Coherent neocortical 40‐Hz oscillations are not present during REM sleep

During cognitive processes there are extensive interactions between various regions of the cerebral cortex. Oscillations in the gamma frequency band (≈40 Hz) of the electroencephalogram (EEG) are involved in the binding of spatially separated but temporally correlated neural events, which results in a unified perceptual experience. The extent of these interactions can be examined by means of a mathematical algorithm called ‘coherence’, which reflects the ‘strength’ of functional interactions between cortical areas. The present study was conducted to analyse EEG coherence in the gamma frequency band of the cat during alert wakefulness (AW), quiet wakefulness (QW), non‐rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. Cats were implanted with electrodes in the frontal, parietal and occipital cortices to monitor EEG activity. Coherence values within the gamma frequency (30–100 Hz) from pairs of EEG recordings were analysed. A large increase in coherence occurred between all cortical regions in the 30–45 Hz frequency band during AW compared with the other behavioral states. As the animal transitioned from AW to QW and from QW to NREM sleep, coherence decreased to a moderate level. Remarkably, there was practically no EEG coherence in the entire gamma band spectrum (30–100 Hz) during REM sleep. We conclude that functional interactions between cortical areas are radically different during sleep compared with wakefulness. The virtual absence of gamma frequency coherence during REM sleep may underlie the unique cognitive processing that occurs during dreams, which is principally a REM sleep‐related phenomenon.     

Differences in electroencephalographic findings among categories of narcolepsy-spectrum disorders

ObjectiveTo clarify the differences in quantitative electroencephalographic (EEG) measures and their relation to clinical symptoms among narcolepsy-spectrum disorders.MethodsThe enrolled patients were: 28 with narcolepsy with cataplexy (NA-CA); 16 with NA without cataplexy (NA w/o CA) and HLA-DRB1*1501/DQB1*0602 positive (NA w/o CA HLA+); 22 with NA w/o CA and HLA negative (NA w/o CA HLA−); and 22 with idiopathic hypersomnia without long sleep time (IHS w/o LST). Nocturnal polysomnography (n-PSG) and quantitative EEG evaluation, as well as the Multiple Sleep Latency test (MSLT), were conducted for all patients.ResultsPatients with NA-CA or NA w/o CA HLA+ showed lower alpha power, higher delta and theta power during wakefulness, and higher alpha and beta power during rapid eye movement (REM) sleep, compared to those with NA w/o CA HLA− or IHS w/o LST. The former two groups also showed lower sleep efficiency and a higher rate of positivity of REM-related symptoms than the other two groups.ConclusionsIn narcolepsy, the presence of cataplexy and HLA positivity are associated with EEG slowing during wakefulness and increased fast EEG activity during REM sleep, REM-related symptoms and disrupted nocturnal sleep in narcolepsy.     

Brainstem carbachol injections in the urethane anesthetized rat produce hippocampal theta rhythm and cortical desynchronization: a comparison of pedunculopontine tegmental versus nucleus pontis oralis injections

Previous research has demonstrated that brainstem injections of acetylcholine agonists (e.g., carbachol) produced electrophysiological indicators of rapid-eye-movement (REM) sleep in the cat. Recent reports now indicate that this phenomenon may hold true for rats as well. Relatively few reports, however, have examined the effect of these injections on REM indicators in the anesthetized rat, a preparation useful for elucidating underlying neurobiological mechanisms controlling REM sleep processes. The present study compared the effect of injections of carbachol (5 μg in 250 nl) into the pedunculopontine tegmental nucleus (PPTg) or the nucleus pontis oralis (NPO) on two tonic indicators of REM sleep in the urethane-anesthetized rat. Namely, changes in the hippocampal EEG and in the cortical EEG. Carbachol injections into either site produced a change in both the hippocampal EEG and cortical EEG to a REM-like state at short latencies. The length of these changes (duration of effect), however, was site-dependent. Thus, PPTg carbachol injections induced significantly longer lasting effects in both the hippocampal and cortical EEG than did NPO injections. The results suggest that brainstem carbachol injections in rats, as in cats, may provide a useful model for investigating tonic REM sleep processes.     

