The EEG microstate topography is predominantly determined by intracortical sources in the alpha band.

Human brain electric activity can be measured at high temporal and fairly good spatial resolution via electroencephalography (EEG). The EEG microstate analysis is an increasingly popular method used to investigate this activity at a millisecond resolution by segmenting it into quasi-stable states of approximately 100 ms duration. These so-called EEG microstates were postulated to represent atoms of thoughts and emotions and can be classified into four classes of topographies A through D, which explain up to 90% of the variance of continuous EEG. The present study investigated whether these topographies are primarily driven by alpha activity originating from the posterior cingulate cortex (all topographies), left and right posterior cortices, and the anterior cingulate cortex (topographies A, B, and C, respectively). We analyzed two 64-channel resting state EEG datasets (N = 61 and N = 78) of healthy participants. Sources of head-surface signals were determined via exact low resolution electromagnetic tomography (eLORETA). The Hilbert transformation was applied to identify instantaneous source strength of four EEG frequency bands (delta through beta). These source strength values were averaged for each participant across time periods belonging to a particular microstate. For each dataset, these averages of the different microstate classes were compared for each voxel. Consistent differences across datasets were identified via a conjunction analysis. The intracortical strength and spatial distribution of alpha band activity mainly determined whether a head-surface topography of EEG microstate class A, B, C, or D was induced. EEG microstate class C was characterized by stronger alpha activity compared to all other classes in large portions of the cortex. Class A was associated with stronger left posterior alpha activity than classes B and D, and class B was associated with stronger right posterior alpha activity than A and D. Previous results indicated that EEG microstate dynamics reflect a fundamental mechanism of the human brain that is altered in different mental states in health and disease. They are characterized by systematic transitions between four head-surface topographies, the EEG microstate classes. Our results show that intra-cortical alpha oscillations, which likely reflect decreased cortical excitability, primarily account for the emergence of these classes. We suggest that microstate class dynamics reflect transitions between four global attractor states that are characterized by selective inhibition of specific intra-cortical regions.

Different Effects of Sleep Deprivation and Torpor on EEG Slow-Wave Characteristics in Djungarian Hamsters.

It has been shown previously in Djungarian hamsters that the initial electroencephalography (EEG) slow-wave activity (power in the 0.5-4.0 Hz band; SWA) in non-rapid eye movement (NREM) sleep following an episode of daily torpor is consistently enhanced, similar to the SWA increase after sleep deprivation (SD). However, it is unknown whether the network mechanisms underlying the SWA increase after torpor and SD are similar. EEG slow waves recorded in the neocortex during sleep reflect synchronized transitions between periods of activity and silence among large neuronal populations. We therefore set out to investigate characteristics of individual cortical EEG slow waves recorded during NREM sleep after 4 h SD and during sleep after emergence from an episode of daily torpor in adult male Djungarian hamsters. We found that during the first hour after both SD and torpor, the SWA increase was associated with an increase in slow-wave incidence and amplitude. However, the slopes of single slow waves during NREM sleep were steeper in the first hour after SD but not after torpor, and, in contrast to sleep after SD, the magnitude of change in slopes after torpor was unrelated to the changes in SWA. Furthermore, slow-wave slopes decreased progressively within the first 2 h after SD, while a progressive increase in slow-wave slopes was apparent during the first 2 h after torpor. The data suggest that prolonged waking and torpor have different effects on cortical network activity underlying slow-wave characteristics, while resulting in a similar homeostatic sleep response of SWA. We suggest that sleep plays an important role in network homeostasis after both waking and torpor, consistent with a recovery function for both states.

Changes of cerebral tissue oxygen saturation at sleep transitions in adolescents.

