Changes In Delta Power Research Articles

Short-Term Changes in Hypsarrhythmia Assessed by Spectral Analysis: Group and Individual Assessments.

Objectives: To perform spectral analysis on previously recorded electroencephalograms (EEGs) containing hypsarrhythmia in an initial recording and to assess changes in spectral power (µV2) in a follow-up recording after a period of 10-25 days. Methods: Fifty participants, aged 2-39 months, with hypsarrhythmia in an initial recording (R1), were compared with regard to their spectral findings in a later recording (R2). Typically, anticonvulsant therapy was initiated or modified after R1. Average delta, theta, alpha, and beta power was derived from approximately 3 min of artifact-free EEG data recorded from 19 electrode derivations. Group and individual changes in delta power between R1 and R2 formed the main analyses. Results: Delta accounted for 84% of the total power. In group comparisons, median delta power decreased statistically significantly between R1 and R2 in all 19 derivations, for example, from 3940 µV2 in R1 to 1722 µV2 in R2, Cz derivation. When assessing individual participants, delta power decreases in R2 were >50% in 60% of the participants, but <25% in 24% of the participants. Conclusion: Spectral analysis may be used as an additional tool for providing a potential biomarker in the assessment of short-term changes in hypsarrhythmia, including the effects of treatment.

Lateralization of delta band power in magnetoencephalography (MEG) in patients with unilateral focal epilepsy and its relation to verbal fluency.

Delta power is a clinically established biomarker for abnormal brain processes. However, in patients with unilateral focal epilepsy (FE) it is still not well understood, how it relates to the epileptogenic zone and to neurocognitive functioning. The aim of the present study was thus to assess how delta power relates to the affected hemisphere, whether lateralization strength differs between the patients, and how changes in delta power correlate with cognitive functioning. We retrospectively studied patients with left (LFE) and right FE (RFE) who had undergone a resting-state magnetoencephalography measurement. We computed global and hemispheric delta power and lateralization indices and examined whether delta power correlates with semantic and letter verbal fluency (former being a marker for language and verbal memory, latter for executive functions) in 26 FE patients (15 LFE, 11 RFE) and 10 healthy controls. Delta power was increased in FE patients compared to healthy controls. However, the increase across hemispheres was related to the site of the epileptic focus: On group level, LFE patients showed higher delta power in both hemispheres, whereas RFE patients primarily exhibited higher delta power in the ipsilateral right hemisphere. Both groups showed co-fluctuations of delta power between the hemispheres. Besides, delta power correlated negatively only with letter verbal fluency. The findings confirm and provide further evidence that delta power is a marker of pathological activity and abnormal brain processes in FE. Delta power dynamics differ between patient groups, indicating that delta power could offer additional diagnostic value. The negative association of delta power and letter verbal fluency suggests that executive dysfunctions are related to low frequency abnormalities.

The M1 Muscarinic Acetylcholine Receptor Positive Allosteric Modulator (PAM) VU0453595 and M4 PAM VU0467154 Normalize Sleep‐Wake Architecture Deficits in Aged Mice

AbstractBackgroundDeclining basal forebrain cholinergic integrity has been associated with disturbances in sleep‐wake architecture in Alzheimer’s Disease (AD). Acetylcholinesterase inhibitors (AChEIs) provide symptomatic treatment for the cognitive deficits in AD through nonselective enhancement of cholinergic signaling. Additionally, AChEIs promote wakefulness, but reduce NREM sleep quality and produce dose limiting side effects through nonselective activation of peripheral muscarinic acetylcholine receptors (mAChR). Selectively targeting different mAChRs with positive allosteric modulators (PAMs) provides an alternate approach. In the current study, we assessed the effects of the M1 PAM VU0453595 and the M4 PAM VU0467154 on sleep‐wake architecture and arousal following dosing across the circadian cycle in aged mice.MethodsYoung (3‐4 month‐old, n = 13‐14 per group) and aged (19‐21 month‐old, n = 14 per group) C57/BL6 mice were implanted with HD‐X02 telemetry devices (DSI) for electroencephalography (EEG) recording. The M1 PAM VU0453595 (3‐30mg/kg IP) or the M4 PAM VU0467154 (1‐30mg/kg IP) were dosed 2‐hours into the active or inactive phases of the circadian cycle. EEG was recorded for 24‐hours, with sleep stages scored in 5‐second epochs. Arousal was assessed through changes in gamma power during wake, and sleep quality was measured through changes in delta power during NREM sleep. Statistical comparisons involved repeated measures one‐ or two‐way ANOVAs as appropriate, with Dunnett’s or Sidak’s multiple comparisons applied in all cases.ResultsThe M1 PAM VU0453595 increased wakefulness and arousal with inactive phase dosing in young and aged mice. During the active phase, VU0453595 increased wakefulness and arousal only in aged mice. The M4 PAM VU0467154 increased NREM sleep in young and aged mice when dosed in both phases. In the inactive phase, suppression of REM sleep in young and aged mice is also observed. During NREM sleep, VU0467154 increased delta power in young and aged mice.ConclusionThese findings suggest that M1 and M4 PAMs may be valuable as treatments in AD at different phases of the circadian cycle. M1 PAMs could be beneficial with morning dosing in clinical populations as they enhanced wakefulness and arousal. M4 PAMs could be advantageous with evening dosing in clinical population as they enhanced NREM sleep quantity and quality.

