Slow EEG Oscillations Research Articles

Relationship between speech perception and cortical temporal information processing in noise

It has been known for many years that some listeners with normal hearing report difficulties in speech reception under the presence of competing sounds. The symptom is called hidden hearing loss. For the elucidation of the mechanism of hidden hearing loss, we examined the relationship between speech-in-noise reception performance and cortical temporal information processing. It has been reported that delta and theta oscillations were phase-locked to speech envelopes, and the synchronization depends on the intelligibility of degraded synthesized speech. However, it remains unclear whether and how the slow oscillations reflect speech-in-noise reception performances. We measured slow-rate (below 8 Hz) electroencephalogram (EEG) oscillations during speech reception under noise with different signal-to-noise ratio (-5 dB to -14 dB). In a control condition, EEG oscillations were measured by the same stimuli, but the participants watched a self-selected movie with subtitles, ignoring the stimuli. The power of the EEG oscillations during speech reception was stronger than those while participants ignored the stimuli. However, we did not find any dependences of the slow EEG oscillations on speech intelligibility changes associated with varying SNR. The enhancement of slow oscillations can be triggered by attention but is not likely to reflect listening effort driven by noise contamination.

The Changes of the Infra-Slow EEG Fluctuations of the Brain Potentials under Influence of Infra-Low Frequency Neurofeedback

This study presents a comparison of the effect on EEG electrical activity in the range of infraslow frequencies of two methods: infra-low frequency EEG biofeedback and heart rate variability training. The study involved 17 healthy subjects aged 21 to 50 years with minor symptoms of a physiological or psychological nature, who did not have a history of neurological or psychiatric diseases. To evaluate the results of the training, we analyzed the spectral power of slow EEG oscillations during the performance of the attention test (Visual Go/NoGo), recorded before and after twenty sessions of biofeedback. Both the subjective assessment of the physiological and psychological state and the results of the visual test showed more pronounced positive changes under the influence of EEG biofeedback compared to the cases of heart rate variability training. A significant increase in the amplitudes of oscillations in the infraslow EEG range was observed only after EEG biofeedback.

P 57. Effect of Infra-Low Frequency Neurofeedback on Infra-Slow EEG Fluctuations

Infra-low frequency neurofeedback (ILF NF) has been proposed as an alternative or complementary treatment method. Previous studies have reported a good effect of ILF training on the subjective perception of positive psychological changes after training. Here we study whether the objective physiological parameters reflecting the brain function also change under the influence of ILF NF. Eight participants 21–50 years of age with no history of neurological or psychiatric diseases, but reporting about some physiological or psychological complaints, performed 20 sessions of infra-low frequency neurofeedback training. EEG in visual Go/NoGo test was recorded before the course of Neurofeedback and after its completion. The spectral power of slow EEG oscillations in the post-training recording was compared with the pretraining baseline. After 20 sessions of ILF training, the pattern of ILF activity at rest changed dramatically. The main difference was an increase in the amplitude of the ILF activity up to 0.3–1.0 mV in all recording sites. These results indicate that ILF training modified the baseline brain state in each case. Furthermore, after completion of 20 NFB sessions, all participants indicated improvement of their state. Most of them noticed a decrease of inner tension and reactivity to stressful factors. Further, they reported on stability of mood, improved body and space awareness, increase of energy level and of cognitive performance. Along with this remission of the clinical complaints, significant increase of spectral power in 0–0.5 Hz frequency band was observed in all eight participants in the post-training EEG patterns compared to the pretraining EEG. Our study has shown the changes in the amplitude distribution within the ILF spectral range in all participants that seems to be induced by the ILF training. In other words, the ILF training leads to the changes of the functional state of the brain. We suggest that the modification of the baseline ILF EEG pattern may reflect the normalization in the metabolic balance in the brain tissue and increasing efficiency of compensatory mechanisms in the stress regulation systems.

Temporal associations between sleep slow oscillations, spindles and ripples.

