Increased EEG sigma and beta power during NREM sleep in primary insomnia

Spiegelhalder, Kai; Regen, Wolfram; Feige, Bernd; Holz, Johannes; Piosczyk, Hannah; Baglioni, Chiara; Riemann, Dieter; Nissen, Christoph

doi:10.1016/j.biopsycho.2012.08.009

Cited by 160 publications

(145 citation statements)

References 30 publications

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“…There is no specific evidence that the observed spectral EEG changes with GABA A modulators are a precursor to or are direct evidence of the AEs associated with these compounds. However, it has been reported that changes in the frequencies involved in sleep spindles (or sigma power bands; bursts of oscillatory brain activity during stage 2 sleep) are related to amnesia, changes in the beta band are related to sensorimotor control and cognition, and changes in the slower delta band are related to subjective sleep complaints (Espa et al, 2000;Krystal et al, 2002;Spiegelhalder et al, 2012). In humans, the distinct typical spectral EEG change in delta sleep induced by benzodiazepine and benzodiazepine-like hypnotics, including zolpidem and zopiclone, have been well characterized (Achermann and Borbely, 1987;Aeschbach et al, 1994;Feige et al, 1999;Lundahl et al, 2012;Trachsel et al, 1990).…”

Section: Discussionmentioning

confidence: 98%

Quantitative Electroencephalography Within Sleep/Wake States Differentiates GABAA Modulators Eszopiclone and Zolpidem From Dual Orexin Receptor Antagonists in Rats

Fox

Gotter

Tye

et al. 2013

Neuropsychopharmacol

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Dual orexin receptor antagonists (DORAs) induce sleep by blocking orexin 1 and orexin 2 receptor-mediated activities responsible for regulating wakefulness. DORAs represent a potential alternative mechanism to the current standard of care that includes the γ-aminobutyric acid (GABA)A receptor-positive allosteric modulators, eszopiclone and zolpidem. This work uses an innovative method to analyze electroencephalogram (EEG) spectral frequencies within sleep/wake states to differentiate the effects of GABAA modulators from DORA-22, an analog of the DORA MK-6096, in Sprague-Dawley rats. The effects of low, intermediate, and high doses of eszopiclone, zolpidem, and DORA-22 were examined after first defining each compound's ability to promote sleep during active-phase dosing. The EEG spectral frequency power within specific sleep stages was calculated in 1-Hz intervals from 1 to 100 Hz within each sleep/wake state for the first 4 h after the dose. Eszopiclone and zolpidem produced marked, dose-responsive disruptions in sleep stage-specific EEG spectral profiles compared with vehicle treatment. In marked contrast, DORA-22 exhibited marginal changes in the spectral profile, observed only during rapid eye movement sleep, and only at the highest dose tested. Moreover, while eszopiclone- and zolpidem-induced changes were evident in the inactive period, the EEG spectral responses to DORA-22 were absent during this phase. These results suggest that DORA-22 differs from eszopiclone and zolpidem whereby DORA-22 promotes somnolence without altering the neuronal network EEG activity observed during normal sleep.

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Section: Discussionmentioning

confidence: 98%

Quantitative Electroencephalography Within Sleep/Wake States Differentiates GABAA Modulators Eszopiclone and Zolpidem From Dual Orexin Receptor Antagonists in Rats

Fox

Gotter

Tye

et al. 2013

Neuropsychopharmacol

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“…Although the significance of alpha power reduction for sleep/wake regulation remains unclear, it is consistent with the increased cortical GABAergic transmission as diazepam also suppresses alpha oscillations [50]. In human, beta oscillations (15-30 Hz) are reflective of cortical arousal within sleep [37, 45]. Although, the changes in beta power in patients with insomnia are variable during REM sleep [45], several reports have demonstrated increased beta power in REM sleep in patients with primary insomnia [37, 41, 55].…”

Section: Discussionmentioning

confidence: 99%

“…In human, beta oscillations (15-30 Hz) are reflective of cortical arousal within sleep [37, 45]. Although, the changes in beta power in patients with insomnia are variable during REM sleep [45], several reports have demonstrated increased beta power in REM sleep in patients with primary insomnia [37, 41, 55]. It is plausible the increased beta oscillations during REM sleep may also suggest poor sleep quality in Nlgn3 R451C mice.…”

Section: Discussionmentioning

confidence: 99%

Neuroligin 3 R451C mutation alters electroencephalography spectral activity in an animal model of autism spectrum disorders

et al. 2017

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Human studies demonstrate that sleep impairment is a concurrent comorbidity of autism spectrum disorders (ASD), but its etiology remains largely uncertain. One of the prominent theories of ASD suggests that an imbalance in synaptic excitation/inhibition may contribute to various aspects of ASD, including sleep impairments. Following the identification of Nlgn3 R451C mutation in patients with ASD, its effects on synaptic transmission and social behaviours have been examined extensively in the mouse model. However, the contributory role of this mutation to sleep impairments in ASD remains unknown. In this study, we showed that Nlgn3 R451C knock-in mice, an established genetic model for ASD, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep.

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“…Effect sizes for polysomnographically determined sleep were taken from the same meta-analysis [25•]. With respect to physiological variables, standardized mean effect sizes were calculated for NREM EEG beta activity [22,[26][27][28][29][30][31][32][33] and resting heart rate [34][35][36][37][38][39][40] as the two most frequently investigated putative physiological indicators of hyperarousal in insomnia. Effect sizes for daytime cognitive performance were taken from the meta-analysis of Fortier-Brochu et al [5].…”

Section: The Promise Of Neuroimagingmentioning

confidence: 99%

Neuroimaging Insights into Insomnia

Spiegelhalder

Regen

Baglioni

et al. 2015

Curr Neurol Neurosci Rep

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Insomnia is one of the most prevalent health complaints afflicting approximately 10% of the population in Western industrialized countries at a clinical level. Despite the proposition that both biological and psychological factors play a role in the experience of insomnia, the field continues to puzzle over so-called "discrepancies" between objective and subjective measurements of sleep and daytime functioning. The promise of neuroimaging is to uncover physiological processes that may readily explain patient reports. However, while there has been an explosion in the number of studies investigating the neural correlates of insomnia with neuroimaging technologies, there appears to be little consistency in findings across studies. We suggest a number of methodological reasons which may, at least partially, explain variability in findings across neuroimaging studies in insomnia.

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Increased EEG sigma and beta power during NREM sleep in primary insomnia

Cited by 160 publications

References 30 publications

Quantitative Electroencephalography Within Sleep/Wake States Differentiates GABAA Modulators Eszopiclone and Zolpidem From Dual Orexin Receptor Antagonists in Rats

Quantitative Electroencephalography Within Sleep/Wake States Differentiates GABAA Modulators Eszopiclone and Zolpidem From Dual Orexin Receptor Antagonists in Rats

Neuroligin 3 R451C mutation alters electroencephalography spectral activity in an animal model of autism spectrum disorders

Neuroimaging Insights into Insomnia

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