EEG spectral analysis of wakefulness and REM sleep in high functioning autistic spectrum disorders.

OBJECTIVE: The aim of this study was to investigate the involvement of temporo-occipital regions in the pathophysiology of autistic spectrum disorders (ASD) by using REM sleep and waking EEG. METHODS: The EEG recordings of 9 persons with ASD and 8 control participants were recorded using a 12-electrode montage. Spectral analysis (0.75-19.75 Hz) was performed on EEG activity recorded upon two activated states: REM sleep and wakefulness. RESULTS: During REM sleep, persons with ASD showed a selective, significantly lower absolute beta (13.0-19.75 Hz) spectral amplitude over the primary (O(1), O(2)) and associative (T(5), T(6)) cortical visual areas compared to controls. Persons with ASD showed significantly higher absolute theta (4.0-7.75 Hz) spectral amplitude over the left frontal pole region (Fp1) compared to controls during evening wakefulness, but not during morning wakefulness. SIGNIFICANCE: The results of waking EEG are consistent with previously reported observations of neuropsychological signs of frontal atypicalities in ASD; results from REM sleep are the first EEG evidence to support the hypothesis of abnormal visuoperceptual functioning in ASD. Altogether, these results point toward atypical thalamo-cortical mechanisms subserving the neural processing of information in ASD.     

Characterization of the mu rhythm during rapid eye movement sleep.

OBJECTIVE: The rolandic mu rhythm, a resting activity of somatosensory cortex, is a striking feature of the waking human electroencephalogram. This study will demonstrate that activity with identical features occurs during rapid eye movement (REM) sleep. METHODS: Eye and chin leads were added during prolonged closed circuit television (video) electroencephalographic (EEG) recording with scalp (12 patients) or subdural electrodes including 64 contract grids over the frontoparietal cortices (5 patients). Sleep staging was performed by reformatting into standard polysomnography montages (using two EEG channels, and eye and chin channels) and applying standard scoring criteria. The recordings were then reviewed using all EEG channels to assess rhythmic EEG activity by a reader blinded to the sleep staging. RESULTS: During scalp recordings, 7-10 Hz central rhythms were seen during wakefulness in 7 patients, with 6 of these also having similar rhythms during REM sleep. Similar activity was seen over somatosensory cortex during wakefulness and REM in all invasively recorded patients. This activity was blocked by contralateral body movement or contralateral somatosensory stimuli, even during REM sleep. It was absent in other sleep stages. CONCLUSIONS: This REM sleep activity recapitulates all the characteristics of the waking rolandic mu rhythm. This demonstrates functional similarity between the states of wakefulness and REM sleep.     

Electroencephalographic correlates of cataplectic attacks in narcoleptic canines

Cataplectic attacks were monitored behaviorally and polygraphically in 4 narcoleptic dogs, of which three inherited the disorder. The recorded EEG signals were evaluated by power spectral analysis. We found 3 distinct stages of cataplexy: an initial stage which resembled wakefulness with tonic suppression of EMG activity, a later stage which was highly similar to REM sleep, and a final transitional stage to wakefulness or NREM sleep. The first stage of cataplexy was characterized by full postural collapse, a waking-like EEG spectrum, visual tracking, and a hypotonic EMG. The second stage of cataplexy differed electrographically from the previous stage by the onset of hypersynchronous hippocampal theta activity, a REM-like EEG spectrum, larger amplitude EEG signals, and a higher peak theta frequency. Glazed eyes, sporadic rapid eye movements and muscle twitches were also present. The final stage of cataplexy was characterized by mixed amplitude, mixed frequency EEG activity, and by the absence of rapid eye movements, visual tracking, directed movements, and muscle twitches. The EEG spectra of two other narcoleptic phenomena, sleep-onset REM periods and NREM sleep onsets from cataplexy, were nearly identical to the spectra of the normally occurring REM and NREM sleep periods.     