In adults, cerebral oxy-([O2Hb]) and deoxyhemoglobin concentrations ([HHb]) change characteristically at transitions of sleep stages. The aims were to assess these changes in adolescents and additionally to measure tissue oxygen saturation (StO2) by near infrared spectroscopy (NIRS). Previously it was reported that in adults [O2Hb] increased and [HHb] decreased at the transition from non-rapid eye movement sleep (NREMS) to REMS and wakefulness. Transitions to NREMS from REMS/wakefulness led to a decrease in [O2Hb] and an increase in [HHb]. We measured [O2Hb], [HHb] and tissue oxygenation (StO2) with NIRS approximately above the left prefrontal cortex in 12 healthy adolescent males (aged 10-16 years). We found comparable signs and magnitudes of changes in [O2Hb] and [HHb] as observed in adults. StO2 increased at the transitions from NREMS to REMS and decreased from REMS to NREMS and at sleep onset (all p < 0.01, linear mixed effects model). Changes in oxygen metabolism during sleep transitions are similar in adolescents and adults. In addition, we show for the first time temporal changes of StO2 at sleep transitions.

No increased sensitivity in brain activity of adolescents exposed to mobile phone-like emissions.

OBJECTIVE: To examine the potential sensitivity of adolescents to radiofrequency electromagnetic field (RF EMF) exposures, such as those emitted by mobile phones. METHODS: In a double-blind, randomized, crossover design, 22 adolescents aged 11-13 years (12 males) underwent three experimental sessions in which they were exposed to mobile phone-like RF EMF signals at two different intensities, and a sham session. During exposure cognitive tasks were performed and waking EEG was recorded at three time-points subsequent to exposure (0, 30 and 60 min). RESULTS: No clear significant effects of RF EMF exposure were found on the waking EEG or cognitive performance. CONCLUSIONS: Overall, the current study was unable to demonstrate exposure-related effects previously observed on the waking EEG in adults, and also provides further support for a lack of an influence of mobile phone-like exposure on cognitive performance. SIGNIFICANCE: Adolescents do not appear to be more sensitive than adults to mobile phone RF EMF emissions.

Ammonia-related changes in cerebral electrogenesis in healthy subjects and patients with cirrhosis.

OBJECTIVE: To study the effect of hyperammonaemia on the wake electroencephalogram (EEG) of patients with cirrhosis and healthy volunteers. METHODS: Wake EEGs were recorded prior to and after the induction of controlled hyperammonaemia in 10 patients with cirrhosis and 10 matched healthy volunteers. RESULTS: At baseline, patients had higher ammonaemia than healthy volunteers and their dominant EEG rhythm was slower and of higher amplitude. Induced hyperammonaemia resulted in increased spectral power over most of the scalp in healthy volunteers and decreased frequency along the anterior-posterior midline in patients. CONCLUSIONS: These findings suggest different effects of hyperammonaemia on the wake EEG in relation to baseline/peak ammonia levels. SIGNIFICANCE: The wake EEG is sensitive to hyperammonaemia and power-based EEG parameters may help in its neurophysiological definition, which, to date, has generally been based on EEG frequency indices.

Dissipation of sleep pressure is stable across adolescence.

The sleep electroencephalogram (EEG) undergoes many changes during adolescence. We assessed whether sleep homeostasis is altered across adolescent development using two measures: the dissipation of slow-wave activity (SWA, 0.6-4.6Hz) across the night and the rate of build-up of SWA in the first non-rapid eye movement (NREM) sleep episode. Furthermore, we examined the association between homeostatic and circadian measures, by correlating the build-up of SWA in the first non-rapid eye movement (NREM) sleep episode with circadian phase. Finally, we compared the dissipation of SWA in individuals with (PH+) and without (PH-) a parental history of alcohol abuse/dependence. Twenty children (8 PH+) and 25 teens (10 PH+) underwent two consecutive polysomnographic recordings at ages 9/10 and 15/16 years and again 1.5-3 years later. Thirteen young adults (ages 20-23 years; no PH+) were assessed one time. The decay of Process S was modeled for each individual at each assessment using data from both recordings. Four parameters of Process S were derived for EEG derivation C3/A2: time constant of the decay, lower asymptote (LA), the level of S at sleep onset (S(SO)), and S(SO) minus LA. We found no change in these parameters between assessments for the children and teen cohorts. Between-subject analysis of the follow-up assessment for children (ages 11-13 years) and the initial assessment for teens (ages 15/16 years) showed no difference in these parameters, nor did follow-up assessment of teens (ages 17-19 years) compared to the single assessment of young adults (ages 20-23 years). Similarly, we observed no developmental changes in the rate of the build-up of SWA in the first NREM sleep episode for our within- and between-subject analyses, or a correlation between this measure and circadian phase for either cohort. With regard to parental alcohol history, we found no difference in the dissipation of sleep pressure between PH+ and PH- children and teens. These results indicate that the dissipation of sleep pressure does not change across adolescent development, is not correlated with circadian phase, and does not differ between PH+ and PH- children and teens.