Screening of non-restorative sleep by quantitative EEG

BackgroundNon-restorative sleep is the major cause of excessive daytime sleepiness and causes injures of the central nervous system. The most common cause of Excessive day sleepiness in a clinical setting is obstructive sleep apnea. Sleepiness scales can assess multiple aspects of the sleep and include subjective and objective measures. The present study aim to disclose the capability of quantitative electroencephalography to screen, as well as to know the pathogenesis of non-restorative sleep in patients with excessive day time sleepiness.ResultsTwenty obstructive sleep apnea patients and 20 healthy control subjects were recruited. All patients were subjected to Epworth sleepiness scale and polysomnography. Quantitative electroencephalography and Karolinska sleepiness scale were done before and after sleep for patients as well as controls. The patients group revealed a significant power reduction in delta and alpha bands, comparing before and after sleep records. Interestingly, there was a significant change in delta power in the temporal delta waves power. Yet, the changes were opposite among cases (significant decrease) versus controls (significant increase). In addition, there were significant correlations between sleepiness scales; Epworth sleepiness scale and Karolinska Sleepiness Scale scores, and alpha band results in quantitative electroencephalography.ConclusionQuantitative electroencephalography with further research, could provide us with clues to the pathogenesis of EDS and non-restorative sleep accompanying OSA and an objective screening tool.

Sleep Quality and Electroencephalogram Delta Power.

Delta activity on electroencephalogram (EEG) is considered a biomarker of homeostatic sleep drive. Delta power is often associated with sleep duration and intensity. Here, we reviewed the literature to explore how sleep quality was influenced by changes in delta power. However, we found that both the decrease and increase in delta power could indicate a higher sleep quality due to the various factors below. First, the differences in changes in delta power in patients whose sleep quality is lower than that of the healthy controls may be related to the different diseases they suffered from. We found that the patients mainly suffered from borderline personality disorder, and Rett syndrome may have a higher delta power than healthy individuals. Meanwhile, patients who are affected by Asperger syndrome, respiratory failure, chronic fatigue, and post-traumatic stress disorder have lower delta power. Second, if the insomnia patients received the therapy, the difference may be caused by the treatment method. Cognitive or music therapy shows that a better therapeutic effect is associated with decreased delta power, whereas in drug treatment, there is an opposite change in delta power. Last, for healthy people, the difference in delta change may be related to sleep stages. The higher sleep quality is associated with increased delta power during the NREM period, whereas a deceased delta change accompanies higher sleep quality during the REM period. Our work summarizes the effect of changes in delta power on sleep quality and may positively impact the monitoring and intervention of sleep quality.