Directional information flows between brain hemispheres across waking,non-REM and REM sleep states: An EEG study

The present electroencephalographic (EEG) study evaluated the hypothesis of a preferred directionality of communication flows between brain hemispheres across 24 h (i.e., during the whole daytime and nighttime), as an extension of a recent report showing changes in preferred directionality from pre-sleep wake to early sleep stages.Scalp EEGs were recorded in 10 normal volunteers during daytime wakefulness (eyes closed; first period: from 10:00 to 13:00 h; second period: from 14:00 to 18:00 h; third period: from 19:00 to 22:00 h) and nighttime sleep (four NREM-REM cycles). EEG rhythms of interest were delta (1–4 Hz), theta (5–7 Hz), alpha (8–11 Hz), sigma (12–15 Hz) and beta (16–28 Hz). The direction of the inter-hemispheric information flow was evaluated by computing the directed transfer function (DTF) from these EEG rhythms.Inter-hemispheric directional flows varied as a function of the state of consciousness (wake, NREM sleep, REM sleep) and in relation to different cerebral areas. During the daytime, alpha and beta rhythms conveyed inter-hemispheric signals with preferred Left-to-Right hemisphere direction in parietal and central areas, respectively. During the NREM sleep periods of nighttime, the direction of inter-hemispheric DTF information flows conveyed by central beta rhythms was again preponderant from Left-to-Right hemisphere in the stage 2, independent of cortical areas. No preferred direction emerged across the REM periods.These results support the hypothesis that specific directionality of communication flows between brain hemispheres is associated with wakefulness, NREM (particularly stage 2) and REM states during daytime and nighttime. They also reinforce the suggestive hypothesis of a relationship between inter-hemispheric directionality of EEG functional coupling and frequency of the EEG rhythms.     

Nasal respiration entrains neocortical long‐range gamma coherence during wakefulness

Recent studies have shown that slow cortical potentials in archi‐, paleo‐ and neocortex can phase‐lock with nasal respiration. In some of these areas, gamma activity (γ: 30–100 Hz) is also coupled to the animal's respiration. It has been hypothesized that these functional relationships play a role in coordinating distributed neural activity. In a similar way, inter‐cortical interactions at γ frequency have also been associated as a binding mechanism by which the brain generates temporary opportunities necessary for implementing cognitive functions. The aim of the present study is to explore whether nasal respiration entrains inter‐cortical functional interactions at γ frequency during both wakefulness and sleep. Six adult cats chronically prepared for electrographic recordings were employed in this study. Our results show that during wakefulness, slow cortical respiratory potentials are present in the olfactory bulb and several areas of the neocortex. We also found that these areas exhibit cross‐frequency coupling between respiratory phase and γ oscillation amplitude. We demonstrate that respiratory phase modulates the inter‐cortical gamma coherence between neocortical electrode pairs. On the contrary, slow respiratory oscillation and γ cortical oscillatory entrainments disappear during non‐rapid eye movement and rapid eye movement sleep. These results suggest that a single unified phenomenon involves cross‐frequency coupling and long‐range γ coherence across the neocortex. This fact could be related to the temporal binding process necessary for cognitive functions during wakefulness.     

Theta and gamma coherence across the septotemporal axis during distinct behavioral states

Theta (4-12 Hz) and gamma (40-100 Hz) field potentials represent the interaction of synchronized synaptic input onto distinct neuronal populations within the hippocampal formation. Theta is quite prominent during exploratory activity, locomotion, and REM sleep. Although it is generally acknowledged that theta is coherent throughout most of the hippocampus, there is significant variability in theta, as well as gamma, coherence across lamina at any particular septotemporal level of the hippocampus. Larger differences in theta coherence are observed across the septotemporal (long) axis. We have reported that during REM sleep there is a decrease in theta coherence across the long axis that varies with the topography of CA3/mossy cell input rather than the topography of the prominent entorhinal input. On the basis of differences in the rat's behavior as well as the activity of neuromodulatory inputs (e.g., noradrenergic and serotonergic), we hypothesized that theta coherence across the long axis would be greater during locomotion than REM sleep and exhibit a pattern more consistent with the topography of entorhinal inputs. We examined theta and gamma coherence indices at different septotemporal and laminar sites during distinct theta states: locomotion during maze running, REM sleep, following acute treatment with a θ-inducing cholinomimetic (physostigmine) and for comparison during slow-wave sleep. The results demonstrate a generally consistent pattern of theta and gamma coherence across the septotemporal axis of the hippocampus that is quite indifferent to sensory input and overt behavior. These results are discussed with regards to the neurobiological mechanisms that generate theta and gamma and the growing body of evidence linking theta and gamma indices to memory and other cognitive functions.     

