evoked oscillations, compatible with an influence of circadian timing on inhibitory interneuron activity. In silico inferences of cell-to-cell excitatory and inhibitory connectivity and GABA/Glutamate receptor time constant based on neural mass modeling within the Dynamic causal modeling framework, further suggested excitation/inhibition balance was under a strong circadian influence. These results indicate that circadian changes in EEG spectral properties, in measure of excitatory/inhibitory connectivity and in GABA/glutamate receptor function could support the maintenance of cognitive performance during a normal waking day, but also during overnight wakefulness. More generally, these findings demonstrate a slow daily regulation of cortical excitation/inhibition balance, which depends on circadian-timing and prior sleep-wake history

    Sleep as a window for evaluating neurodevelopmental outcome: which impact on the brain of preterm infants? A prospective study on prematurity from a biological neuropsychiatry perspective

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    Background. Newborns and infants spend most of their time sleeping an immature sleep, which allows brain maturation a good neurodevelopment. Preterm birth is associated with abnormal brain development and alterations in later-in-life sleep patterns, carrying a high social burden, even when not accompanied by major neurological damages. Which impact prematurity itself can have on early sleep architecture, which influence it can have on well- known adverse outcomes, and which role brain lesions play in determining sleep patterns in preterm infants are still matter of debate. This exploratory pilot study aimed to describe the distribution of sleep states among very low birth weight (VLBW) infants, and to correlate it with neurobehavioral assessment at 35 weeks of post-menstrual age (PMA), and to observe if these persisted at term equivalent age (TEA) and at 6 months of corrected age (CA). Secondly, it aimed to assess if the presence of a major or minor brain lesion detected at MRI can affect sleep duration, distribution and quality. Methods. 10 VLBW were assessed at 34±2 weeks PMA with a 24-hours video- polysomnographic recording and received a neurobehavioral examination at the moment of the recording and at TEA (with Neonatal Behavior Assessment Scale; Hammersmith Neurological Neonatal Examination, and the neonatal visual battery). They were followed- up at 6 months CA with Griffiths’ Mental Development Scale III edition. Analysis of sleep stages distribution and spectra was conducted. Results. Total sleep time and total amount of transitional sleep (TS) significantly positively correlated with neurological, and neurobehavioral assessment at 34 weeks PMA, at TEA and with neurodevelopment at 6 months CA, while Sleep Onset Active Sleep (SOAS) had a negative association. Infants carrying severe-moderate brain lesions showed lower Total Sleep time (66.9% ± 7.39 vs 72.2% ± 3.52, p = 0.047) accompanied by a higher prevalence of SOAS (23.9% ± 10.2 vs 12.26% ± 5.5 p = 0.048), and showed a gradient for higher power of posterior slow activity (slow δ and δ) during SOAS from the posterior cerebral regions. Conclusions. Understanding sleep mechanism among preterm infants might provide future therapeutic/management strategies, which need to encompass sleep care. Further analyses with larger samples and more complex methods are claimed

    Cortico-autonomic local arousals and heightened somatosensory arousability during NREMS of mice in neuropathic pain.

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    Frequent nightly arousals typical for sleep disorders cause daytime fatigue and present health risks. As such arousals are often short, partial, or occur locally within the brain, reliable characterization in rodent models of sleep disorders and in human patients is challenging. We found that the EEG spectral composition of non-rapid eye movement sleep (NREMS) in healthy mice shows an infraslow (~50 s) interval over which microarousals appear preferentially. NREMS could hence be vulnerable to abnormal arousals on this time scale. Chronic pain is well-known to disrupt sleep. In the spared nerve injury (SNI) mouse model of chronic neuropathic pain, we found more numerous local cortical arousals accompanied by heart rate increases in hindlimb primary somatosensory, but not in prelimbic, cortices, although sleep macroarchitecture appeared unaltered. Closed-loop mechanovibrational stimulation further revealed higher sensory arousability. Chronic pain thus preserved conventional sleep measures but resulted in elevated spontaneous and evoked arousability. We develop a novel moment-to-moment probing of NREMS vulnerability and propose that chronic pain-induced sleep complaints arise from perturbed arousability
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