High delta and gamma EEG power in resting state characterise dementia in Parkinson’s patients

• We compare EEG power changes in PD with or without dementia. • Higher power in delta and gamma bands differentiate PD dementia stage form PD non-dementia stage. • Changes in delta power occur globally over the scalp. • Power in gamma band changes in right frontal and centro-parietal regions. Parkinson’s disease (PD) is a chronic neurodegenerative disease with appearance of dementia as the disease progresses. Dementia in PD worsens the quality of life and poses a burden on caregivers. Objective markers of the presence and as well as onset of dementia needs to be explored to improve the quality of life. We attempted to identify EEG abnormalities that differentiate PD patients with or without dementia using high density EEG. The differential changes in the EEG spectral activity could mark the early stage as well as onset of dementia in Parkinson’s disease (PD). The present study was designed to find out the resting eyes-closed (EC) EEG characteristics in PD with dementia (PDD) and without dementia (PDND) compared to healthy controls (CON) of both gender using high density EEG. Absolute power of seven frequency bands based on individual alpha frequency was estimated by Fast Fourier transform algorithm in 58 PD patients (30 PDND and 28 PDD) and 26 CON. Compared to CON, PDND had higher power in theta and lower alpha1 bands while PDD had higher power in delta, theta, lower alpha1 and beta bands. Higher delta and gamma power with no difference in theta and lower alpha 1 power was the characteristic feature of PD patients with dementia compared to non-dementia. This cross-sectional study proposes to use these differential changes in power as EEG signatures of appearance of dementia in PD. Absence of high delta power, but presence of high theta and lower alpha 1 power defined PDND group compared to CON.

Change in functional networks for transitions between states of consciousness during midazolam-induced sedation.

How brain dynamics change across conscious states, including reliable signatures of the transitions between unconsciousness and consciousness, remains unclear. In this work, we addressed the changes in functional brain networks during self-titrated midazolam sedation using high-density electroencephalography (EEG) in ten subjects. We were particularly interested in the underlying network alterations, identified with graph theory, associated with transitions between states of consciousness. The weighted Phase Lag Index (wPLI) was used as the connectivity estimator between two signals. Based on wPLI, we calculated network properties such as characteristic path length, clustering coefficient, and small-worldness for measuring the integration and segregation of the brain network. We found significant changes in power and wPLI at different levels of consciousness. During unconsciousness, wPLI over the parietal region was higher in the delta band (1-4Hz). The frontal-parietal interaction in the delta band was also stronger during the transition from consciousness to unconsciousness. There was the significant difference of wPLI over the frontal region between consciousness and unconsciousness in the sigma band (12-15Hz). The topological properties across conscious states were significantly changed in the delta band and sigma band. Our results showed parietal brain dynamics is associated with consciousness. Our data also suggest that reversible changes in delta power and connectivity underlie changes in conscious state.

The Relationship Between Estrogen and the Decline in Delta Power During Adolescence.

During adolescence, there is a precipitous decrease in slow-wave sleep (SWS) and its spectral correlate, delta power, which may reflect cortical reorganization. The temporal association between the decrease in delta power and puberty suggests that sex steroids may initiate these changes. This association has not been previously investigated. To determine whether estrogen triggers the adolescent decline in delta power, we compared delta power in 14 girls with central precocious puberty (CPP) and 6 age-matched, prepubertal controls. Five CPP participants were re-studied 7-14 months after pubertal suppression to determine if the changes in delta power are reversible after restoring a prepubertal hormonal milieu. The change in delta power was also compared between CPP participants and five historic controls from a longitudinal polysomnographic study. CPP participants (6.7-10.5 years) spent 30% of the night in SWS. Delta power (3.7 × 106 ± 2.7 × 105 µV2) predominated in the first 2 non-rapid eye movement episodes and decayed exponentially (tau 0.006 minutes). Age-matched controls demonstrated similar sleep staging (24% SWS) and delta dynamics (3.3 × 106 ± 5.1 × 105 µV2, tau 0.004 minutes). Four out of 5 CPP participants had a significant decrease (26%) in delta power after hormone suppression (p < .05), similar to historic controls. Using an innovative model of girls with CPP studied before and after estrogen suppression, the effects of puberty on the decline in delta power were dissociated from those of chronologic age. The current studies suggest that increased estrogen does not cause the adolescent decline in delta power and indicate that neurodevelopmental changes per se or other factors associated with puberty drive these sleep changes.

