Beta EEG activity and insomnia

Perlis, Michael L.; Merica, Helli; Smith, Michael T.; Giles, Donna E.

doi:10.1053/smrv.2001.0151

Cited by 291 publications

(243 citation statements)

References 57 publications

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“…[32][33][34] The excess arousal refers to the exaggerated cortical, somatic, and cognitive activation, which leads to increased sensory information processing and inability to initiate or maintain sleep. 5,35 These studies provided supported evidence that the hyperarousal model is a core predisposing or perpetuating factor of chronic insomnia. 36 Our previous sleep deprivation study found that the female sleep deprivation subjects showed hyperarousal re-activation in the bilateral occipital gyrus compared with the GS-Fs, 21 and our previous regional homogeneity study demonstrated the excessive hyperarousal reactivities in the temporal lobe in the PCPIs, PCPI-Ms and PCPI-Fs, and the excessive hyperarousal reactivation in the occipital cortex in the PCPI-Fs.…”

Section: Discussionsupporting

confidence: 52%

Gender Differences in Regional Brain Activity in Patients with Chronic Primary Insomnia: Evidence from a Resting-State fMRI Study

Dai

Nie

Liu

et al. 2016

Journal of Clinical Sleep Medicine

115

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Study Objectives: To explore the regional brain activities in patients with chronic primary insomnia (PCPIs) and their sex differences. Methods: Forty-two PCPIs (27 females, 15 males) and 42 good sleepers (GSs; 24 females, 18 males) were recruited. Six PCPIs (3 males, 3 females) were scanned twice by MRI to examine the test-retest reliability. Amplitude of low frequency fluctuation (ALFF) method was used to assess the local brain features. The mean signal values of the different ALFF areas were analyzed with a receiver operating characteristic (ROC) curve. Simple linear regression analysis was performed to investigate the relationships between clinical features and different brain areas. Results: Both female and male PCPIs showed higher ALFF in the temporal lobe and occipital lobe, especially in female PCPIs. Female PCPIs had lower ALFF in the bilateral cerebellum posterior lobe, left dorsolateral prefrontal cortex, and bilateral limbic lobe; however, male PCPIs showed lower ALFF in the left occipital gyrus. The mean signal value of the cerebellum in female PCPIs showed negative correlations with negative emotions. Compared with male PCPIs, female PCPIs showed higher ALFF in the bilateral middle temporal gyrus and lower ALFF in the left limbic lobe. The different areas showed high testretest stability (Clusters of contiguous volumes ≥ 1080 mm 3 with an intraclass correlation coefficient ≥ 0.80) and high degree of sensitivity and specificity. Conclusions: Female PCPIs showed more regional brain differences with higher and lower ALFF responses than male PCPIs. However, they shared analogous excessive hyperarousal mechanism and wide variations in aberrant brain areas. I NTRO DUCTI O NPatients with chronic primary insomnia (PCPIs), who underwent the subjective experience of chronically disturbed sleep, sleep loss, non-refreshing sleep, and heightened arousal in bed with impaired quality of life, showed a decreased ability to disengage from external information processing at sleep onset.1-3 Occasional episodes of insomnia symptoms are reported in half of all adults, while chronic insomnia is prevalent in 10-15% of the adult population. 4 In spite of a recent increase in neuroimaging research into PCPIs, it has not gleaned a consistent conclusion about its neuropathology after reviewing the neuroimaging studies of primary insomnia, especially with regard to the structural studies of brain alterations. 5 The results of structural studies are either contradictory or required replication. Altena et al. found that PCPIs had a smaller volume of reduced gray matter in the precuneus and left orbitofrontal cortex which strongly correlated with the subjective severity of insomnia, but increased gray matter volume was not found. 6 Joo et al. demonstrated significantly reduced gray matter concentrations in the dorsolateral prefrontal and pericentral cortices, superior temporal gyrus, and cerebellum, and decreased gray matter volumes in the medial frontal lobe and middle temporal lobe in PCPIs compared with good sleepers (GSs), ...