The systems consolidation of memory during slow-wave sleep (SWS) is thought to rely on a dialogue between hippocampus and neocortex that is regulated by an interaction between neocortical slow oscillations (SOs), thalamic spindles and hippocampal ripples. Here, we examined the occurrence rates of and the temporal relationships between these oscillatory events in rats, to identify the possible direction of interaction between these events under natural conditions. To facilitate comparisons with findings in humans, we combined frontal and parietal surface EEG with local field potential (LFP) recordings in medial prefrontal cortex (mPFC) and dorsal hippocampus (dHC). Consistent with a top-down driving influence, EEG SO upstates were associated with an increase in spindles and hippocampal ripples. This increase was missing in SO upstates identified in mPFC recordings. Ripples in dHC recordings always followed the onset of spindles consistent with spindles timing ripple occurrence. Comparing ripple activity during co-occurring SO-spindle events with that during isolated SOs or spindles, suggested that ripple dynamics during SO-spindle events are mainly determined by the spindle, with only the SO downstate providing a global inhibitory signal to both thalamus and hippocampus. As to bottom-up influences, we found an increase in hippocampal ripples ~200ms before the SO downstate, but no similar increase of spindles preceding SO downstates. Overall, the temporal pattern is consistent with a loop-like scenario where, top-down, SOs can trigger thalamic spindles which, in turn, regulate the occurrence of hippocampal ripples. Ripples, bottom-up, and independent from thalamic spindles, can contribute to the emergence of neocortical SOs.

A hypothesis regarding how sleep can calibrate neuronal excitability in the central nervous system and thereby offer stability, sensitivity and the best possible cognitive function

The function of sleep in mammal and other vertebrates is one of the great mysteries of biology. Many hypotheses have been proposed, but few of these have made even the slightest attempt to explain the essence of sleep – the uncompromising need for reversible unconsciousness. During sleep, epiphenomena – often of a somatic character – occur, but these cannot explain the core function of sleep. One answer could be hidden in the observations made for long periods of time of the function of the central nervous system (CNS). The CNS is faced with conflicting requirements on stability and excitability. A high level of excitability is desirable, and is also a prerequisite for sensitivity and quick reaction times; however, it can also lead to instability and the risk of feedback, with life-threatening epileptic seizures. Activity-dependent negative feedback in neuronal excitability improves stability in the short term, but not to the degree that is required. A hypothesis is presented here demonstrating how calibration of individual neurons – an activity which occurs only during sleep – can establish the balanced and highest possible excitability while also preserving stability in the CNS. One example of a possible mechanism is the observation of slow oscillations in EEGs made on birds and mammals during slow wave sleep. Calibration to a genetically determined level of excitability could take place in individual neurons during the slow oscillation. This is only possible offline, which explains the need for sleep. The hypothesis can explain phenomena such as the need for unconsciousness during sleep, with the disconnection of sensory stimuli, slow EEG oscillations, the relationship of sleep and epilepsy, age, the effects of sleep on neuronal firing rate and the effects of sleep deprivation and sleep homeostasis. This is with regard primarily to mammals, including humans, but also all other vertebrates.

Ketamine-induced regulation of TrkB-GSK3β signaling is accompanied by slow EEG oscillations and sedation but is independent of hydroxynorketamine metabolites

Subanesthetic rather than anesthetic doses are thought to bring the rapid antidepressant effects of the NMDAR (N-methyl-d-aspartate receptor) antagonist ketamine. Among molecular mechanisms, activation of BDNF receptor TrkB along with the inhibition of GSK3β (glycogen synthase kinase 3β) are considered as critical molecular level determinants for ketamine's antidepressant effects. Hydroxynorketamines (2R,6R)-HNK and (2S,6S)–HNK), non-anesthetic metabolites of ketamine, have been proposed to govern the therapeutic effects of ketamine through a mechanism not involving NMDARs. However, we have shown that nitrous oxide, another NMDAR blocking anesthetic and a putative rapid-acting antidepressant, evokes TrkB-GSK3β signaling alterations during rebound slow EEG (electroencephalogram) oscillations. We investigated here the acute effects of ketamine, 6,6-d2-ketamine (a ketamine analogue resistant to metabolism) and cis-HNK that contains (2R,6R) and (2S,6S) enantiomers in 1:1 ratio, on TrkB-GSK3β signaling and concomitant electroencephalographic (EEG) alterations in the adult mouse cortex. Ketamine dose-dependently increased slow oscillations and phosphorylations of TrkBY816 and GSK3βS9 in crude brain homogenates (i.e. sedative/anesthetic doses (>50 mg/kg, i.p.) produced more prominent effects than a subanesthetic dose (10 mg/kg, i.p.)). Similar, albeit less obvious, effects were seen in crude synaptosomes. A sedative dose of 6,6-d2-ketamine (100 mg/kg, i.p.) recapitulated the effects of ketamine on TrkB and GSK3β phosphorylation while cis-HNK at a dose of 20 mg/kg produced negligible acute effects on TrkB-GSK3β signaling or slow oscillations. These findings suggest that the acute effects of ketamine on TrkB-GSK3β signaling are by no means restricted to subanesthetic (i.e. antidepressant) doses and that cis-HNK is not responsible for these effects.