Separating the Contribution of Glucocorticoids and Wakefulness to the Molecular and Electrophysiological Correlates of Sleep Homeostasis

The sleep-deprivation-induced changes in delta power, an electroencephalographical correlate of sleep need, and brain transcriptome profiles have importantly contributed to current hypotheses on sleep function. Because sleep deprivation also induces stress, we here determined the contribution of the corticosterone component of the stress response to the electrophysiological and molecular markers of sleep need in mice. N/A SETTINGS: Mouse sleep facility. C57BL/6J, AKR/J, DBA/2J mice. Sleep deprivation, adrenalectomy (ADX). Sleep deprivation elevated corticosterone levels in 3 inbred strains, but this increase was larger in DBA/2J mice; i.e., the strain for which the rebound in delta power after sleep deprivation failed to reach significance. Elimination of the sleep-deprivation-associated corticosterone surge through ADX in DBA/2J mice did not, however, rescue the delta power rebound but did greatly reduce the number of transcripts affected by sleep deprivation. Genes no longer affected by sleep deprivation cover pathways previously implicated in sleep homeostasis, such as lipid, cholesterol (e.g., Ldlr, Hmgcs1, Dhcr7, -24, Fkbp5), energy and carbohydrate metabolism (e.g., Eno3, G6pc3, Mpdu1, Ugdh, Man1b1), protein biosynthesis (e.g., Sgk1, Alad, Fads3, Eif2c2, -3, Mat2a), and some circadian genes (Per1, -3), whereas others, such as Homer1a, remained unchanged. Moreover, several microRNAs were affected both by sleep deprivation and ADX. Our findings indicate that corticosterone contributes to the sleep-deprivation-induced changes in brain transcriptome that have been attributed to wakefulness per se. The study identified 78 transcripts that respond to sleep loss independent of corticosterone and time of day, among which genes involved in neuroprotection prominently feature, pointing to a molecular pathway directly relevant for sleep function.

Cold Exposure and Sleep in the Rat: Effects on Sleep Architecture and the Electroencephalogram

Acute exposure to low ambient temperature modifies the wake-sleep cycle due to stage-dependent changes in the capacity to regulate body temperature. This study was carried out to make a systematic analysis of sleep parameters during the exposure to different low ambient temperatures and during the following recoveries at ambient temperature 24 degrees C. Electroencephalographic activity, hypothalamic temperature, and motor activity were studied during a 24-hour exposure to ambient temperatures ranging from 10 degrees C to -10 degrees C and for 4 days during the recovery. Laboratory of Physiological Regulation during the Wake-Sleep Cycle, Department of Human and General Physiology, Alma Mater Studiorum-University of Bologna. Twenty-four male albino rats. Animals were implanted with electrodes for electroencephalographic recording and a thermistor for measuring hypothalamic temperature. Wake-sleep stage duration and the electroencephalographic spectral analysis performed by fast Fourier transform were compared among baseline, exposure, and recovery conditions. The amount of non-rapid eye movement sleep was slightly depressed by cold exposure, but no rebound was observed during the recovery period. Delta power during non-rapid eye movement sleep was decreased in animals exposed to the lowest ambient temperatures and increased during the first day of the recovery. In contrast, rapid eye movement sleep was greatly depressed by cold exposure and showed an increase during the recovery. Both of these effects were dependent on the ambient temperature of the exposure. Moreover, theta power was increased during rapid eye movement sleep in both the exposure and the first day of the recovery. These findings show that sleep-stage duration and electroencephalogram power are simultaneously affected by cold exposure. The effects on rapid eye movement sleep appear mainly as changes in the duration, whereas those on non-rapid eye movement sleep are shown by changes in delta power. These effects are temperature dependent, and the decrease of both parameters during the exposure is reciprocated by an increase in the subsequent recovery.

The Homeostatic Regulation of Sleep Need Is under Genetic Control

Delta power, a measure of EEG activity in the 1-4 Hz range, in slow-wave sleep (SWS) is in a quantitative and predictive relationship with prior wakefulness. Thus, sleep loss evokes a proportional increase in delta power, and excess sleep a decrease. Therefore, delta power is thought to reflect SWS need and its underlying homeostatically regulated recovery process. The neurophysiological substrate of this process is unknown and forward genetics might help elucidate the nature of what is depleted during wakefulness and recovered during SWS. We applied a mathematical method that quantifies the relationship between the sleep-wake distribution and delta power to sleep data of six inbred mouse strains. The results demonstrated that the rate at which SWS need accumulated varied greatly with genotype. This conclusion was confirmed in a "dose-response" study of sleep loss and changes in delta power; delta power strongly depended on both the duration of prior wakefulness and genotype. We followed the segregation of the rebound of delta power after sleep deprivation in 25 BXD recombinant inbred strains by quantitative trait loci (QTL) analysis. One "significant" QTL was identified on chromosome 13 that accounted for 49% of the genetic variance in this trait. Interestingly, the rate at which SWS need decreases did not vary with genotype in any of the 31 inbred strains studied. These results demonstrate, for the first time, that the increase of SWS need is under a strong genetic control, and they provide a basis for identifying genes underlying SWS homeostasis.