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Section: Discussionsupporting

confidence: 52%

Gender Differences in Regional Brain Activity in Patients with Chronic Primary Insomnia: Evidence from a Resting-State fMRI Study

Dai

Nie

Liu

et al. 2016

Journal of Clinical Sleep Medicine

115

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“…Supporting a role for A 2A receptors in human sleep, caffeine increased higher-frequency (> 16 Hz) EEG activity prominently in the C/C genotype (15.3 ± 3.1 %, n = 6), intermediately in the C/T genotype (6.9 ± 3.0 %, n = 10), and was ineffective in the T/T genotype (-0.2 ± 5.1 %, n = 3) [16]. Elevated highfrequency activity in nonREM sleep reflects reduced sleep intensity and may be characteristic of patients with primary insomnia when compared to healthy good sleepers [152].…”

Section: Studies Of Sleep Pharmacogeneticsmentioning

confidence: 99%

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

Landolt

2008

CPD

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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.

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“…Despite these operational issues, prior work suggested that SL misperception was linked to increased EEG beta frequency power at or near sleep latency. 24,25 Similarly, a study of memory consolidation suggested that auditory stimuli recollection was increased in those with elevated beta activity in the first 10 minutes of sleep, suggesting conscious processing in some individuals may be linked to EEG frequencies. 26 In addition, Nofzinger et al reported increased brain metabolism on functional imaging (during wake and sleep) of insomnia patients, although misperception was not explicitly measured.…”

Section: Sleep Latency: Physiology and Perceptionmentioning

confidence: 99%

Sleep Fragmentation Does Not Explain Misperception of Latency or Total Sleep Time

Saline

Goparaju

Bianchi

2016

Journal of Clinical Sleep Medicine

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Study Objectives: Perception of sleep-wake times may differ from objective measures, although the mechanisms remain elusive. Quantifying the misperception phenotype involves two operational challenges: defining objective sleep latency and treating sleep latency and total sleep time as independent factors. We evaluated a novel approach to address these challenges and test the hypothesis that sleep fragmentation underlies misperception. Methods: We performed a retrospective analysis on patients with or without obstructive sleep apnea during overnight diagnostic polysomnography in our laboratory (n = 391; n = 252). We compared subjective and objective sleep-wake durations to characterize misperception. We introduce a new metric, sleep during subjective latency (SDSL), which captures latency misperception without defining objective sleep latency and allows correction for latency misperception when assessing total sleep time (TST) misperception. Results:The stage content of SDSL is related to latency misperception, but in the opposite manner as our hypothesis: those with > 20 minutes of SDSL had less N1%, more N3%, and lower transition frequency. After adjusting for misperceived sleep during subjective sleep latency, TST misperception was greater in those with longer bouts of REM and N2 stages (OSA patients) as well as N3 (non-OSA patients), which also did not support our hypothesis. Conclusions: Despite the advantages of SDSL as a phenotyping tool to overcome operational issues with quantifying misperception, our results argue against the hypothesis that light or fragmented sleep underlies misperception. Further investigation of sleep physiology utilizing alternative methods than that captured by conventional stages may yield additional mechanistic insights into misperception. I NTRO DUCTI O NAssessment of sleep often includes subjective reports of sleepwake durations, in clinical practice as well as epidemiological studies of sleep duration.1 However, when concurrent objective sleep measurements are available, it is not uncommon to observe that the subjective responses may differ. Underestimation of total sleep time has been previously observed in healthy adults under experimental circumstances, as well as insomnia patients during polysomnography (PSG).2-4 This phenomenon, sometimes termed misperception, may manifest as either overestimating sleep latency (SL) or underestimating total sleep time (TST), or both.4 Some patients with obstructive sleep apnea (OSA) may also exhibit misperception, though perhaps not to the same extent as those with insomnia symptoms. 5-7Several hypotheses have arisen regarding the basis for misperception, although a unified explanation remains elusive. For example, misperception has been linked with anxiety and mood, 3,8 personality traits, and sleep physiology measures such as electroencephalogram patterns of alpha-delta sleep or cyclic alternating pattern and high frequency electroencephalography (EEG) content. [9][10][11][12][13] In addition, we previously investigated possible relat...

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Beta EEG activity and insomnia

Cited by 291 publications

References 57 publications

Gender Differences in Regional Brain Activity in Patients with Chronic Primary Insomnia: Evidence from a Resting-State fMRI Study

Gender Differences in Regional Brain Activity in Patients with Chronic Primary Insomnia: Evidence from a Resting-State fMRI Study

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

Sleep Fragmentation Does Not Explain Misperception of Latency or Total Sleep Time

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