Developmental changes in brain connectivity assessed using the sleep EEG.

Adolescence represents a time of significant cortical restructuring. Current theories posit that during this period connections between frequently utilized neural networks are strengthened while underutilized synaptic connections are discarded. The aim of the present study was to examine the developmental evolution of connectivity between brain regions using the sleep EEG. All-night sleep EEG recordings in two longitudinal cohorts (children and teens) followed at 1.5-3 year intervals and one cross-sectional cohort (adults) were analyzed. The children and teen cohorts were 9/10 and 15/16 years at the initial assessment; ages of the adults were 20 to 23 years. Intrahemispheric, interhemispheric, and diagonal coherence was measured between all six possible pairings of two central (C3/A2 and C4/A1) and two occipital (O2/A1 and O1/A2) derivations during slow wave, stage 2, and, REM sleep. Within-subjects analyses were performed for the children and teen cohorts, and a linear regression analysis was performed across every assessment of all cohorts. Within-subject analyses revealed a maturational increase in coherence for both age cohorts, though the frequencies, sleep states, and regions differed between cohorts. Regression analysis across all age cohorts showed an overall linear increase in left and right intrahemispheric coherence for all sleep states across frequencies. Furthermore, coherence between diagonal electrode pairs also increased in a linear manner for stage 2 and REM sleep. No age-related trend was found in interhemispheric coherence. Our results indicate that sleep EEG coherence increases with age and that these increases are confined to specific brain regions. This analysis highlights the utility of the sleep EEG to measure developmental changes in brain maturation.

Correlation between sleep and cognitive functions after hemispheric ischaemic stroke.

BACKGROUND: The aim of this study was to test the hypothesis of a link between sleep and cognitive functions, particularly memory and attention, after stroke. METHODS: We studied 11 consecutive patients with first-ever hemispheric ischaemic stroke within eight days after symptoms onset and nine of them at least three months after stroke. Sleep EEG was recorded with a portable system. Cognitive functions were assessed using a standardized battery of tests allowing the estimation of the most relevant domains of cognition. Five age-matched healthy subjects served as controls. RESULTS: The patients were aged 43 +/- 12 years (18-59). In five patients stroke was right-sided and in six patients left-sided. In the acute stroke phase a correlation between attention and amounts of slow wave sleep (SWS), Rapid eye movement (REM) sleep and sleep efficiency was found. In the recovery phase verbal/figural memory and attention significantly improved in most patients. Furthermore, an association between (i) verbal/figural (non-verbal) memory and amounts of SWS, REM sleep and sleep efficiency, and between (ii) attention and sleep efficiency was observed. CONCLUSIONS: The results point to a link between sleep and cognitive functions and their recovery after hemispheric stroke. Further studies are needed to determine the specific nature of this link.

Sleep homeostasis in the rat in the light and dark period.