Behavioral and Neurophysiological Effects of Transcranial Direct Current Stimulation (tDCS) in Fronto-Temporal Dementia.

Fronto-temporal dementia (FTD) is the clinical-diagnostic term that is now preferred to describe patients with a range of progressive dementia syndromes associated with focal atrophy of the frontal and anterior temporal cerebral regions. Currently available FTD medications have been used to control behavioral symptoms, even though they are ineffective in some patients, expensive and may induce adverse effects. Alternative therapeutic approaches are worth pursuing, such as non-invasive brain stimulation with transcranial direct current (tDCS). tDCS has been demonstrated to influence neuronal excitability and reported to enhance cognitive performance in dementia. The aim of this study was to investigate whether applying Anodal tDCS (2 mA intensity, 20 min) over the fronto-temporal cortex bilaterally in five consecutive daily sessions would improve cognitive performance and behavior symptoms in FTD patients, also considering the neuromodulatory effect of stimulation on cortical electrical activity measured through EEG. We recruited 13 patients with FTD and we tested the effect of Anodal and Sham (i.e., placebo) tDCS in two separate experimental sessions. In each session, at baseline (T0), after 5 consecutive days (T1), after 1 week (T2), and after 4 weeks (T3) from the end of the treatment, cognitive and behavioral functions were tested. EEG (21 electrodes, 10–20 international system) was recorded for 5 min with eyes closed at the same time points in nine patients. The present findings showed that Anodal tDCS applied bilaterally over the fronto-temporal cortex significantly improves (1) neuropsychiatric symptoms (as measured by the neuropsychiatric inventory, NPI) in FTD patients immediately after tDCS treatment, and (2) simple visual reaction times (sVRTs) up to 1 month after tDCS treatment. These cognitive improvements significantly correlate with the time course of the slow EEG oscillations (delta and theta bands) measured at the same time points. Even though further studies on larger samples are needed, these findings support the effectiveness of Anodal tDCS over the fronto-temporal regions in FTD on attentional processes that might be correlated to a normalized EEG low-frequency pattern.

Cortical Excitability and Activation of TrkB Signaling During Rebound Slow Oscillations Are Critical for Rapid Antidepressant Responses

Rapid antidepressant effects of ketamine become most evident when its psychotomimetic effects subside, but the neurobiological basis of this “lag” remains unclear. Laughing gas (N2O), another NMDA-R (N-methyl-d-aspartate receptor) blocker, has been reported to bring antidepressant effects rapidly upon drug discontinuation. We took advantage of the exceptional pharmacokinetic properties of N2O to investigate EEG (electroencephalogram) alterations and molecular determinants of antidepressant actions during and immediately after NMDA-R blockade. Effects of the drugs on brain activity were investigated in C57BL/6 mice using quantitative EEG recordings. Western blot and qPCR were used for molecular analyses. Learned helplessness (LH) was used to assess antidepressant-like behavior. Immediate-early genes (e.g., bdnf) and phosphorylation of mitogen-activated protein kinase—markers of neuronal excitability—were upregulated during N2O exposure. Notably, phosphorylation of BDNF receptor TrkB and GSK3β (glycogen synthase kinase 3β) became regulated only gradually upon N2O discontinuation, during a brain state dominated by slow EEG activity. Subanesthetic ketamine and flurothyl-induced convulsions (reminiscent of electroconvulsive therapy) also evoked slow oscillations when their acute pharmacological effects subsided. The correlation between ongoing slow EEG oscillations and TrkB-GSK3β signaling was further strengthened utilizing medetomidine, a hypnotic-sedative agent that facilitates slow oscillations directly through the activation of α2-adrenergic autoreceptors. Medetomidine did not, however, facilitate markers of neuronal excitability or produce antidepressant-like behavioral changes in LH. Our results support a hypothesis that transient cortical excitability and the subsequent regulation of TrkB and GSK3β signaling during homeostatic emergence of slow oscillations are critical components for rapid antidepressant responses.