Comparative study on the behavioral and EEG changes induced by diazepam, buspirone and a novel anxioselective anxiolytic, DN-2327, in the cat.

Behavioral and EEG effects of 2-(7-chloro-1,8-naphthyridin-2-yl)-3-[(1,4)-dioxa-8-(azas piro-[4.5]dec-8- yl)carbonylmethyl]isoindolin-1-one (DN-2327; 1, 5 and 20 mg/kg p.o.) were compared to those of diazepam (0.2 and 1 mg/kg p.o.) and buspirone (1 and 5 mg/kg p.o.) in freely moving cats. DN-2327 did not affect motor coordination or the relative percentages of the three sleep-wakefulness stages. Diazepam (1 mg/kg) increased wakefulness and non-REM sleep, and buspirone (5 mg/kg) also increased wakefulness and decreased REM sleep. In addition, diazepam (1 mg/kg) caused severe motor disturbance, but buspirone did not. The cortical EEG power density spectra during wakefulness were changed almost dose-dependently by DN-2327 (decreased: 2-7.75 Hz; increased: 20-49.75 Hz), and dose-dependently by diazepam (decreased: 2-7.75 Hz; increased 13-49.75 Hz) and buspirone (decreased: 4-9.75 and 13-19.75 Hz). The effect of DN-2327 on the cortical EEG varied with the sleep-wakefulness stage. The power of the 4- to 7.75-Hz frequency (theta) band of the hippocampal EEG during wakefulness was decreased by diazepam and buspirone but not by DN-2327, while the peak frequency of its spectra was decreased only by diazepam. On the other hand, during non-REM sleep, DN-2327 decreased the power of the theta band as did diazepam. These results indicate that the behavioral and EEG effects of DN-2327 differ completely from those of buspirone and considerably from those of diazepam and that the EEG effect of DN-2327 varies with the sleep-wakefulness stage.     

Selective Immunolesion of the Basal Forebrain Cholinergic Neurons: Effects on Hippocampal Activity During Sleep and Wakefulness in the Rat

Intracerebroventricular injection of the toxin 192 IgG-saporin (4μg) kills the cholinergic neurons of the basal forebrain bearing the low affinity NGF receptor (NGFr). The effect of this cholinergic denervation on the hippocampal and cortical electrical activity (EEG) was studied during sleep and wakefulness. EEG was recorded under freely-moving conditions in lesioned (n=10) and control (n=6) rats (8–16 days post-injection). In lesioned rats, active (AW) and quiet (QW) wakefulness episode durations were similar to those of controls whereas the REM sleep duration was reduced, 8 days post-lesion (P<0.01). Bouts of REM sleep were more numerous but shorter. The hippocampal theta activity was still present in lesioned-rats during AW (type 1 theta), QW (type 2 theta) and REM sleep. The frequency was unchanged but the amplitude of the three types of theta was significantly reduced (P<0.01). Type 2 theta occurred with shorter and less regular bouts (P<0.05). Abnormal slow waves (2–4 Hz) were observed during wakefulness. Histology showed a dramatic loss of NGFr-positive neurons in the basal forebrain and a decline in hippocampal and cortical acetylcholinesterase activity. These results suggest that the cholinergic septohippocampal input is not the primary pacemaker for the hippocampal theta rhythm.     

Human alpha oscillations in wakefulness, drowsiness period, and REM sleep: different electroencephalographic phenomena within the alpha band.