Sleep is regulated by the interaction of a homeostatic (Process S) and a circadian component. The duration of prior wakefulness is the main factor influencing subsequent sleep duration and its intensity. We investigated in the rat whether the sleep-wake history before sleep deprivation (SD) contributes to the effects of sleep loss incurred during the SD. A 24-h baseline recording was followed by 6 h SD at light onset (SD-Light, n=7), or at dark onset (SD-Dark, n=8) and 18 h recovery. Both SDs led to a pronounced increase in slow wave activity (SWA, EEG power between 0.75 and 4.0 Hz) in NREM sleep and increased sleep consolidation. The prolongation of sleep episodes was associated with increased intra-episode SWA. The amount of waking before the SD correlated positively with the SWA increase during recovery, and SWA levels before SD were negatively correlated with their subsequent increase. The time-course of SWA (Process S) as well as of single frequency bins within the SWA band was successfully simulated based on vigilance-state distribution. The time constant of the exponential monotonic decay (Td) was higher for the 0.75-1.0 Hz bin compared to all remaining frequency bins of the SWA band, reflecting a slower process determining the slow EEG component during sleep. The data show that the homeostatic response after SD, consisting of increased sleep intensity and sleep consolidation is determined by a combination of SD and the preceding vigilance-state history. The slower dynamics of low frequency delta power compared to fast delta frequencies point to heterogeneity within the traditionally defined SWA band.

Sleep-wake disturbances in sporadic Creutzfeldt-Jakob disease.

BACKGROUND: The prevalence and characteristics of sleep-wake disturbances in sporadic Creutzfeldt-Jakob disease (sCJD) are poorly understood. METHODS: Seven consecutive patients with definite sCJD underwent a systematic assessment of sleep-wake disturbances, including clinical history, video-polysomnography, and actigraphy. Extent and distribution of neurodegeneration was estimated by brain autopsy in six patients. Western blot analyses enabling classification and quantification of the protease-resistant isoform of the prion protein, PrPSc, in thalamus and occipital cortex was available in four patients. RESULTS: Sleep-wake symptoms were observed in all patients, and were prominent in four of them. All patients had severe sleep EEG abnormalities with loss of sleep spindles, very low sleep efficiency, and virtual absence of REM sleep. The correlation between different methods to assess sleep-wake functions (history, polysomnography, actigraphy, videography) was generally poor. Brain autopsy revealed prominent changes in cortical areas, but only mild changes in the thalamus. No mutation of the PRNP gene was found. CONCLUSIONS: This study demonstrates in sporadic Creutzfeldt-Jakob disease, first, the existence of sleep-wake disturbances similar to those reported in fatal familial insomnia in the absence of prominent and isolated thalamic neuronal loss, and second, the need of a multimodal approach for the unambiguous assessment of sleep-wake functions in these patients.

Trait-like individual differences in the human sleep electroencephalogram.

We aimed to examine whether commonly observed individual differences in sleep architecture and the sleep electroencephalogram reflect individual traits, which are amenable to a genetic investigation of human sleep. We studied intra-individual stability and inter-individual variation in sleep and sleep electroencephalogram spectra across four baseline recordings of eight healthy young men. A similarity concept based on Euclidean distances between vectors was applied. Visually scored sleep variables served as feature vector components, along with electroencephalogram power spectra in non-rapid-eye-movement and rapid-eye-movement sleep. The distributions of similarity coefficients of feature vectors revealed a clear distinction between high within-subject similarity (i.e. stability), and low between-subject similarity (i.e. variation). Moreover, a cluster analysis based on electroencephalogram spectra in both non-rapid-eye-movement and rapid-eye-movement sleep segregated all four baseline nights of each individual into a distinct cluster. To investigate whether high and low sleep pressure affects the similarity coefficients, normalized non-rapid-eye-movement sleep electroencephalogram spectra of the first and second half of the recordings were compared. Because the electroencephalogram changes systematically in the course of the night, within-subject variation no longer differed from between-subject variation. In conclusion, our data provide evidence for trait-like characteristics in the sleep electroencephalogram. Further studies may help to identify distinct phenotypes to search for genes underlying functional aspects of undisturbed human sleep.