Auditory closed-loop stimulation of EEG slow oscillations strengthens sleep and signs of its immune-supportive function

Sleep is essential for health. Slow wave sleep (SWS), the deepest sleep stage hallmarked by electroencephalographic slow oscillations (SOs), appears of particular relevance here. SWS is associated with a unique endocrine milieu comprising minimum cortisol and high aldosterone, growth hormone (GH), and prolactin levels, thereby presumably fostering efficient adaptive immune responses. Yet, whether SWS causes these changes is unclear. Here we enhance SOs in men by auditory closed-loop stimulation, i.e., by delivering tones in synchrony with endogenous SOs. Stimulation intensifies the hormonal milieu characterizing SWS (mainly by further reducing cortisol and increasing aldosterone levels) and reduces T and B cell counts, likely reflecting a redistribution of these cells to lymphoid tissues. GH remains unchanged. In conclusion, closed-loop stimulation of SOs is an easy-to-use tool for probing SWS functions, and might also bear the potential to ameliorate conditions like depression and aging, where disturbed sleep coalesces with specific hormonal and immunological dysregulations.

Association of Electroencephalography (EEG) Power Spectra with Corneal Nerve Fiber Injury in Retinoblastoma Patients.

BackgroundIn our clinical experience we discovered that EEG band power may be correlated with corneal nerve injury in retinoblastoma patients. This study aimed to investigate biomarkers obtained from electroencephalography (EEG) recordings to reflect corneal nerve injury in retinoblastoma patients.Material/MethodsOur study included 20 retinoblastoma patients treated at the Department of Ophthalmology, Affiliated Hospital of Weifang Medical University between 2010 and 2014. Twenty normal individuals were included in the control group. EEG activity was recorded continuously with 32 electrodes using standard EEG electrode placement for detecting EEG power. A cornea confocal microscope was used to examine corneal nerve injury in retinoblastoma patients and normal individuals. Spearman rank correlation analysis was used to analyze the correlation between corneal nerve injury and EEG power changes. The sensitivity and specificity of changed EEG power in diagnosis of corneal nerve injury were also analyzed.ResultsThe predominantly slow EEG oscillations changed gradually into faster waves in retinoblastoma patients. The EEG pattern in retinoblastoma patients was characterized by a distinct increase of delta (P<0.01) and significant decrease of theta power P<0.05). Corneal nerves were damaged in corneas of retinoblastoma patients. Corneal nerve injury was positively correlated with delta EEG spectra power and negatively correlated with theta EEG spectra power. The diagnostic sensitivity and specificity by compounding in the series were 60% and 67%, respectively.ConclusionsChanges in delta and theta of EEG appear to be associated with occurrence of corneal nerve injury. Useful information can be provided for evaluating corneal nerve damage in retinoblastoma patients through analyzing EEG power bands.

Distinction in EEG slow oscillations between chronic mild traumatic brain injury and PTSD

Spectral information from resting state EEG is altered in acute mild traumatic brain injury (mTBI) and in disorders of consciousness, but there is disagreement about whether mTBI can elicit long term changes in the spectral profile. Even when identified, any long-term changes attributed to TBI can be confounded by psychiatric comorbidities such as PTSD, particularly for combat-related mTBI where postdeployment distress is commonplace. To address this question, we measured spectral power during the resting state in a large sample of service members and Veterans varying in mTBI history and active PTSD diagnosis but matched for having had combat blast exposure. We found that PTSD was associated with decreases in low frequency power, especially in the right temporoparietal region, while conversely, blast-related mTBI was associated with increases in low frequency power, especially in prefrontal and right temporal areas. Results support the idea that long-term neurophysiological effects of mTBI share some features with states of reduced arousal and cognitive dysfunction, suggesting a role for EEG in tracking the trajectory of recovery and persisting vulnerabilities to injury. Additionally, results suggest that EEG power reflects distinct pathophysiologies for current PTSD and chronic mTBI.

Odors enhance slow-wave activity in non-rapid eye movement sleep.