Cortical oscillations in the range of alpha activity (8-13 Hz) are one of the fundamental electrophysiological phenomena of the human electroencephalogram (EEG). Evidence from quantitative EEG data has shown that their electrophysiological features, cortical generation mechanisms, and therefore, their functional correlates vary along the sleep-wake continuum. Specifically, spectral microstructure and EEG coherence levels between anterior and posterior cortical regions permit to differentiate among alpha activity spontaneously appearing in relaxed wakefulness with eyes closed, drowsiness period, and REM sleep, by reflecting distinct properties of neural networks involved in its cortical generation as well as a different interplay between cortical generators, respectively. Besides, the dissimilar spatiotemporal features of brain electrical microstates within the alpha range reveals a different geometry of active neural structures underlying each alpha variant or, simply, changes in the stability level of neural networks during each brain state. Studies reviewed in this paper support the hypothesis that two different alpha variants occur during human REM sleep: 'background responsive alpha activity', blocked over occipital regions when rapid eye movements are present, and 'REM-alpha bursts', non modulated by the alteration of tonic and phasic periods. Altogether, evidence suggests that electrophysiological features of human cortical oscillations in the alpha frequency range vary across different behavioural states, as well as within state, reflecting different cerebral phenomena with probably dissimilar functional meaning.     

Rapid eye movement sleep behavior disorder and rapid eye movement sleep without atonia in narcolepsy

Narcolepsy is a rare disabling hypersomnia disorder that may include cataplexy, sleep paralysis, hypnagogic hallucinations, and sleep-onset rapid eye movement (REM) periods, but also disrupted nighttime sleep by nocturnal awakenings, and REM sleep behavior disorder (RBD). RBD is characterized by dream-enacting behavior and impaired motor inhibition during REM sleep (REM sleep without atonia, RSWA). RBD is commonly associated with neurodegenerative disorders including Parkinsonisms, but is also reported in narcolepsy in up to 60% of patients. RBD in patients with narcolepsy is, however, a distinct phenotype with respect to other RBD patients and characterized also by absence of gender predominance, elementary rather than complex movements, less violent behavior and earlier age at onset of motor events, and strong association to narcolepsy with cataplexy/hypocretin deficiency. Patients with narcolepsy often present dissociated sleep features including RSWA, increased density of phasic chin EMG and frequent shift from REM to NREM sleep, with or without associated clinical RBD. Most patients with narcolepsy with cataplexy lack the hypocretin neurons in the lateral hypothalamus. Tonic and phasic motor activities in REM sleep and dream-enacting behavior are mostly reported in presence of cataplexy. Narcolepsy without cataplexy is a condition rarely associated with hypocretin deficiency. We proposed that hypocretin neurons are centrally involved in motor control during wakefulness and sleep in humans, and that hypocretin deficiency causes a functional defect in the motor control involved in the development of cataplexy during wakefulness and RBD/RSWA/phasic motor activity during REM sleep.     

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age- and gender-matched healthy subjects. During wakefulness, RBD patients showed a considerably higher theta power in frontal, temporal, and occipital regions with a lower beta power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, beta power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders.     

Absence of sleep spindles in human medial and basal temporal lobes

All-night recordings from subdural electrocorticographic (ECoG) electrodes on the human medial and basal temporal lobes were analysed to examine spindling activities during sleep. Subjects were three males and three females who were candidates for neurosurgical treatments of partial epilepsy. Subdural electrodes were attached to the medial and basal temporal lobe cortices, allowing ECoG and electroencephalogram from the scalp vertex (Cz EEG) to be recorded simultaneously during all night sleep. In one case, subdural electrodes were attached also on the parietal lobe. Fast Fourier transformation (FFT) analyses were performed on the ECoG and Cz EEG signals. No organized sleep spindles or sigma band (12-16 Hz) peaks in FFT power spectra were observed from the medial or basal temporal lobes of the non-epileptogenic hemispheres during non-rapid eye movement (NREM) sleep. In a case with parietal electrodes, organized spindle bursts were observed in parietal signals synchronized with Cz spindles. Although delta band (0.3-3 Hz) power from both the medial and basal temporal lobes fluctuated across each night as expected, sigma activity changed little. However, 14 Hz oscillatory bursts were observed in the medial basal temporal lobe of epileptogenic hemisphere in two cases and bilaterally in one case during not only NREM sleep but rapid eye movement (REM) sleep and wakefulness. From the present study we conclude that sleep spindle activities are absent in the medial and basal temporal lobes. Fourteen Hz oscillatory bursts observed from the medial or basal temporal lobe in some cases were not considered to be sleep spindles since they also appeared during REM sleep and wakefulness. These waveforms could have originated due to epileptic pathology, since they frequently appeared in epileptic regions.     