Analysis of oscillatory patterns in the human sleep EEG using a novel detection algorithm.

The different brain states during sleep are characterized by the occurrence of distinct oscillatory patterns such as spindles or delta waves. Using a new algorithm to detect oscillatory events in the electroencephalogram (EEG), we studied their properties and changes throughout the night. The present approach was based on the idea that the EEG may be described as a superposition of stochastically driven harmonic oscillators with damping and frequency varying in time. This idea was implemented by fitting autoregressive models to the EEG data. Oscillatory events were detected, whenever the damping of one or more frequencies was below a predefined threshold. Sleep EEG data of eight healthy young males were analyzed (four nights per subject). Oscillatory events occurred mainly in three frequency ranges, which correspond roughly to the classically defined delta (0-4.5 Hz), alpha (8-11.5 Hz) and sigma (11.5-16 Hz) bands. Their incidence showed small intra- but large inter-individual differences, in particular with respect to alpha events. The incidence and frequency of the events was characteristic for sleep stages and non-rapid eye movement (REM)-REM sleep cycles. The mean event frequency of delta and sigma (spindle) events decreased with the deepening of sleep. It was higher in the second half of the night compared with the first one for delta, alpha and sigma oscillations. The algorithm provides a general framework to detect and characterize oscillatory patterns in the EEG and similar signals.

Exposure to pulse-modulated radio frequency electromagnetic fields affects regional cerebral blood flow.

We investigated the effects of radio frequency electromagnetic fields (RF EMF) similar to those emitted by mobile phones on waking regional cerebral blood flow (rCBF) in 12 healthy young men. Two types of RF EMF exposure were applied: a 'base-station-like' and a 'handset-like' signal. Positron emission tomography scans were taken after 30 min unilateral head exposure to pulse-modulated 900 MHz RF EMF (10 g tissue-averaged spatial peak-specific absorption rate of 1 W/kg for both conditions) and sham control. We observed an increase in relative rCBF in the dorsolateral prefrontal cortex on the side of exposure. The effect depended on the spectral power in the amplitude modulation of the RF carrier such that only 'handset-like' RF EMF exposure with its stronger low-frequency components but not the 'base-station-like' RF EMF exposure affected rCBF. This finding supports our previous observation that pulse modulation of RF EMF is necessary to induce changes in the waking and sleep EEG, and substantiates the notion that pulse modulation is crucial for RF EMF-induced alterations in brain physiology.

The dynamics of spindles and EEG slow-wave activity in NREM sleep in mice.

A quantitative analysis of spindles and spindle-related EEG activity was performed in C57BL/6 mice. The hypothesis that spindles are involved in sleep regulatory mechanisms was tested by investigating their occurrence during 24 h and after 6 h sleep deprivation (SD; n = 7). In the frontal derivation distinct spindle events were characterized as EEG oscillations with a dominant frequency approximately at 11 Hz. Spindles were most prominent during NREM sleep and increased before NREM-REM sleep transitions. Whereas spindles increased concomitantly with slow wave activity (SWA, EEG power between 0.5 and 4.0 Hz) at the beginning of the NREM sleep episode, these measures showed an opposite evolution prior to the transition to REM sleep. The 24-h time course of spindles showed a maximum at the end of the 12-h light period, and was a mirror image of SWA in NREM sleep. After 6 h SD the spindles in NREM sleep were initially suppressed, and showed a delayed rebound. In contrast, spindles occurring immediately before the transition to REM sleep were enhanced during the first 2 h of recovery. The data suggest that spindles in NREM sleep may be involved in sleep maintenance, while spindles heralding the transition to REM sleep may be related to mechanisms of REM sleep initiation.

Sleep and rest facilitate auditory learning.