EEG delta power during sleep in young and old rats

Delta EEG power density, which has been viewed as a measure of intensity of NREM sleep, declines across the lifetime in humans, cats, and hamsters, but data in rats have been unclear. It is also uncertain whether older rats differ from younger animals in the degree of change in delta power during recovery sleep following short-term sleep deprivation. We have examined delta power density in NREM sleep under baseline conditions and following 48 h of sleep deprivation in young (3 months), middle-aged (12 months), and older (24 months) rats. The presence or absence of age effects was highly dependent on the method of normalizing the data. When expressed as a fraction of total NREM EEG power, there was no age effect on baseline delta power density, or on the change from baseline to recovery conditions. When expressed as a multiple of delta power in REM under the same condition, the younger rats had higher delta power density than the middle-aged and older rats. For all the ages combined, there was an increase in delta power density in the recovery condition. When examined by age, the younger rats (which started from a higher level of delta power density than the other groups) did not have an increase in delta during recovery; the middle-aged rats tended to, and the older rats (which started from lower baseline levels) significantly increased delta power density in the recovery condition. This suggests that the lower delta power seen during baseline in older rats is not due to decreased ability to generate delta activity.

Topography of visual EEG reactivity in school-age children.

In order to quantify the visual reactivity of EEG to opening the eyes, the topography of EEG power spectra for a sample of 72 healthy subjects of age ranging from 7 to 15 years was investigated. The EEGs were recorded from 16 scalp sites with eyes open (EOP) and eyes closed (ECL). Ln-transformed absolute EEG powers, acquired under these two states, were tested with Wilcoxon's paired test for differences between the powers. The absolute powers in alpha band and in total, were significantly higher in all derivations, under the ECL, as compared with the EOP, condition. Absolute powers in theta band under the ECL condition were also significantly higher than those under the EOP condition, except for frontal derivations. Changes in delta power were insignificant. Beta 1 band activity, when eyes were closed, was maximal in posterior and minimal in anterior derivations. When the eyes were open, the greatest beta 1 power was found in the frontal derivations. Beta 2 was the only band in which a frequent increase in power took place with eyes opening. Eyes opening appeared to decrease significantly, the beta 1 and beta 2 powers only in posterior derivations. The results showed that the visual blocking of EEG was mostly due to a higher degree of EEG desynchronization for the subjects aged 7-5 years.

Delta (0.5–1.5 Hz) and sigma (11.5–15.5 Hz) EEG power dynamics throughout quiet sleep in infants

Twenty-eight healthy infants, split into 3 groups according to age (group 1: 2–6 weeks, n =10; group 2: 7–14 weeks, n = 10; and group 3: 4–12 months, n = 8), were recorded during the whole night. For each infant, the longest quiet sleep (QS) phase occurring between 8 p.m. and midnight was selected for EEG power spectral analysis. The power in the frequency band related to low-frequency delta waves (0.5–1.5 Hz, “delta band”) and the power in the frequency band related to sigma spindles (11.5–15.5 Hz, “sigma band”) were analyzed. Group 1 infants showed no significant modification of the power in the sigma band in the course of the QS phase; the power in the delta band showed a significant increase between the second and the third 5 min segment and a decrease thereafter. Group 2 infants showed a progressive reduction of the power in the sigma band, whereas the power in the delta band increased during the first 15 min. In group 3 infants, the sigma band power significantly decreased between the third and the fifth 5 min segment without further changes. The power in the delta band, on the contrary, increased progressively for the first 20 min and showed a second progressive increase beyond 35 min. For both group 2 and group 3 infants, it appeared that the change in delta power preceded the change in sigma power. The above results provide quantitative evidence that a well-defined temporal inhomogeneity pattern in the EEG of the QS phase may appear between 7 and 14 weeks of age and continues from the fourth month on.