Most forms of suprathreshold sensory stimulation perturb sleep. In contrast, presentation of pure olfactory or mild trigeminal odorants does not lead to behavioral or physiological arousal. In fact, some odors promote objective and subjective measures of sleep quality in humans and rodents. The brain mechanisms underlying these sleep-protective properties of olfaction remain unclear. Slow oscillations in the electroencephalogram (EEG) are a marker of deep sleep, and K complexes (KCs) are an EEG marker of cortical response to sensory interference. We therefore hypothesized that odorants presented during sleep will increase power in slow EEG oscillations. Moreover, given that odorants do not drive sleep interruption, we hypothesized that unlike other sensory stimuli odorants would not drive KCs. To test these hypotheses we used polysomnography to measure sleep in 34 healthy subjects (19 women, 15 men; mean age 26.5 ± 2.5 yr) who were repeatedly presented with odor stimuli via a computer-controlled air-dilution olfactometer over the course of a single night. Each participant was exposed to one of four odorants, lavender oil (n = 13), vetiver oil (n = 5), vanillin (n = 12), or ammonium sulfide (n = 4), for durations of 5, 10, and 20 s every 9-15 min. Consistent with our hypotheses, we found that odor presentation during sleep enhanced the power of delta (0.5-4 Hz) and slow spindle (9-12 Hz) frequencies during non-rapid eye movement sleep. The increase was proportionate to odor duration. In addition, odor presentation did not modulate the occurrence of KCs. These findings imply a sleep-promoting olfactory mechanism that may deepen sleep through driving increased slow-frequency oscillations.

Resting state EEG correlates of memory consolidation

Numerous studies demonstrate that post-training sleep benefits human memory. At the same time, emerging data suggest that other resting states may similarly facilitate consolidation. In order to identify the conditions under which non-sleep resting states benefit memory, we conducted an EEG (electroencephalographic) study of verbal memory retention across 15min of eyes-closed rest. Participants (n=26) listened to a short story and then either rested with their eyes closed, or else completed a distractor task for 15min. A delayed recall test was administered immediately following the rest period. We found, first, that quiet rest enhanced memory for the short story. Improved memory was associated with a particular EEG signature of increased slow oscillatory activity (<1Hz), in concert with reduced alpha (8–12Hz) activity. Mindwandering during the retention interval was also associated with improved memory. These observations suggest that a short period of quiet rest can facilitate memory, and that this may occur via an active process of consolidation supported by slow oscillatory EEG activity and characterized by decreased attention to the external environment. Slow oscillatory EEG rhythms are proposed to facilitate memory consolidation during sleep by promoting hippocampal–cortical communication. Our findings suggest that EEG slow oscillations could play a significant role in memory consolidation during other resting states as well.

Interactions between perceptual and endogenous processes as reflected in slow EEG oscillations

Interactions between perceptual and endogenous processes as reflected in slow EEG oscillations

Control of sleep and wakefulness.

This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

The role of NREM sleep instability in child cognitive performance.

Based on recent reports of the involvement of cyclic alternating pattern (CAP) in cognitive functioning in adults, we investigated the association between CAP parameters and cognitive performance in healthy children. Polysomnographic assessment and standardized neurocognitive testing in healthy children. Sleep laboratory. Forty-two children aged 7.6 ± 2.7 years, with an even distribution of body mass percentile (58.5 ± 25.5) and SES reflective of national norms. Analysis of sleep macrostructure following the R&K criteria and of cyclic alternating pattern (CAP). The neurocognitive tests were the Stanford Binet Intelligence Scale (5(th) edition) and a Neuropsychological Developmental Assessment (NEPSY) RESULTS: Fluid reasoning ability was positively associated with CAP rate, particularly during SWS and with A1 total index and A1 index in SWS. Regression analysis, controlling for age and SES, showed that CAP rate in SWS and A1 index in SWS were significant predictors of nonverbal fluid reasoning, explaining 24% and 22% of the variance in test scores, respectively. This study shows that CAP analysis provides important insights on the role of EEG slow oscillations (CAP A1) in cognitive performance. Children with higher cognitive efficiency showed an increase of phase A1 in total sleep and in SWS.

Effects of replacement therapy on sleep architecture in children with growth hormone deficiency

Children with GH deficiency (GHD) show a general decrease in electroencephalographic (EEG) arousability represented by a significant global decrease in Cyclic Alternating Pattern (CAP). The aim of the present study was to evaluate if sleep structure is influenced by GH substitutive therapy by analyzing the classical sleep architecture parameters and sleep microstructure by means of CAP. Laboratory polysomnographic sleep recordings were obtained from five children affected by GHD (two girls and three boys; mean age: 4.6 ± 3.1 years), at baseline and after GH therapy, and from 10 normal healthy children (four girls and six boys, mean age: 5.6 ± 2.2 years). Compared to controls, GHD subjects showed a reduced total sleep time with increased wakefulness and a consequent decrease in sleep efficiency; GH therapy was associated with an increase of the awakenings/hour and a large effect size was evident for sleep latency, sleep efficiency, and stage N3, which were decreased, and for stage W, which was increased. CAP appeared to be globally reduced and all phase A subtypes and CAP cycle showed a longer duration in GHD children vs. controls. GH substitutive treatment was followed by an increase in CAP rate (total, in N2, and in N3); additionally, A1 index was also significantly increased, especially during stage N3, with a very large effect size. On the other hand, A2 and A3 index and CAP cycle mean duration were reduced. Sleep stage architecture seems to be influenced by the GH status, but the analysis of sleep microstructure by means of CAP reveals an enhancement of EEG slow oscillations in GHD patients (demonstrated by an increase in CAP rate and A1 index during N3) after the start of GH replacement therapy. These findings deserve to be verified in a larger trial.