Decreased coherence in higher frequency ranges (beta and gamma) between central and frontal EEG in patients with schizophrenia: A preliminary report

Schizophrenia is associated with a dysfunction of cognitive integration that may be due to abnormalities in inhibitory neural circuitry. A previous study found a failure of gamma band (25-45 Hz) synchronization in patients with schizophrenia compared to controls. Another recent study also stressed the importance of investigating high frequencies in the scalp-recorded sleep electroencephalogram (EEG). In this study, we compared coherence between first episode drug-na?ve patients with schizophrenia (n=8) and age- and sex-matched normal controls (n=8) using two 32-s epochs of C4 and F4 EEG. The coherence was obtained using 4096 data points (128 Hz signal) using cross-spectral analysis with Blackman-Tukey window in beta (15.25-24.75 Hz) and gamma (25-44.75 Hz) frequency bands. We used wake, non-rapid eye movement (NREM) and rapid eye movement (REM) sleep periods for the analyses. Our results show a significant decrease in coherence in both beta and gamma frequency bands in patients. Post-hoc 't' tests revealed a significantly lower coherence only during the wake stage in patients with schizophrenia in beta as well as gamma frequency bands. These results further support the importance of the analyses of high-frequency bands in the EEG and support previous findings of abnormal neural synchrony in patients with schizophrenia. These results have been discussed further in relation to wake and sleep stages.     

State-dependent control of lumbar motoneurons by the hypocretinergic system

Neurons in the lateral hypothalamus (LH) that synthesize hypocretins (Hcrt-1 and Hcrt-2) are active during wakefulness and excite lumbar motoneurons. Because hypocretinergic cells also discharge during phasic periods of rapid eye movement (REM) sleep, we sought to examine their action on the activity of motoneurons during this state. Accordingly, cat lumbar motoneurons were intracellularly recorded, under α-chloralose anesthesia, prior to (control) and during the carbachol-induced REM sleep-like atonia (REMc). During control conditions, LH stimulation induced excitatory postsynaptic potentials (composite EPSP) in motoneurons. In contrast, during REMc, identical LH stimulation induced inhibitory PSPs in motoneurons. We then tested the effects of LH stimulation on motoneuron responses following the stimulation of the nucleus reticularis gigantocellularis (NRGc) which is part of a brainstem–spinal cord system that controls motoneuron excitability in a state-dependent manner. LH stimulation facilitated NRGc stimulation-induced composite EPSP during control conditions whereas it enhanced NRGc stimulation-induced IPSPs during REMc. These intriguing data indicate that the LH exerts a state-dependent control of motor activity. As a first step to understand these results, we examined whether hypocretinergic synaptic mechanisms in the spinal cord were state dependent. We found that the juxtacellular application of Hcrt-1 induced motoneuron excitation during control conditions whereas motoneuron inhibition was enhanced during REMc. These data indicate that the hypocretinergic system acts on motoneurons in a state-dependent manner via spinal synaptic mechanisms. Thus, deficits in Hcrt-1 may cause the coexistence of incongruous motor signs in cataplectic patients, such as motor suppression during wakefulness and movement disorders during REM sleep.     