Sleep is superior to waking for promoting performance improvements between sessions of visual perceptual and motor learning tasks. Few studies have investigated possible effects of sleep on auditory learning. A key issue is whether sleep specifically promotes learning, or whether restful waking yields similar benefits. According to the "interference hypothesis," sleep facilitates learning because it prevents interference from ongoing sensory input, learning and other cognitive activities that normally occur during waking. We tested this hypothesis by comparing effects of sleep, busy waking (watching a film) and restful waking (lying in the dark) on auditory tone sequence learning. Consistent with recent findings for human language learning, we found that compared with busy waking, sleep between sessions of auditory tone sequence learning enhanced performance improvements. Restful waking provided similar benefits, as predicted based on the interference hypothesis. These findings indicate that physiological, behavioral and environmental conditions that accompany restful waking are sufficient to facilitate learning and may contribute to the facilitation of learning that occurs during sleep.

Interhemispheric coherence of the sleep electroencephalogram in mice with congenital callosal dysgenesis.

Regional differences in the effect of sleep deprivation on the sleep electroencephalogram (EEG) may be related to interhemispheric synchronization. To investigate the role of the corpus callosum in interhemispheric EEG synchronization, coherence spectra were computed in mice with congenital callosal dysgenesis (B1) under baseline conditions and after 6-h sleep deprivation, and compared with the spectra of a control strain (C57BL/6). In B1 mice coherence was lower than in controls in all vigilance states. The level of coherence in each of the three totally acallosal mice was lower than in the mice with only partial callosal dysgenesis. The difference between B1 and control mice was present over the entire 0.5-25 Hz frequency range in non-rapid eye movement sleep (NREM sleep), and in all frequencies except for the high delta and low theta band (3-7 Hz) in rapid eye movement (REM) sleep and waking. In control mice, sleep deprivation induced a rise of coherence in the Delta band of NREM sleep in the first 2 h of recovery. This effect was absent in B1 mice with total callosal dysgenesis and attenuated in mice with partial callosal dysgenesis. In both strains the effect of sleep deprivation dissipated within 4 h. The results show that EEG synchronization between the hemispheres in sleep and waking is mediated to a large part by the corpus callosum. This applies also to the functional changes induced by sleep deprivation in NREM sleep. In contrast, interhemispheric synchronisation of theta oscillations in waking and REM sleep may be mediated by direct interhippocampal connections.

Dimensional complexity and spectral properties of the human sleep EEG. Electroencephalograms.

OBJECTIVE: The relevance of the dimensional complexity (DC) for the analysis of sleep EEG data is investigated and compared to linear measures. METHODS: We calculated DC of artifact-free 1 min segments of all-night sleep EEG recordings of 4 healthy young subjects. Non-linearity was tested by comparing with DC values of surrogate data. Linear properties of the segments were characterized by estimating the self-similarity exponent alpha based on the detrended fluctuation analysis which quantifies the persistence of the signal and by calculating spectral power in the delta, theta, alpha and sigma bands, respectively. RESULTS: We found weak nonlinear signatures in all sleep stages, but most pronounced in sleep stage 2. Strong correlations between DC and linear measures were established for the self-similarity exponent alpha and delta power, respectively. CONCLUSIONS: The dimensional complexity of the sleep EEG is influenced by both linear and nonlinear features. It cannot be directly interpreted as a nonlinear synchronization measure of brain activity, but yields valuable information when combined with the analysis of linear measures.

Electromagnetic fields, such as those from mobile phones, alter regional cerebral blood flow and sleep and waking EEG.