Resting posterior minus frontal EEG slow oscillations is associated with extraversion and DRD2 genotype

The agency facet of extraversion has been hypothesized to be based on individual differences in dopamine activity. Recent work suggests that resting posterior minus frontal electroencephalographic (EEG) slow oscillations (delta, theta) is both consistently associated with extraversion and sensitive to dopamine D2 receptor antagonist-induced changes in dopaminergic activity. Here we examine for the first time the interrelations between polymorphisms of the dopamine D2 receptor (DRD2) gene (rs1800497 [previously termed TAQ1A], rs1076560, rs1799732 [−141C Ins/Del]), extraversion and resting posterior minus frontal (Pz–Fz) slow oscillations. As predicted, we found an association between DRD2 and resting Pz–Fz slow oscillations in a sample of 141 individuals participating in an eyes-closed resting EEG session. Moreover, we replicated the association between extraversion and Pz–Fz slow oscillations. Our findings strongly suggest that the posterior–frontal distribution of slow oscillations constitutes a useful brain-based intermediate phenotype for investigating the dopaminergic basis of extraversion.

Large-scale microelectrode recordings of high-frequency gamma oscillations in human cortex during sleep.

Gamma oscillations (40-120 Hz), usually associated with waking functions, can be recorded in the deepest stages of sleep in animals. The full details of their large-scale coordination across multiple cortical networks are still unknown. Furthermore, it is not known whether oscillations with similar characteristics are also present in the human brain. In this study, we examined the existence of gamma oscillations during polysomnographically defined sleep-wake states using large-scale microelectrode recordings (up to 56 channels), with single-cell and spike-time precision, in epilepsy patients. We report that low (40-80 Hz) and high (80-120 Hz) gamma oscillations recurrently emerged over time windows of several hundreds of milliseconds in all investigated cortical areas during slow-wave sleep. These patterns were correlated with positive peaks of EEG slow oscillations and marked increases in local cellular discharges, suggesting that they were associated with cortical UP states. These gamma oscillations frequently appeared at approximately the same time in many different cortical areas, including homotopic regions, forming large spatial patterns. Coincident firings with millisecond precision were strongly enhanced during gamma oscillations but only between cells within the same cortical area. Furthermore, in a significant number of cases, cortical gamma oscillations tended to occur within 100 ms after hippocampal ripple/sharp wave complexes. These data confirm and extend earlier animal studies reporting that gamma oscillations are transiently expressed during UP states during sleep. We speculate that these high-frequency patterns briefly restore "microwake" activity and are important for consolidation of memory traces acquired during previous awake periods.

Reduced NREM sleep instability in benign childhood epilepsy with centro-temporal spikes

To analyze sleep architecture and NREM sleep instability by means of the cyclic alternating pattern (CAP) in children with benign epilepsy with rolandic spikes (BERS). Ten children with BERS, drug free at the time of the study and 10 age-matched normal controls were included in this study. Sleep was visually scored for sleep architecture and CAP using standard criteria. Sleep architecture in BERS showed only few significant differences vs. controls with a reduction of total sleep time, sleep efficiency, and REM sleep percentage. CAP analysis revealed several significant differences: reduced total CAP rate, mainly in sleep stage 2, and reduced EEG slow oscillations and arousals during stages N1 and N2. Sleep architecture is not importantly affected in BERS but CAP analysis reveals a decrease of NREM instability, mainly in sleep stage 2. Since there is a spindle-related spike activation in BERS, we speculate that the decrease of CAP and of EEG slow oscillations and arousals might be linked with the inhibitory action of spindling activity and spikes on arousals. CAP analysis discloses sleep structure abnormalities in children with BERS not shown by the classical sleep scoring. Spike activity and CAP A1 subtypes seem to be mutually exclusive probably because centro-temporal spikes disturb the physiological synchronization mechanisms needed for the generation of slow-wave components of CAP.