Cortical oscillations in human medial temporal lobe during wakefulness and all-night sleep

We have recorded human medial temporal lobe electrocorticogram during wakefulness and natural sleep in epileptic patients with subdural electrodes. From these recordings, we have found gamma (30-150 Hz) [Neuroscience 90 (1999) 1149] and beta-1 (10-20 Hz) [NeuroReport 10 (1999) 3055] activities during wakefulness in human medial temporal lobe. In this paper, we will report changes of these frequencies across wake and natural sleep. Electrocorticograms during wake, slow wave sleep and rapid eye movement (REM) sleep were subjected to fast Fourier transformation analysis. During wake two spectral enhancements, beta-1 and gamma, were consistently observed across subjects. In the raw signal, beta-1 was observed as a regular rhythmic oscillation. In slow wave sleep, the beta-1 peak disappeared but gamma remained, although slightly reduced in power. During REM sleep, beta-1 appeared again, but the peak frequency was significantly lower than during wake (mean frequency: wake=16.6, REM=12.8 Hz). The gamma peak was also present in REM sleep. It has been known that the rhythmic slow activity (RSA) or theta is observed in some animals. However, it is unclear whether the human hippocampus displays similar activity. Since human beta-1 appears during wake and REM sleep when RSA is observed in other species, and since beta-1 is also a regular rhythmic oscillation, we propose that beta-1 may be the functional equivalent of hippocampal RSA (theta) observed in some animals. Functional significances of the gamma activity should be further investigated.     

The diagnostic value of power spectra analysis of the sleep electroencephalography in narcoleptic patients

ObjectiveManifestations of narcolepsy with cataplexy (NC) include disturbed nocturnal sleep – hereunder sleep–wake instability, decreased latency to rapid eye movement (REM) sleep, and dissociated REM sleep events. In this study, we characterized the electroencephalography (EEG) of various sleep stages in NC versus controls.MethodsEEG power spectral density (PSD) was computed in 136 NC patients and 510 sex- and age-matched controls. Features reflecting differences in PSD curves were computed. A Lasso-regularized regression model was used to find an optimal feature subset, which was validated on 19 NC patients and 708 non-NC patients from a sleep clinic. Reproducible features were analyzed using receiver operating characteristic (ROC) curves.ResultsThirteen features were selected based on the training dataset. Three were applicable in the validation dataset, indicating that NC patients show (1) increased alpha power in REM sleep, (2) decreased sigma power in wakefulness, and (3) decreased delta power in stage N1 versus wakefulness. Sensitivity of these features ranged from 4% to 10% with specificity around 98%, and it did not vary substantially with and without treatment.ConclusionsEEG spectral analysis of REM sleep, wake, and differences between N1 and wakefulness contain diagnostic features of NC. These traits may represent sleepiness and dissociated REM sleep in patients with NC. However, the features are not sufficient for differentiating NC from controls, and further analysis is needed to completely evaluate the diagnostic potential of these features.     

Long-term changes in sleep and electroencephalographic activity by chronic vagus nerve stimulation in cats

We previously reported the effect of vagus nerve electrical stimulation (VNS) on sleep and behavior in cats. The aim of the present study is to analyze the long-term effects of VNS on the electroencephalographic (EEG) power spectrum and on the different stages of the sleep-wakefulness cycle in the freely moving cat. To achieve this, six male cats were implanted with electrodes on the left vagal nerve and submitted to 15 rounds of 23 h continuous sleep recordings in three categories: baseline (BL), VNS and post-stimulus recording (PSR). The following parameters were analyzed: EEG power spectrum, total time and number of sleep phases, ponto-geniculo-occipital (PGO) wave density of the rapid eye movement (REM) sleep, and the number of times the narcoleptic reflex was present (sudden transition from wakefulness to REM sleep). Significant changes were detected, such as an enhancement of slow-wave sleep (SWS) stage II; a power increase in the bands corresponding to sleep spindles (8-14 Hz) and delta waves (1-4 Hz) with VNS and PSR; an increase in the total time, number of stages, and density of PGO wave in REM sleep with VNS; a decrease of wakefulness in PSR, and the eventual appearance of the narcoleptic reflex with VNS. The results show that the effect of the VNS changes during different stages of the sleep-wakefulness cycle. In REM sleep, the effect was present only during VNS, while the SWS II was affected beyond VNS periods. This suggests that ponto-medullar and thalamic mechanisms of slow EEG activity may be due to plastic changes elicited by vagal stimulation.