Usage of mobile phones is rapidly increasing, but there is limited data on the possible effects of electromagnetic field (EMF) exposure on brain physiology. We investigated the effect of EMF vs. sham control exposure on waking regional cerebral blood flow (rCBF) and on waking and sleep electroencephalogram (EEG) in humans. In Experiment 1, positron emission tomography (PET) scans were taken after unilateral head exposure to 30-min pulse-modulated 900 MHz electromagnetic field (pm-EMF). In Experiment 2, night-time sleep was polysomnographically recorded after EMF exposure. Pulse-modulated EMF exposure increased relative rCBF in the dorsolateral prefrontal cortex ipsilateral to exposure. Also, pm-EMF exposure enhanced EEG power in the alpha frequency range prior to sleep onset and in the spindle frequency range during stage 2 sleep. Exposure to EMF without pulse modulation did not enhance power in the waking or sleep EEG. We previously observed EMF effects on the sleep EEG (A. A. Borbély, R. Huber, T. Graf, B. Fuchs, E. Gallmann and P. Achermann. Neurosci. Lett., 1999, 275: 207-210; R. Huber, T. Graf, K. A. Cote, L. Wittmann, E. Gallmann, D. Matter, J. Schuderer, N. Kuster, A. A. Borbély, and P. Achermann. Neuroreport, 2000, 11: 3321-3325), but the basis for these effects was unknown. The present results show for the first time that (1) pm-EMF alters waking rCBF and (2) pulse modulation of EMF is necessary to induce waking and sleep EEG changes. Pulse-modulated EMF exposure may provide a new, non-invasive method for modifying brain function for experimental, diagnostic and therapeutic purposes.

Power and coherence of sleep spindle frequency activity following hemispheric stroke.

Brainstem and thalamic structures are known to play a critical role in modulating sleep-wake cycles, but the extent to which the cerebral hemispheres are involved remains unclear. To study the role of the cerebral hemispheres in generating sleep EEG patterns, all-night polysomnographic recordings were collected in subjects with brain damage (n = 30) caused by hemispheric stroke and in hospitalized controls (n = 12). Recordings were made in the acute (< or =10 days post-stroke), subchronic (11-35 days post-stroke) and chronic (>60 days post-stroke) phases of stroke. Bipolar and referential EEG derivations were recorded. Standard sleep stage scoring was conducted using the referential derivation placed opposite the lesion. Sleep stage 2 power and coherence spectra were calculated based on recordings from bipolar derivations. In the mean spectra, the highest spindle frequency peak was identified and its size was calculated relative to the background spectrum. Analysis of visually scored EEG data indicated that, compared with controls, acute phase brain-damaged subjects had lower sleep efficiency and increased waking after sleep onset. The durations of rapid eye movement and non-rapid eye movement sleep stages did not differ significantly between brain-damaged subjects and hospitalized controls. Spectral analyses revealed that, compared with hospitalized controls, brain-damaged subjects had significantly reduced spindle peak sizes in the power and coherence spectra from derivations ipsilateral to the lesion. Within-subject comparisons across time demonstrated that the power and coherence of sleep spindle frequency activity increased significantly from the acute to the chronic phases of stroke, suggesting that plastic mechanisms allowed the possibility of recovery. Our findings provide novel evidence that the cerebral hemispheres are important in generating coherent sleep spindles in humans, and they are consonant with prior empirical and theoretical evidence that corticothalamic projections modulate the generation of synchronous spindle oscillations. Because spindle oscillations are thought to be involved in blocking sensory input to the cortex during sleep, the decrease in synchronous spindle frequency activity following hemispheric stroke may contribute to the observed reduction in sleep continuity.

Brain sources of EEG gamma frequency during volitionally meditation-induced, altered states of consciousness, and experience of the self.

Multichannel EEG of an advanced meditator was recorded during four different, repeated meditations. Locations of intracerebral source gravity centers as well as Low Resolution Electromagnetic Tomography (LORETA) functional images of the EEG 'gamma' (35-44 Hz) frequency band activity differed significantly between meditations. Thus, during volitionally self-initiated, altered states of consciousness that were associated with different subjective meditation states, different brain neuronal populations were active. The brain areas predominantly involved during the self-induced meditation states aiming at visualization (right posterior) and verbalization (left central) agreed with known brain functional neuroanatomy. The brain areas involved in the self-induced, meditational dissolution and reconstitution of the experience of the self (right fronto-temporal) are discussed in the context of neural substrates implicated in normal self-representation and reality testing, as well as in depersonalization disorders and detachment from self after brain lesions.